The NK gene complex (NKC) controls murine cytomegalovirus (MCMV) immunity through Cmv1-dependent natural killer (NK) cell responses. Ly49H expression correlates with Cmv1 phenotypes in different inbred strains, is required for MCMV resistance in C57BL/6 (B6) mice, and its interaction with the MCMV encoded m157 protein leads to NK cell-mediated destruction of virus-infected cells. However, genetic mapping studies have previously indicated that Cmv1 should reside in the D6Wum9-16 NKC interval, distal to Ly49h. Since these data suggested that multiple NKC-linked loci could regulate viral immunity, a putative MCMV resistance control ( Mrc) locus was pinpointed to within the D6Wum9-16 interval on a NKC-aligned bacterial artificial chromosome (BAC). Sequence analysis of BAC 151 revealed several novel G-protein coupled receptor genes, an HMG-1 remnant and many additional polymorphic microsatellites that were useful in determining the minimal genetic interval for the Mrc locus. Moreover, comparison of B6, BALB/c, A/J and recombinant Mrc alleles restricted the genetic interval to approximately 470 bp and showed that it was also a hotspot for recombination. MCMV challenge of novel NKC recombinant mice demonstrated that Mrc(B6) was not required for MCMV resistance nor could it directly complement the Ly49(BALB) haplotype to rescue MCMV susceptibility. Taken together, these data show that while Mrc apparently guides recombination, Ly49H expression is sufficient for MCMV resistance in B6 mice. A direct role for Mrc(B6) in virus resistance is excluded in the novel mice.
In unstimulated mature microvascular networks, NG2 expression is limited to perivascular cells located in the arterial tree (e.g. arterial vascular smooth muscle cells) and along capillaries (e.g. pericytes). NG2 expression according to immunohistochemistry is notably absent in the perivascular cells present in the venule tree. During microvascular remodeling in response to an inflammatory or hypoxic stimulus, however, the NG2 proteoglycan is transiently expressed by perivascular cells (e.g. smooth muscle cells) in venules. Expression of NG2 by perivascular cells in venules spatially and temporally coincides with an abundance of angiogenic capillary sprouting from venules in the rat mesentery, for example. The objective of this study is to determine, using immunohistochemistry, the spatial and temporal expression profile of NG2 in the microvasculature of the murine spinotrapezius muscle, a thin stabilizing muscle that enables en face visualization of entire microvascular networks, in young vs. old mice, before and after ischemic insult, and in healthy vs. obese (ob/ob) and diabetic (db/db) mice. Results suggest that NG2 exhibits a differential expression pattern in the perivascular cells of arterial vs. venous trees in the quiescent spinotrapezius muscle, and ischemic insult induces NG2 expression by smooth muscle cells along remodeling capillaries. Support provided by: NIH‐HL082838‐02.
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