Overview

This strain is currently unavailable due to replenishing of cryopreserved stocks. Interested customers can register interest.

Homozyous Postn (periostin, osteoblast specific factor) targeted mutation mice are more prone to ventricular rupture in the first 10 days after a myocardial infarction, but surviving mice show less fibrosis and better ventricular performance. They also show less fibrosis and hypertrophy following long-term pressure overload. This strain may be useful in studies of cardiac remodeling and hypertrophy.

Donating Investigator

Jeffery D. Molkentin, Cincinnati Children's Hospital

Genetic overview

Genetic Background	Generation

Postn^tm1Jmol

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Postn	periostin, osteoblast specific factor

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Research Applications

Cardiovascular Research

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Details

Detailed Description

Homozyous targeted mutation mice are more prone to ventricular rupture in the first 10 days after a myocardial infarction, but surviving mice show less fibrosis and better ventricular performance. They also show less fibrosis and hypertrophy following long-term pressure overload. The developing feet and hearts of 1-day-old mice show no expression of protein. No significant protein is found in the extracellular matrix of the heart after postnatal development, although the valves show persistent expression within fibroblasts. Homozygotes are slightly smaller than wild-type and heterozygous animals. This strain may be useful in studies of cardiac remodeling and hypertrophy.

Development

Exons 4-10 were replaced with a neomycin resistance cassette placed in the reverse transcriptional orientation. A 129-derived embryonic stem (ES) cell line was used to create the mutation. Chimeric mice were crossed to C57BL/6. This line was maintained on a mixed C57BL/6 and 129 genetic background by the donating laboratory.

Control Suggestions

Approximate Controls

101045 B6129SF2/J

Additional Information

Considerations for Choosing Controls

Selected References

Oka T; Xu J; Kaiser RA; Melendez J; Hambleton M; Sargent MA; Lorts A; Brunskill EW; Dorn GW 2nd; Conway SJ; Aronow BJ; Robbins J; Molkentin JD. 2007. Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling. Circ Res 101(3):313-21PubMed: 17569887 MGI: J:140301

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Genetics

Postn^tm1Jmol

Allele Symbol: Postn^tm1Jmol

Allele Name	targeted mutation 1, Jeffery D Molkentin
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Pn^-
Gene Symbol and Name	Postn, periostin, osteoblast specific factor
Gene Synonym(s)
Strain of Origin	129/Sv
Chromosome	3
Molecular Note	Exons 4 through 10 were replaced with a neo cassette. The absence of protein expression was confirmed by western blot analysis on P1 developing foot and heart extracts.
Mutations Made By	Jeffery Molkentin, Cincinnati Children's Hospital

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Cardiovascular Research
- Heart Abnormalities
  - cardiomyopathy

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Postn^tm1Jmol/Postn^tm1Jmol
involves: 129S/SvEv

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - cyclosporine A-treated mice exhibit normal hypertrophic cardiomyopathy

The following phenotype relates to a compound genotype created using this strain

Genotype: Postn^tm1Jmol/Postn^tm1Jmol
involves: 129/Sv * C57BL/6

cardiovascular system phenotype

abnormal response to cardiac infarction
- following induced myocardial infarct, mice exhibit less of an increase in the number of fibroblasts in the left ventricle compared to in wild-type mice
- following induced myocardial infarct, mice exhibit an increase in death during the first 10 days and a 2-fold increase in the rate of ventricular wall rupture but reduced fibrosis and overall size of scaring compared to similarly treated wild-type mice
- Normal - however, mice maintain better cardiac function compared to wild-type mice over the 8 weeks following the initial scar formation

small heart
- slightly

cellular phenotype

abnormal cell adhesion
- isolated fibroblasts exhibit reduced adhesion to neonatal cardiomyocytes compared to wild-type fibroblasts

growth/size/body region phenotype

decreased body weight
- as adults

homeostasis/metabolism phenotype

abnormal response to cardiac infarction
- following induced myocardial infarct, mice exhibit less of an increase in the number of fibroblasts in the left ventricle compared to in wild-type mice
- following induced myocardial infarct, mice exhibit an increase in death during the first 10 days and a 2-fold increase in the rate of ventricular wall rupture but reduced fibrosis and overall size of scaring compared to similarly treated wild-type mice
- Normal - however, mice maintain better cardiac function compared to wild-type mice over the 8 weeks following the initial scar formation

decreased susceptibility to injury
- Normal - however, initial response during the first 2 weeks after pressure overload is normal
- following transverse aortic constriction to induce pressure overload, mice exhibit less cardiac hypertrophy with reduced myocyte cross-section diameter and increased ventricular function after 8 weeks compared to similarly treated wild-type mice

References

Oka T; Xu J; Kaiser RA; Melendez J; Hambleton M; Sargent MA; Lorts A; Brunskill EW; Dorn GW 2nd; Conway SJ; Aronow BJ; Robbins J; Molkentin JD. 2007. Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling. Circ Res 101(3):313-21PubMed: 17569887 MGI: J:140301

Additional - Postn^tm1Jmol related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Postn STD PCR
- Probe:Postn Probe
- Genotyping resources and troubleshooting
Breeding Considerations

The donating investigator reports that homozygous females do not breed.
- Additional Breeding and Husbandry Support
Citation
When using the B6;129-Postn^tm1Jmol/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #009067 in your Materials and Methods section.

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Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Donating Investigator

Genetic overview

Research Applications

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Postntm1Jmol

Allele Symbol: Postntm1Jmol

Disease Terms

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Postntm1Jmol/Postntm1Jmolinvolves: 129S/SvEv

mammalian phenotype

Genotype: Postntm1Jmol/Postntm1Jmolinvolves: 129/Sv * C57BL/6

cardiovascular system phenotype

cellular phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

References

Additional - Postntm1Jmol related

Genotyping Protocols

Breeding Considerations

Citation

Strain Interest Registration

Contact Information

Interest

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

Postn^tm1Jmol

Allele Symbol: Postn^tm1Jmol

Genotype: Postn^tm1Jmol/Postn^tm1Jmol
involves: 129S/SvEv

Genotype: Postn^tm1Jmol/Postn^tm1Jmol
involves: 129/Sv * C57BL/6

Additional - Postn^tm1Jmol related