JAX Mouse Strain Datasheet - 000659

C3H/HeJ

Stock No:: 000659 |; C3H

Inbred Strain

Readily Available

Overview

Also Known As: C3H, C3, C3H Heston

C3H/HeJ mice, commonly called C3H, are used as a general purpose strain in a wide variety of research areas including cancer, infectious disease, sensorineural, and cardiovascular biology research. A spontaneous mutation in Tlr4 occurred in C3H/HeJ at the lipopolysaccharide response locus (mutation in toll-like receptor 4 gene, Tlr4^Lps-d) making C3H/HeJ mice more resistant to endotoxin. C3H/HeJ mice are highly susceptible to infection by Gram-negative bacteria such as Salmonella enterica. The C3H substrains at The Jackson Laboratory are homozygous for the retinal degeneration 1 mutation (Pde6b^rd1), causing blindness by weaning age.

Genetic overview

Genetic Background	Generation
	Contact Technical Support (27-JUL-18)

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Research Applications

Cancer Research
Cardiovascular Research
Immunology, Inflammation and Autoimmunity Research
Neurobiology Research
Research Tools
Sensorineural Research

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Base Price

Starting at:

$25.33 Domestic price for male 3-week

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Details

Important Note

This strain does not carry mouse mammary tumor virus (MMTV). This strain is homozygous for retinal degeneration allele Pde6b^rd1, the defective lipopolysaccharide response allele Tlr4^Lps-d, and for a chromosomal inversion on Chromosome 6. A sighted alternative is Stock No. 003648, C3Sn.BLiA-Pde6b⁺/DnJ.

Detailed Description

C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6b^rd1), which causes blindness by weaning age, but lack the nob5 allele of Gpr179 (Chang, 2015). White belly spots, ranging in phenotype from a few white hairs to a defined spot are common in C3H/HeJ mice. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687). C3H/HeJ mice spontaneously develop alopecia areata (AA) at a reported incidence of approximately 0.25% by 5 months of age. In older mice (12-18 months old), incidences as high as approximately 20% are reported. Females as young as 3-5 months can develop AA, but onset typically is delayed until after 6 months in males. Alopecia areata can be surgically-induced by grafting a small piece of skin from an older, donor animal with AA onto a younger, isogenic C3H/HeJ recipient.

A spontaneous mutation occurred in C3H/HeJ at the lipopolysaccharide response locus (later identified as a mutation in the toll-like receptor 4 gene, Tlr4^Lps-d) making C3H/HeJ mice endotoxin resistant. C3H/HeJ (Tlr4^Lps-d) mice are highly susceptible to infection by Gram-negative bacteria such as Salmonella enterica. Mice infected with Salmonella exhibit delayed chemokine production, impaired nitric oxide generation and attenuated cellular immune responses. Mortality in infected mice appears to result from enhanced bacterial growth within the liver Kupffer cell network (Vazquez-Torres et al., 2004).The C3H/HeJ substrain is homozygous for an inversion on Chromosome 6 (symbol: In(6)1J). The inversion covers 20% of Chromosome 6 between D6Mit124 (~30.3 cM) and D6Mit150 (~51.0 cM), but results in no reported phenotype. Results from screening other C3H substrains and cryopreserved stock from C3H/HeJ suggest that the mutation arose after 1952. The spontaneous mutation, spike wave discharge 1 (Gria4^spkw1), is present in C3H/HeJ, but not C3HeB/FeJ. Mice homozygous for this mutation exhibit a modest incidence of absence seizures. This strain is also homozygous for a hypomorphic allele in Pcnx2, which is caused by an IAP insertion and which dampens the severity of the absence seizure phenotype caused by Gria4^spkw1 (Frankel et al., 2014).

Development

The C3H parent strain was developed by LC Strong in 1920 from a cross of a Bagg albino female with a DBA male followed by selection for high incidence of mammary tumors. This high incidence resulted from exogenous mouse mammary tumor virus (MMTV) transmitted through the mother's milk. The Jackson Laboratory maintains four C3H substrains, C3H/HeJ (Stock No. 000659), C3H/HeOuJ (Stock No. 000635), C3HeB/FeJ (Stock No. 000658) and C3H/HeSnJ (Stock No. 000661) that are now free of exogenous MMTV. C3H/HeJ and C3H/HeOuJ mice previously carried MMTV but were rederived in 1999 during planned efforts to increase the overall health status of the mice and the virus was not reintroduced. C3H/HeJ and C3H/HeOuJ substrains were separated in 1952 and are genetically very similar. However, a spontaneous mutation occurred in C3H/HeJ sometime between 1960 and 1968 at lipopolysaccharide response locus (mutation in toll-like receptor 4 gene, Tlr4^lps) making C3H/HeJ mice endotoxin resistant while the other three C3H strains are endotoxin sensitive.

Selected References

Akeson EC; Donahue LR; Beamer WG; Shultz KL; Ackert-Bicknell C; Rosen CJ; Corrigan J; Davisson MT. 2006. Chromosomal inversion discovered in C3H/HeJ mice. Genomics 87(2):311-3. PubMed: 16309882 MGI: J:105810
Chang B. 2015. Survey of the nob5 mutation in C3H substrains. Mol Vis 21:1101-5. PubMed: 26396487 MGI: J:224435
Cheers C; McKenzie IF. 1978. Resistance and susceptibility of mice to bacterial infection: genetics of listeriosis. Infect Immun 19(3):755-62. PubMed: 305895 MGI: J:5965
Dragani TA; Manenti G; Gariboldi M; Degregorio L; Pierotti MA. 1995. Genetics of liver tumor susceptibility in mice. Toxicol Lett 82-3:613-619. PubMed: 8597117 MGI: J:31816
Frankel WN; Mahaffey CL; McGarr TC; Beyer BJ; Letts VA. 2014. Unraveling genetic modifiers in the gria4 mouse model of absence epilepsy. PLoS Genet 10(7):e1004454. PubMed: 25010494 MGI: J:228536
Heston WE; Vlahakis G. 1971. Mammary tumors, plaques, and hyperplastic alveolar nodules in various combinations of mouse inbred strains and the different lines of the mammary tumor virus. Int J Cancer 7(1):141-8. PubMed: 4322934 MGI: J:24674
Outzen HC; Corrow D; Shultz LD. 1985. Attenuation of exogenous murine mammary tumor virus virulence in the C3H/HeJ mouse substrain bearing the Lps mutation. J Natl Cancer Inst 75(5):917-23. PubMed: 2997536 MGI: J:24864
Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11. PubMed: 15081119 MGI: J:89298

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Genetics

Ahr^b-2

Allele Symbol: Ahr^b-2

Allele Name	b-2 variant
Allele Type	Not Applicable
Allele Synonym(s)	Ah^b-2; Ah^h
Gene Symbol and Name	Ahr, aryl-hydrocarbon receptor
Gene Synonym(s)	Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity
Strain of Origin	BALB/cBy
Chromosome	12
General Note	C57BL/6 carries the responsive Ahr^b allele; DBA/2 carries nonresponsive Ahr^d. Heterozygotes (Ahr^b/Ahr^d) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahr^b-1; Ahr^b-2 is carried by BALB/cBy, A, and C3H; and Ahr^b-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahr^b-1 and Ahr^d have been determined (J:17460). Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains
Molecular Note	This allele encodes a high affinity, heat labile, 104 kDa receptor containing 848 amino acids. Sequencing studies of cDNA from C57BL/6J congenic mice homozygous for this allele identified nucleotide substitutions in the ORF that would cause 5 amino acid differences between the C57BL/6J and BALB/cBy peptides, and 2 amino acid differences between the BALB/cBy and DBA/2J peptides. A T to C transition in exon 11 replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the BALB/cBy allele. This change would extend translation of the BALB/cBy mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa, vs 95 kDa for the C57BL/6J allele).

Cd5^a

Allele Symbol: Cd5^a

Allele Name	a variant
Allele Type	Spontaneous (Not Applicable)
Allele Synonym(s)	CD5.1; Ly-1.1
Gene Symbol and Name	Cd5, CD5 antigen
Gene Synonym(s)	LEU1; Ly-1; Ly-1; Ly-12; Ly-12; Ly-A; Lyt-1; Lyt-1; T-lymphocyte antigen 1; T1; lymphocyte antigen 1; lymphocyte antigen 12
Strain of Origin	multiple strains
Chromosome	19
Molecular Note	Sequence analysis of C3H/HeJ showed that this polymorphic variant has point mutations relative to the b variant that result in valine instead of isoleucine at amino acid 9, leucine instead of glutamine at amino acid 52, and isoleucine instead of phenylalanine at amino acid 71, all within the amino terminal scavenger receptor cysteine-rich D1 domain, in addition to 7 silent point mutations. This allele is found in many inbred strains including CBA/J, C3H and DBA substrains.

Gria4^spkw1

Allele Symbol: Gria4^spkw1

Allele Name	spike wave discharge 1
Allele Type	QTL
Allele Synonym(s)	Gria4^IAP
Gene Symbol and Name	Gria4, glutamate receptor, ionotropic, AMPA4 (alpha 4)
Gene Synonym(s)	GLUR4; GLUR4C; GLURD; GluA4; GluR-D; GluR4; Glur-4; Glur-4; Glur4; Glur4; Gluralpha4; NEDSGA; glutamate receptor 4; spike wave 1; spkw1; spkw1
Strain of Origin	C3H/HeJ
Chromosome	9
General Note	This allele interacts with spkw2. Animals with the highest incidence of spike wave discharges are homozygous for C3H/HeJ-derived alleles at spkw1 and heterozygous for C57BL/6J and C3H/HeJ alleles at spkw2.
Molecular Note	This mutation was originally identified as a QTL allele conferring increased incidence of spike wave discharges in the brains of C3H/HeJ mice as compared to C57BL/6J. Genomic PCR and sequencing showed a full-length intracisternal A-particle (IAP) proviral insertion in the last intron of Gria4 in C3H/HeJ mice. qRT-PCR showed a 10-fold difference in C3H/HeJ and C3HeB/FeJ substrains in transcripts detected between exons flanking the IAP-containing intron, and a neglible difference between upstream exon transcript levels in these substrains. Gria4 protein levels in C3H/HeJ cerebella are reduced compared with controls.

In(6)1J

Allele Symbol: In(6)1J

Allele Name	inversion, Chr 6, Jackson 1
Allele Type	Spontaneous
Allele Synonym(s)
Gene Symbol and Name	In(6)1J, inversion, Chr 6, Jackson 1
Gene Synonym(s)
Strain of Origin	C3H/HeJ
Chromosome	6
General Note	C3H/HeJ and C3H/HeJBir carry this inversion; C3H/HeSnJ and C3HeB/FeJ do not. Examination of recombination distances in Recombinant Inbred (RI) strain sets developed using C3H/HeJ as a progenitor suggest none of these harbor the inversion. Mouse strains carrying spontaneous mutations that arose on the C3H/HeJ background after 1965-1970 could carry the inversion and are expected to if the mutation arose after the early 1970s.
Molecular Note	The In(6)1J inversion covers approximately 20% of Chr 6 in C3H/HeJ mice. Therefore, linkage crosses using C3H/HeJ will show no recombination in this region of Chr 6. Genetic analyses of congenic construction crosses suggested that the suppressed region lies between D6Mit124 (cytological band 6C3) and D6Mit150 (cytological band 6F1). FISH analyses using flanking BACs detected a paracentric chromosomal region between ~73 Mb and ~116 Mb.

Pcnx2^C3H/HeJ

Allele Symbol: Pcnx2^C3H/HeJ

Allele Name	C3H/HeJ
Allele Type	Spontaneous (Hypomorph)
Allele Synonym(s)	Pcnxl2^IAP
Gene Symbol and Name	Pcnx2, pecanex homolog 2
Gene Synonym(s)	AU067631; E330039K12Rik; E330039K12Rik; PCNXL2; Pcnxl2; Pcnxl2; RGD1305883; RIKEN cDNA E330039K12 gene; expressed sequence AU067631; pecanex-like 2 (Drosophila)
Strain of Origin	C3H/HeJ
Chromosome	8
Molecular Note	This IAP insertion in intron 19 causes diminished expression of this gene by RT-PCR in C3H/HeJ and is not found in C3HeB/FeJ, C3H/HeOuJ, or C3H/HeSnJ.

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Allele Name	retinal degeneration 1
Allele Type	Spontaneous
Allele Synonym(s)	Pdeb^rd1; rd; rd-1; rd1; rodless retina
Gene Symbol and Name	Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Gene Synonym(s)	CSNB3; CSNBAD2; GMP-PDEbeta; PDEB; Pdeb; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; r; rd; rd; rd-1; rd1; rd1; rd10; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10
Strain of Origin	various
Chromosome	5
General Note	The following inbred strains are known to be homozygous for Pde6b: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.
Molecular Note	Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested.

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Allele Name	defective lipopolysaccharide response
Allele Type	Spontaneous
Allele Synonym(s)	TLR4-M; TLR4-Mu; TLR4^lps-def; TLR4d; Tlr4^-; Tlr4^d; Tlr^Lps-d; lps^d; mutant TLR4
Gene Symbol and Name	Tlr4, toll-like receptor 4
Gene Synonym(s)	ARMD10; CD284; Lps; Lps; RAS-like, family 2, locus 8; Rasl2-8; Rasl2-8; TLR-4; TOLL; lipopolysaccharide response; lipopolysaccharide response
Strain of Origin	C3H/HeJ
Chromosome	4
General Note	C3H/HeJ mice carry this allele. Various combinations of Lps-associated traits have been followed in crosses between C3H/HeJ and other C3H substrains, and the traits have in all cases segregated together (J:30692, J:5557, J:5593, J:5938). Some of the traits show dominance of the Tlr4^lps-n allele; others, including Tlr4^Lps-d, show codominance. Genbank ID for this allele: AF095353
Molecular Note	This allele corresponds to a mutation in the third exon of the gene. A C to A substitution at nucleotide position 2342 results in an amino acid substitution that replaces proline with histidine at position 712.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Cancer Research
- Increased Tumor Incidence
  - Hepatomas
  - Mammary Gland Tumors
  - Mammary Gland Tumors: late onset
Cardiovascular Research
- Diet-Induced Atherosclerosis
  - Relatively Resistant
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - Tlr deficiency
Neurobiology Research
- Epilepsy
Research Tools
- General Purpose
- Infectious Disease
  - Anthrax
Sensorineural Research
- Retinal Degeneration
  - Homozygous for Pde6b^rd1

Genotype: Pde6b^rd1 related

Sensorineural Research
- Retinal Degeneration

Genotype: Tlr4^Lps-d related

Immunology, Inflammation and Autoimmunity Research
- CD Antigens, Antigen Receptors, and Histocompatibility Markers
  - Tlr deficiency
- Immunodeficiency
  - Tlr deficiency
- Inflammation
  - Tlr deficiency

Mammalian Phenotype Terms by Genotype

Genotype: Ahr^b-2/Ahr^b-2
C3H/He

mortality/aging

increased sensitivity to xenobiotic induced morbidity/mortality
- mice are susceptible to DMBA induced lethality

homeostasis/metabolism phenotype

increased physiological sensitivity to xenobiotic
- mice are susceptible to the pathological effects of DMBA and exhibit lethality, weight loss, peritonitis, decreased spleen weight, and decreased thymus weight

increased sensitivity to xenobiotic induced morbidity/mortality
- mice are susceptible to DMBA induced lethality

Genotype: Gria4^spkw1/Gria4^spkw1
C3H/HeJ

behavior/neurological phenotype

absence seizures
- mice show higher spike wave discharge incidence than C3HeB/FeJ or C57BL/6 mice

nervous system phenotype

absence seizures
- mice show higher spike wave discharge incidence than C3HeB/FeJ or C57BL/6 mice

Genotype: In(6)1J/In(6)1J
C3H/HeJ

normal phenotype

no abnormal phenotype detected
- no phenotype is known to be associated with this chromosomal inversion

Genotype: Pde6b^rd1/Pde6b^rd1
C3H/HeJ

vision/eye phenotype

abnormal retinal outer nuclear layer morphology
- nearly complete absence of outer nuclear layer

absent photoreceptor outer segment

retinal degeneration
- entire outer retina is destroyed, however the inner retina remains intact

vision/eye phenotype
- despite the absence of rods, mice exhibit normal photopotentiation (defined as a 50% augmentation in pupillary light response (PLR) compared to pre-bright light PLR during a one minute dim blue light exposure after bright light exposure)

nervous system phenotype

absent photoreceptor outer segment

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
involves: C3H/HeJ

immune system phenotype

abnormal T-helper 2 physiology
- Th2 responses elevated after induction of autoimmune arthritis

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

abnormal tumor necrosis factor level
- diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion
- macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage

increased susceptibility to bacterial infection
- increased K. pneumoniae levels in the lung
- increased sensitivity to gram (-) infection
- low responsiveness of spleen cells to lipopolysaccharides
- significantly shortened survival after infection with Klebsiella pneumoniae

increased susceptibility to induced arthritis
- reduced susceptibility to arthritis induced by type II collagen

hearing/vestibular/ear phenotype

hearing/vestibular/ear phenotype
- cisplatin and lipopolysaccharide treatment does not lead to significant increases in auditory brainstem response as is observed in controls

behavior/neurological phenotype

hyporesponsive to tactile stimuli
- reduced mechanical allodynia after nerve injury

increased thermal nociceptive threshold
- attenuated response to heat

skeleton phenotype

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

increased susceptibility to induced arthritis
- reduced susceptibility to arthritis induced by type II collagen

muscle phenotype

muscle phenotype
- MCP-1 (monocyte chemoattractant protein-1) release from isolated mouse aorta smooth muscle cells (MAoSMC) by stimulation with dsRNA is normal relative to controls

integument phenotype

hyporesponsive to tactile stimuli
- reduced mechanical allodynia after nerve injury

increased thermal nociceptive threshold
- attenuated response to heat

nervous system phenotype

abnormal glial cell apoptosis
- isolated microglia exposed to LPS are resistant to apoptosis

homeostasis/metabolism phenotype

abnormal circulating enzyme level
- increased HO-1 expression
- myeloperoxidase levels are reduced after 90 minutes of liver ischemia followed by 6 hours of reperfusion

abnormal tumor necrosis factor level
- diminished TNF alpha expression after 90 minutes of liver ischemia followed by 6 hours of reperfusion
- macrophage primary but not secondary necrotic cells with residual stimulatory affect on TNF alpha production by macrophage

decreased circulating alanine transaminase level
- serum levels decreased after 90 minutes of liver ischemia followed by 6 hours of reperfusion

hematopoietic system phenotype

abnormal T-helper 2 physiology
- Th2 responses elevated after induction of autoimmune arthritis

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

cellular phenotype

abnormal glial cell apoptosis
- isolated microglia exposed to LPS are resistant to apoptosis

abnormal osteoclast differentiation
- antibody to IFN-beta or to IFNAR1 reverses inhibition of osteoclast formation induced by RANKL
- lipopolysaccharide fails to inhibit RANKL induced osteoclast formation as it does in controls

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C3H/HeJ-Tlr4^Lps-d

mortality/aging

decreased sensitivity to induced morbidity/mortality
- bacterial lipoteichoic acid exposure after priming by IFNgamma and sensitization with D-galactosamine induces lethal shock in Tlr4-deficient mutants, while Tlr2- and Tlr2/4-doubly deficient mice are protected
- heat-inactivated E. coli exposure results in fatal toxemia as in wild type mice
- heat-inactivated E. coli exposure results in fatal toxemia as in wild-type mice
- systemic challenge with Myr₃-CSK₄ (a synthetic lipopeptide) after D-galactosamine induces lethal shock in wild-type mice, but mutants are protected

increased susceptibility to viral infection induced morbidity/mortality
- 10 days after intranasal infection with 5 x 10⁵ pfu Vac-GFL 70% of mice succumb unlike wild-type controls that all survive

respiratory system phenotype

abnormal pulmonary alveolus morphology
- destruction of normal alveolar structures

abnormal respiratory system morphology

abnormal respiratory system physiology

dilated pulmonary alveolar ducts
- enlarged air spaces distal to the terminal bronchioles

enlarged lung
- significantly increased lung volume at 3 months of age in contrast to normal body weights through 12 months

lung inflammation
- no increase in white blood cells or neutrophiles in bronchoalveolar fluid
- white blood cells and neutrophiles are not detected by myeloperoxidase assay

pulmonary edema
- less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation
- resistant to lipopolysaccharide induced lung interstitial edema

nervous system phenotype

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal myelin sheath morphology
- increased myelin destruction at site of spinal cord injury
- no clear delineation between injured and spared tissues

abnormal nervous system morphology

decreased cerebral infarction size
- damage due to middle cerebral artery occlusion is considerably reduced
- infarctions due to cerebral ischemia/reperfusion are smaller in size

decreased neuron apoptosis
- neurons are resistant to apoptosis caused by glucose deficiency

decreased susceptibility to ischemic brain injury
- less inflammation after cerebral ischemia/reperfusion
- less nerve cell swelling after cerebral ischemia/reperfusion
- reduced brain edema after cerebral ischemia/reperfusion
- reduced neurological impairment after cerebral ischemia/reperfusion

behavior/neurological phenotype

abnormal locomotor behavior
- locomotor recovery impaired as measured 4-6 weeks after spinal cord injury

abnormal motor coordination/balance
- impaired recovery of fore-limb-hindlimb coordination as measured 4-6 weeks after spinal cord injury

skeleton phenotype

decreased susceptibility to bone fracture
- bones resistant to fracture

increased bone mass
- increased bone area of the tibia

increased bone mineral content
- greater mineral content

increased bone mineral density
- density continues to increase over time
- significantly increased bone mineral density at 20 weeks

muscle phenotype

abnormal muscle cell glucose uptake
- insulin stimulated glucose uptake by soleus muscle is not affected by palmitate treatment or by other fatty acids

cellular phenotype

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal muscle cell glucose uptake
- insulin stimulated glucose uptake by soleus muscle is not affected by palmitate treatment or by other fatty acids

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

decreased neuron apoptosis
- neurons are resistant to apoptosis caused by glucose deficiency

growth/size/body region phenotype

decreased body size
- always smaller than controls

decreased body weight
- food intake comparable to controls
- lower body weight than controls after 8 weeks on a high fat diet
- weights are 15% lower than controls after 8 months on a high fat diet

decreased susceptibility to weight loss
- reduced weight loss following infection with Vac-GFL

immune system phenotype

abnormal cytokine level
- keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide
- macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide

abnormal interleukin level
- Il-6 levels in lungs are unaffected by lipopolysaccharide
- il6 levels increase less on a high fat diet than in controls

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal phagocyte morphology
- however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells
- phagocytes fail to respond to LPS stimulation

abnormal spleen weight
- spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls

abnormal tumor necrosis factor level
- TNF alpha levels in lungs are unaffected by lipopolysaccharide
- less increase in TNF alpha on a high fat diet than in controls

altered susceptibility to infection
- following intranasal infection with 1x10⁴ pfu Vac-GFL (a recombinant vaccinia virus that expresses a reporter protein) weight loss is reduced at 1 - 3 and 7 - 8 days after infection but the decrease in body temperature is more severe at 4 - 7 days afteinfection and viral replication is increaseddays afteinfection and viral replication is increased

increased circulating interleukin-6 level
- increased levels after 7 days of dextran sodium sulfate treatment

increased susceptibility to viral infection induced morbidity/mortality
- 10 days after intranasal infection with 5 x 10⁵ pfu Vac-GFL 70% of mice succumb unlike wild-type controls that all survive

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

lung inflammation
- no increase in white blood cells or neutrophiles in bronchoalveolar fluid
- white blood cells and neutrophiles are not detected by myeloperoxidase assay

hematopoietic system phenotype

abnormal macrophage chemotaxis
- robust macrophage response at the site of spinal injury

abnormal microglial cell physiology
- resistant to lipopolysaccharide induced apoptosis

abnormal phagocyte morphology
- however, response to stimulation with TLR9 or TLR7 and TLR8 with their ligands (CpG and R848, respectively) is similar to in wild-type cells
- phagocytes fail to respond to LPS stimulation

abnormal spleen weight
- spleen weight fails to increase with dextran sodium sulfate treatment as it does in controls

hematopoietic system phenotype
- B cell apoptosis in Peyer's patch is not observed after bile duct ligation (BDL)

homeostasis/metabolism phenotype

abnormal circulating glucose level
- faster disappearance of glucose in response to insulin when on a high fat diet

abnormal circulating leptin level
- increase in blood leptin on a high fat diet is 36% less than in controls

abnormal cytokine level
- keratinocyte derived cytokine levels in lungs are unaffected by lipopolysaccharide
- macrophage inflammatory protein-2 levels in lungs are unaffected by lipopolysaccharide

abnormal fatty acid level
- less elevated than for controls on a high fat diet

abnormal gas homeostasis

abnormal glucose homeostasis

abnormal interleukin level
- Il-6 levels in lungs are unaffected by lipopolysaccharide
- il6 levels increase less on a high fat diet than in controls

abnormal lipid level

abnormal tumor necrosis factor level
- TNF alpha levels in lungs are unaffected by lipopolysaccharide
- less increase in TNF alpha on a high fat diet than in controls

decreased body temperature
- more severe reduction in body temperature following infection with Vac-GFL

decreased cerebral infarction size
- damage due to middle cerebral artery occlusion is considerably reduced
- infarctions due to cerebral ischemia/reperfusion are smaller in size

decreased circulating insulin level
- lower blood insulin levels when on a high fat diet

decreased liver triglyceride level
- less increase in hepatic triglycerides on a high fat diet than in controls

decreased respiratory quotient
- lower respiratory exchange ratio

decreased susceptibility to ischemic brain injury
- less inflammation after cerebral ischemia/reperfusion
- less nerve cell swelling after cerebral ischemia/reperfusion
- reduced brain edema after cerebral ischemia/reperfusion
- reduced neurological impairment after cerebral ischemia/reperfusion

homeostasis/metabolism phenotype
- after BDL, serum alanine transaminase levels are not different from controls

improved glucose tolerance
- lower blood glucose in a glucose tolerance test when on a high fat diet

increased adiponectin level
- levels remain elevated on a high fat diet

increased circulating interleukin-6 level
- increased levels after 7 days of dextran sodium sulfate treatment

increased oxygen consumption
- oxygen consumption is higher after 8 weeks on a high fat diet than controls

pulmonary edema
- less protein leakage into bronchoalveolar lavage fluid after lipopolysaccharide inhalation
- resistant to lipopolysaccharide induced lung interstitial edema

liver/biliary system phenotype

abnormal hepatocyte morphology
- confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL

abnormal liver physiology
- liver protected from ischemia/reperfusion injury

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

decreased liver triglyceride level
- less increase in hepatic triglycerides on a high fat diet than in controls

focal hepatic necrosis

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

adipose tissue phenotype

decreased epididymal fat pad weight
- reduced 40% compared to controls when on a high fat diet
- weight similar to controls on a normal diet

decreased fat cell size
- adipocyte size reduced 30% relative to controls on a high fat diet
- reduced aggregation of macrophage around dying adipocytes than in controls

decreased percent body fat/body weight
- 70% less body fat

cardiovascular system phenotype

rectal hemorrhage
- recover from bleeding after 10 days of treatment when 50% of controls are dead
- rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls

digestive/alimentary phenotype

rectal hemorrhage
- recover from bleeding after 10 days of treatment when 50% of controls are dead
- rectal bleeding after 7 days of dextrose sodium sulfate treatment is reduced relative to controls

Phenotype Information

Body Weight Information - JAX^® Mice Strain C3H/HeJ (000659)

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Additional - In(6)1J related

Akeson EC. 2003. Chromosomal inversion discovered in C3H/HeJ mice JAX Notes 491:15. MGI: J:87486

Also Known As: C3H, C3, C3H Heston

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Selected References

Ahrb-2

Allele Symbol: Ahrb-2

Cd5a

Allele Symbol: Cd5a

Gria4spkw1

Allele Symbol: Gria4spkw1

In(6)1J

Allele Symbol: In(6)1J

Pcnx2C3H/HeJ

Allele Symbol: Pcnx2C3H/HeJ

Pde6brd1

Allele Symbol: Pde6brd1

Tlr4Lps-d

Allele Symbol: Tlr4Lps-d

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Pde6brd1 related

Genotype: Tlr4Lps-d related

Mammalian Phenotype Terms by Genotype

Genotype: Ahrb-2/Ahrb-2C3H/He

mortality/aging

homeostasis/metabolism phenotype

Genotype: Gria4spkw1/Gria4spkw1C3H/HeJ

behavior/neurological phenotype

nervous system phenotype

Genotype: In(6)1J/In(6)1JC3H/HeJ

normal phenotype

Genotype: Pde6brd1/Pde6brd1C3H/HeJ

vision/eye phenotype

nervous system phenotype

Genotype: Tlr4Lps-d/Tlr4Lps-dinvolves: C3H/HeJ

immune system phenotype

hearing/vestibular/ear phenotype

behavior/neurological phenotype

skeleton phenotype

muscle phenotype

integument phenotype

nervous system phenotype

homeostasis/metabolism phenotype

hematopoietic system phenotype

cellular phenotype

Genotype: Tlr4Lps-d/Tlr4Lps-dC3H/HeJ-Tlr4Lps-d

mortality/aging

respiratory system phenotype

nervous system phenotype

behavior/neurological phenotype

skeleton phenotype

muscle phenotype

cellular phenotype

growth/size/body region phenotype

immune system phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

adipose tissue phenotype

cardiovascular system phenotype

digestive/alimentary phenotype

Phenotype Information

References

Additional References

Additional - Ahrb-2 related

Additional - Cd5a related

Additional - Gria4spkw1 related

Additional - Pde6brd1 related

Additional - Tlr4Lps-d related

Additional - In(6)1J related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Ahr^b-2

Allele Symbol: Ahr^b-2

Cd5^a

Allele Symbol: Cd5^a

Gria4^spkw1

Allele Symbol: Gria4^spkw1

Pcnx2^C3H/HeJ

Allele Symbol: Pcnx2^C3H/HeJ

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Tlr4^Lps-d

Allele Symbol: Tlr4^Lps-d

Genotype: Pde6b^rd1 related

Genotype: Tlr4^Lps-d related

Genotype: Ahr^b-2/Ahr^b-2
C3H/He

Genotype: Gria4^spkw1/Gria4^spkw1
C3H/HeJ

Genotype: In(6)1J/In(6)1J
C3H/HeJ

Genotype: Pde6b^rd1/Pde6b^rd1
C3H/HeJ

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
involves: C3H/HeJ

Genotype: Tlr4^Lps-d/Tlr4^Lps-d
C3H/HeJ-Tlr4^Lps-d

Additional - Ahr^b-2 related

Additional - Cd5^a related

Additional - Gria4^spkw1 related

Additional - Pde6b^rd1 related

Additional - Tlr4^Lps-d related