C3H Mouse

The C3H strain was developed by STRONG in 1920 from a cross of BAGG ALBINO female with DBA male. It was selected for a high incidence of mammary tumours. This sensitivity to mammary tumours is due to an exogenous virus transmitted by the mother’s milk (the Mouse Mammary Tumour Virus – MMTV). In 1930, STRONG sent a colony to ANDERVONT who in turn sent one to HESTON (at generation F35). HESTON stock was then transferred to the NIH in 1951 (generation F51).  C3H/HeN mice are used in a wide range of studies. They are homozygous for the Pde6brd1 allele and have an early onset severe retinal degeneration that causes blindness at weaning age.

This strain has a high incidence of hepatoma. Even if MMTV is not present, virgin and breeding females can develop mammary tumours. Despite an atherogenic diet, C3H/HeN mice do not develop aortic atherosclerosis, in contrast to the C57BL/6J. There is a genetically mediated difference between the C3H/HeN and the C3H/HeJ regarding their response to bacterial endotoxin (LPS). This response is linked to the TL4 protein (Toll-like receptor 4; previously lps). C3H/HeN are Tlr4lps-n (toll-like receptor 4; normal LPS response), previously LPSn. This strain will have a normal response to an LPS challenge, it is said to be endotoxin-sensitive. Per contra, the C3H/HeJ strain is Tlr4lps-d, previously LPSn and said to be endotoxin-resistant.

Important: This strain no longer carries MMTV (Mouse Mammary
Tumour Virus).

Main application and research fields