In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for these C57BL/6J-congenic miR-22- mice. It should be noted that the phenotype of these mice could vary from that originally described on a 129S genetic background (129S.miR-22-; Stock No. 018155). We may modify the C57BL/6J-congenic miR-22- strain description if necessary as published results become available.
The phenotype for 129S.miR-22- animals is:
Mir22 (microRNA 22) expresson is frequently dysregulated in diseased human hearts. Mice that are homozygous for the knock-out mutation of Mir22 (miR-22-/-) are viable and fertile, but are not produced at expected numbers from heterozygous crosses. Null mice produce small litters of 2 to 3 pups. No gene product (mRNA) is detected by qPCR analysis of heart tissue. Although no evidence of cardiac pathology is evident under basal conditions, homozygous mice are impaired in contractile reserve to dobutamine and intracellular calcium homeostasis. Homozygotes exhibit increased sensitivity to heart failure after transverse aortic constriction (TAC), as evidenced by loss of contractility, ventricular dilatation, and increased fibrosis.
