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10.1152/ajplung.00162.2014 http://scihub22266oqcxt.onion/10.1152/ajplung.00162.2014 25128524!4187037!25128524     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25128524&cmd=llinks): Failed to open stream: HTTP request failed! 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Role of hypoxia-induced transglutaminase 2 in pulmonary artery smooth muscle cell proliferation |pdf=|usr=}}{{25128524}} gab.com Text Role of hypoxia-induced transglutaminase 2 in pulmonary artery smooth muscle cell proliferation JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25128524 #FOAvip We previously reported that transglutaminase 2 (TG2) activity is markedly elevated in lungs of hypoxia-exposed rodent models of pulmonary hypertension (PH). Since vascular remodeling of pulmonary artery smooth muscle cells (PASMCs) is important in PH, we undertook the present study to determine whether TG2 activity is altered in PASMCs with exposure to hypoxia and whether that alteration participates in their proliferative response to hypoxia. Cultured distal bovine (b) and proximal human (h) PASMCs were exposed to hypoxia (3% O2) or normoxia (21% O2). mRNA and protein expression were determined by PCR and Western blot analyses. TG2 activity and function were visualized and determined by fluorescent labeled 5-pentylamine biotin incorporation and immunoblotting of serotonylated fibronectin. Cell proliferation was assessed by [(3)H]thymidine incorporation assay. At 24 h, both TG2 expression and activity were stimulated by hypoxia in bPASMCs. Activation of TG2 by hypoxia was blocked by inhibition of the extracellular calcium-sensing receptor or the transient receptor potential channel V4. In contrast, TG2 expression was blocked by inhibition of the transcription factor hypoxia-inducible factor-1alpha, supporting the presence of separate mechanisms for stimulation of activity and expression of TG2. Pulmonary arterial hypertension patient-derived hPASMCs were found to proliferate significantly more rapidly and respond to hypoxia more strongly than control-derived hPASMCs. Similar to bovine cells, hypoxia-induced proliferation of patient-derived cells was blocked by inhibition of TG2 activity. Our results suggest an important role for TG2, mediated by intracellular calcium fluxes and HIF-1alpha, in hypoxia-induced PASMC proliferation and possibly in vascular remodeling in PH. Twit Text FOAVip Role of hypoxia-induced transglutaminase 2 in pulmonary artery smooth muscle cell proliferation ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25128524 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25128524 #FOAvip English Wikipedia <ref>{{Cite pmid|25128524}}</ref> Role of hypoxia-induced transglutaminase 2 in pulmonary artery smooth muscle cell proliferation #MMPMID25128524 Penumatsa KC; Toksoz D; Warburton RR; Hilmer AJ; Liu T; Khosla C; Comhair SA; Fanburg BL Am J Physiol Lung Cell Mol Physiol 2014[Oct]; 307 (7): L576-85 PMID25128524show ga We previously reported that transglutaminase 2 (TG2) activity is markedly elevated in lungs of hypoxia-exposed rodent models of pulmonary hypertension (PH). Since vascular remodeling of pulmonary artery smooth muscle cells (PASMCs) is important in PH, we undertook the present study to determine whether TG2 activity is altered in PASMCs with exposure to hypoxia and whether that alteration participates in their proliferative response to hypoxia. Cultured distal bovine (b) and proximal human (h) PASMCs were exposed to hypoxia (3% O2) or normoxia (21% O2). mRNA and protein expression were determined by PCR and Western blot analyses. TG2 activity and function were visualized and determined by fluorescent labeled 5-pentylamine biotin incorporation and immunoblotting of serotonylated fibronectin. Cell proliferation was assessed by [(3)H]thymidine incorporation assay. At 24 h, both TG2 expression and activity were stimulated by hypoxia in bPASMCs. Activation of TG2 by hypoxia was blocked by inhibition of the extracellular calcium-sensing receptor or the transient receptor potential channel V4. In contrast, TG2 expression was blocked by inhibition of the transcription factor hypoxia-inducible factor-1alpha, supporting the presence of separate mechanisms for stimulation of activity and expression of TG2. Pulmonary arterial hypertension patient-derived hPASMCs were found to proliferate significantly more rapidly and respond to hypoxia more strongly than control-derived hPASMCs. Similar to bovine cells, hypoxia-induced proliferation of patient-derived cells was blocked by inhibition of TG2 activity. Our results suggest an important role for TG2, mediated by intracellular calcium fluxes and HIF-1alpha, in hypoxia-induced PASMC proliferation and possibly in vascular remodeling in PH. |*Cell Proliferation[MESH] |Animals[MESH] |Calcium Signaling[MESH] |Cattle[MESH] |Cell Hypoxia[MESH] |Cells, Cultured[MESH] |Enzyme Activation[MESH] |Enzyme Induction[MESH] |Enzyme Inhibitors/pharmacology[MESH] |GTP-Binding Proteins/antagonists & inhibitors/*physiology[MESH] |Humans[MESH] |Hypertension, Pulmonary/*enzymology/pathology[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism[MESH] |Muscle, Smooth, Vascular/pathology/physiopathology[MESH] |Myocytes, Smooth Muscle/*enzymology/physiology[MESH] |Protein Glutamine gamma Glutamyltransferase 2[MESH] |Pulmonary Artery/*pathology/physiopathology[MESH] |Receptors, Calcium-Sensing/antagonists & inhibitors/metabolism[MESH] |TRPV Cation Channels/antagonists & inhibitors/metabolism[MESH]Role of hypoxia-induced transglutaminase 2 in pulmonary artery smooth (epmc).pdf DeepDyve Pubget Overpricing