Anti-TGFB2 (aa 250-350) polyclonal antibody

Objective-Although hypertension is the most common risk factor for thoracic aortic diseases, it is not understood how increased pressures on the ascending aorta lead to aortic aneurysms. We investigated the role of angiotensin II type 1 receptor activation in ascending aortic remodeling in response to increased biomechanical forces using a transverse aortic constriction (TAC) mouse model. Approach and Results-Two weeks after TAC, the increased biomechanical pressures led to ascending aortic dilatation and thickening of the medial and adventitial layers of the aorta. There was significant adventitial hyperplasia and inflammatory responses in TAC ascending aortas were accompanied by increased adventitial collagen, elevated inflammatory and proliferative markers, and increased cell density attributable to accumulation of myofibroblasts and macrophages. Treatment with losartan significantly blocked TAC-induced vascular inflammation and macrophage accumulation. However, losartan only partially prevented TAC-induced adventitial hyperplasia, collagen accumulation, and ascending aortic dilatation. Increased Tgfb2 expression and phosphorylated-Smad2 staining in the medial layer of TAC ascending aortas were effectively blocked with losartan. In contrast, the increased Tgfb1 expression and adventitial phospho-Smad2 staining were only partially attenuated by losartan. In addition, losartan significantly blocked extracellular signal-regulated kinase activation and reactive oxygen species production in the TAC ascending aorta. Conclusions-Inhibition of the angiotensin II type 1 receptor using losartan significantly attenuated the vascular remodeling associated with TAC but did not completely block the increased transforming growth factor-1 expression, adventitial Smad2 signaling, and collagen accumulation. These results help to delineate the aortic transforming growth factor- signaling that is dependent and independent of the angiotensin II type 1 receptor after TAC.

The Socorro Warbler (Setophaga pitiayumi graysoni) is currently classified as a subspecies of the Tropical Parula. This bird is endemic to Socorro Island, and due to the island's distance from mainland Mexico and likely low levels of gene flow for this non-migratory species, we expected this form to exhibit significant divergence from its mainland counterparts. Here, we analyzed the phylogenetic position of the Socorro Warbler and examined its taxonomic status. Using blood samples from four individual Socorro Warblers, we performed phylogenetic analyses using the nuclear genes rhodopsin intron 1 (RDPSN) and transforming growth factor beta-2 (TGFB2), and the mitochondrial genes ATPase and cytochrome b. Bayesian inference, maximum-likelihood, and maximum parsimony analyses were employed to determine the genetic relationship of the Socorro Warbler to its mainland counterparts. Results reveal significant genetic divergence and a basal position of the Socorro Warbler relative to its mainland counterparts. Based on its distinct phylogenetic placement and geographical isolation, we recommend returning the Socorro Warbler to its original specific status, Setophaga graysoni, based on its taxonomic history. This case illustrates the importance of preserving island habitats to save unique island biodiversity that otherwise could pass unnoticed.