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10.1172/JCI76327 http://scihub22266oqcxt.onion/10.1172/JCI76327 C4362266!4362266!25664851     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2015 ; 125 (3): 1189-202 Nephropedia Template TP {{tp|p=25664851|t=2015. Lymphocyte adaptor protein LNK deficiency exacerbates hypertension and end-organ inflammation |pdf=|usr=}}{{25664851}} gab.com Text Lymphocyte adaptor protein LNK deficiency exacerbates hypertension and end-organ inflammation JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25664851 #FOAvip The lymphocyte adaptor protein LNK (also known as SH2B3) is primarily expressed in hematopoietic and endothelial cells, where it functions as a negative regulator of cytokine signaling and cell proliferation. Single-nucleotide polymorphisms in the gene encoding LNK are associated with autoimmune and cardiovascular disorders; however, it is not known how LNK contributes to hypertension. Here, we determined that loss of LNK exacerbates angiotensin II?induced (Ang II?induced) hypertension and the associated renal and vascular dysfunction. At baseline, kidneys from Lnk?/? mice exhibited greater levels of inflammation, oxidative stress, and glomerular injury compared with WT animals, and these parameters were further exacerbated by Ang II infusion. Aortas from Lnk?/? mice exhibited enhanced inflammation, reduced nitric oxide levels, and impaired endothelial-dependent relaxation. Bone marrow transplantation studies demonstrated that loss of LNK in hematopoietic cells is primarily responsible for the observed renal and vascular inflammation and predisposition to hypertension. Ang II infusion increased IFN-??producing CD8+ T cells in the spleen and kidneys of Lnk?/? mice compared with WT mice. Moreover, IFN-? deficiency resulted in blunted hypertension in response to Ang II infusion. Together, these results suggest that LNK is a potential therapeutic target for hypertension and its associated renal and vascular sequela. Twit Text FOAVip Lymphocyte adaptor protein LNK deficiency exacerbates hypertension and end-organ inflammation ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25664851 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25664851 #FOAvip English Wikipedia <ref>{{Cite pmid|25664851}}</ref> Lymphocyte adaptor protein LNK deficiency exacerbates hypertension and end-organ inflammation #MMPMID25664851 Saleh MA; McMaster WG; Wu J; Norlander AE; Funt SA; Thabet SR; Kirabo A; Xiao L; Chen W; Itani HA; Michell D; Huan T; Zhang Y; Takaki S; Titze J; Levy D; Harrison DG; Madhur MS J Clin Invest 2015[Mar]; 125 (3): 1189-202 PMID25664851show ga The lymphocyte adaptor protein LNK (also known as SH2B3) is primarily expressed in hematopoietic and endothelial cells, where it functions as a negative regulator of cytokine signaling and cell proliferation. Single-nucleotide polymorphisms in the gene encoding LNK are associated with autoimmune and cardiovascular disorders; however, it is not known how LNK contributes to hypertension. Here, we determined that loss of LNK exacerbates angiotensin II?induced (Ang II?induced) hypertension and the associated renal and vascular dysfunction. At baseline, kidneys from Lnk?/? mice exhibited greater levels of inflammation, oxidative stress, and glomerular injury compared with WT animals, and these parameters were further exacerbated by Ang II infusion. Aortas from Lnk?/? mice exhibited enhanced inflammation, reduced nitric oxide levels, and impaired endothelial-dependent relaxation. Bone marrow transplantation studies demonstrated that loss of LNK in hematopoietic cells is primarily responsible for the observed renal and vascular inflammation and predisposition to hypertension. Ang II infusion increased IFN-??producing CD8+ T cells in the spleen and kidneys of Lnk?/? mice compared with WT mice. Moreover, IFN-? deficiency resulted in blunted hypertension in response to Ang II infusion. Together, these results suggest that LNK is a potential therapeutic target for hypertension and its associated renal and vascular sequela. äLymphocyte adaptor protein LNK deficiency exacerbates hypertension and(epmc).pdf DeepDyve Pubget Overpricing