Integrative Physiology B lood vessels consist of 2 major cell types, endothelial and mural cells, such as pericytes and vascular smooth muscle cells (VSMC), which surround the endothelium. Regulator of G-protein signaling 5 (RGS5) is expressed in mural cells and has emerged as a crucial modulator of vascular pathology in cancer. For instance, we have demonstrated that RGS5 is highly upregulated in angiogenic tumor pericytes.1 Loss of RGS5 results in pericyte maturation and normalization of tumor vasculature.2,3 Moreover, we showed a crucial role for RGS5 in regulating vascular barrier function in tumors and in brain capillaries during ischemia, and also provided the first genetic evidence that RGS5 is involved in vascular wall remodeling in adults. 2A striking feature of RGS5 expression is its dynamic nature in various physiological and pathological states, which indicates a role in adaptive processes. 1,[4][5][6] This is consistent with RGS5 being a member of the extended family of RGS molecules, which are modulators of G-protein-coupled receptors (GPCRs). G-protein signaling pathways rely on rapid on-off kinetics, and RGS molecules act as GTPaseactivating proteins (GAP) for heterotrimeric G proteins and, as such, regulate duration and intensity of signaling events. They contain a highly conserved carboxyl-terminal RGS domain that confers the catalytic function for active Gα subunits. Members of the R4/B subfamily, which include, among others, RGS 2, 4, and 5, are the smallest RGS Original received September 21, 2012; revision received January 7, 2013; accepted January 9, 2013. In December 2012, the average time from submission to first decision for all original research papers submitted to Circulation Research was 14.5 days.
Summary Candida alhicans infections were established in eight inbred strains of mice. Using established histological criteria, only two strains (AKR and CBA/CaH) were found to exhibit severe lesions. The remainder showed only mild tissue damage. Deaths occurred in three strains: CBA/CaH, A/J and DBA/2. The last two strains lack the important complement component C5. Colony counts in the brain varied widely between strains and showed no correlation with the extent or severity of tissue destruction. However, strains lacking C5 had a significantly greater fungal burden in the brain than C5-sufficient mice. The data are discussed in relation to concepts of susceptibility and resistance to C. albicans in experimental infections in mice.
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