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10.1111/jcmm.13030 http://scihub22266oqcxt.onion/10.1111/jcmm.13030 C5387175!5387175!27976512     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Mol+Med 2017 ; 21 (5): 916-28 Nephropedia Template TP {{tp|p=27976512|t=2017. FGF2 antagonizes aberrant TGF? regulation of tropomyosin: role for posterior capsule opacity |pdf=|usr=}}{{27976512}} gab.com Text FGF2 antagonizes aberrant TGF regulation of tropomyosin: role for posterior capsule opacity JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27976512 #FOAvip Transforming growth factor (TGF) ?2 and fibroblast growth factor (FGF) 2 are involved in regulation of posterior capsule opacification (PCO) and other processes of epithelial?mesenchymal transition (EMT) such as cancer progression, wound healing and tissue fibrosis as well as normal embryonic development. We previously used an in vivo rodent PCO model to show the expression of tropomyosin (Tpm) 1/2 was aberrantly up?regulated in remodelling the actin cytoskeleton during EMT. In this in vitro study, we show the Tpms family of cytoskeleton proteins are involved in regulating and stabilizing actin microfilaments (F?actin) and are induced by TGF?2 during EMT in lens epithelial cells (LECs). Importantly, we found TGF?2 and FGF2 played contrasting roles. Stress fibre formation and up?regulation of ??smooth muscle actin (?SMA) induced by TGF?2 could be reversed by Tpm1/2 knock?down by siRNA. Expression of Tpm1/2 and stress fibre formation induced by TGF?2 could be reversed by FGF2. Furthermore, FGF2 delivery to TGF??treated LECs perturbed EMT by reactivating the mitogen?activated protein kinase (MAPK)/ extracellular signal?regulated kinase (ERK) pathway and subsequently enhanced EMT. Conversely, MEK inhibitor (PD98059) abated the FGF2?mediated Tpm1/2 and ?SMA suppression. However, we found that normal LECs which underwent EMT showed enhanced migration in response to combined TGF? and FGF2 stimulation. These findings may help clarify the mechanism reprogramming the actin cytoskeleton during morphogenetic EMT cell proliferation and fibre regeneration in PCO. We propose that understanding the physiological link between levels of FGF2, Tpm1/2 expression and TGF?s?driven EMT orchestration may provide clue(s) to develop therapeutic strategies to treat PCO based on Tpm1/2. Twit Text FOAVip FGF2 antagonizes aberrant TGF regulation of tropomyosin: role for posterior capsule opacity ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27976512 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27976512 #FOAvip English Wikipedia <ref>{{Cite pmid|27976512}}</ref> FGF2 antagonizes aberrant TGF? regulation of tropomyosin: role for posterior capsule opacity #MMPMID27976512 Kubo E; Shibata S; Shibata T; Kiyokawa E; Sasaki H; Singh DP J Cell Mol Med 2017[May]; 21 (5): 916-28 PMID27976512show ga Transforming growth factor (TGF) ?2 and fibroblast growth factor (FGF) 2 are involved in regulation of posterior capsule opacification (PCO) and other processes of epithelial?mesenchymal transition (EMT) such as cancer progression, wound healing and tissue fibrosis as well as normal embryonic development. We previously used an in vivo rodent PCO model to show the expression of tropomyosin (Tpm) 1/2 was aberrantly up?regulated in remodelling the actin cytoskeleton during EMT. In this in vitro study, we show the Tpms family of cytoskeleton proteins are involved in regulating and stabilizing actin microfilaments (F?actin) and are induced by TGF?2 during EMT in lens epithelial cells (LECs). Importantly, we found TGF?2 and FGF2 played contrasting roles. Stress fibre formation and up?regulation of ??smooth muscle actin (?SMA) induced by TGF?2 could be reversed by Tpm1/2 knock?down by siRNA. Expression of Tpm1/2 and stress fibre formation induced by TGF?2 could be reversed by FGF2. Furthermore, FGF2 delivery to TGF??treated LECs perturbed EMT by reactivating the mitogen?activated protein kinase (MAPK)/ extracellular signal?regulated kinase (ERK) pathway and subsequently enhanced EMT. Conversely, MEK inhibitor (PD98059) abated the FGF2?mediated Tpm1/2 and ?SMA suppression. However, we found that normal LECs which underwent EMT showed enhanced migration in response to combined TGF? and FGF2 stimulation. These findings may help clarify the mechanism reprogramming the actin cytoskeleton during morphogenetic EMT cell proliferation and fibre regeneration in PCO. We propose that understanding the physiological link between levels of FGF2, Tpm1/2 expression and TGF?s?driven EMT orchestration may provide clue(s) to develop therapeutic strategies to treat PCO based on Tpm1/2. äFGF2 antagonizes aberrant TGF? regulation of tropomyosin: role for pos(epmc).pdf DeepDyve Pubget Overpricing