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10.14814/phy2.13687 http://scihub22266oqcxt.onion/10.14814/phy2.13687 C5932570!5932570!29722156     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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Physiol+Rep 2018 ; 6 (9): ä Nephropedia Template TP {{tp|p=29722156|t=2018. Hydrostatic pressure suppresses fibrotic changes via Akt/GSK?3 signaling in human cardiac fibroblasts |pdf=|usr=}}{{29722156}} gab.com Text Hydrostatic pressure suppresses fibrotic changes via Akt/GSK 3 signaling in human cardiac fibroblasts JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29722156 #FOAvip Mechanical stresses play important roles in the process of constructing and modifying heart structure. It has been well established that stretch force acting on cardiac fibroblasts induces fibrosis. However, the effects of compressive force, that is, hydrostatic pressure (HP), have not been well elucidated. We thus evaluated the effects of HP using a pressure?loading apparatus in human cardiac fibroblasts (HCFs) in vitro. In this study, high HP (200 mmHg) resulted in significant phosphorylation of Akt in HCFs. HP then greatly inhibited glycogen synthase kinase 3 (GSK?3)?, which acts downstream of the PI3K/Akt pathway. Similarly, HP suppressed mRNA transcription of inflammatory cytokine?6, collagen I and III, and matrix metalloproteinase 1, compared with an atmospheric pressure condition. Furthermore, HP inhibited collagen matrix production in a three?dimensional HCF culture. Taken together, high HP suppressed the differentiation of fibroblasts into the myofibroblast phenotype. HP under certain conditions suppressed cardiac fibrosis via Akt/GSK?3 signaling in HCFs. These results might help to elucidate the pathology of some types of heart disease. Twit Text FOAVip Hydrostatic pressure suppresses fibrotic changes via Akt/GSK 3 signaling in human cardiac fibroblasts ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29722156 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29722156 #FOAvip English Wikipedia <ref>{{Cite pmid|29722156}}</ref> Hydrostatic pressure suppresses fibrotic changes via Akt/GSK?3 signaling in human cardiac fibroblasts #MMPMID29722156 Tanaka R; Umemura M; Narikawa M; Fujita T; Yokoyama U; Ishigami T; Kimura K; Tamura K; Ishikawa Y Physiol Rep 2018[May]; 6 (9): ä PMID29722156show ga Mechanical stresses play important roles in the process of constructing and modifying heart structure. It has been well established that stretch force acting on cardiac fibroblasts induces fibrosis. However, the effects of compressive force, that is, hydrostatic pressure (HP), have not been well elucidated. We thus evaluated the effects of HP using a pressure?loading apparatus in human cardiac fibroblasts (HCFs) in vitro. In this study, high HP (200 mmHg) resulted in significant phosphorylation of Akt in HCFs. HP then greatly inhibited glycogen synthase kinase 3 (GSK?3)?, which acts downstream of the PI3K/Akt pathway. Similarly, HP suppressed mRNA transcription of inflammatory cytokine?6, collagen I and III, and matrix metalloproteinase 1, compared with an atmospheric pressure condition. Furthermore, HP inhibited collagen matrix production in a three?dimensional HCF culture. Taken together, high HP suppressed the differentiation of fibroblasts into the myofibroblast phenotype. HP under certain conditions suppressed cardiac fibrosis via Akt/GSK?3 signaling in HCFs. These results might help to elucidate the pathology of some types of heart disease. äHydrostatic pressure suppresses fibrotic changes via Akt/GSK?3 signali(epmc).pdf DeepDyve Pubget Overpricing