| First Author | Carp RI | Year | 2002 |
| Journal | Mech Ageing Dev | Volume | 123 |
| Issue | 6 | Pages | 575-84 |
| PubMed ID | 11850021 | Mgi Jnum | J:75182 |
| Mgi Id | MGI:2176031 | Doi | 10.1016/s0047-6374(01)00377-3 |
| Citation | Carp RI, et al. (2002) Murine leukemia virus in organs of senescence-prone and -resistant mouse strains. Mech Ageing Dev 123(6):575-84 |
| abstractText | A series of inbred strains of mice have been developed that are either prone (SAMP) or resistant (SAMR) to accelerated senescence. All of these strains originated from an inadvertent cross or crosses between the AKR/J mouse strain and an unknown strain(s). The characteristics of the nine senescence-prone lines differ, with all strains showing generalized aspects of accelerated aging but with each line having a specific aging-related change that is emphasized, e.g. learning and memory deficits, osteoporosis and senile amyloidosis. The senescence-resistant strains have normal patterns of aging and do not show the specific aging-related changes seen in SAMP strains. The fact that AKR mice have high levels of endogenous, ecotropic murine leukemia virus (MuLV) prompted an examination of the expression levels of MuLV in SAM strains. Analysis of brain, spleen and thymus samples revealed that seven of nine SAMP strains had high levels of MuLV and contained the Emv11 provirus (previously termed Akv1) that encodes the predominant MuLV found in AKR mice. In contrast, none of the SAMR strains had Emv11 or significant amounts of virus. The current findings represent an initial step in determining the role of MuLV in the accelerated senescence seen in SAMP strains. |
