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10.1152/ajprenal.00169.2015 http://scihub22266oqcxt.onion/10.1152/ajprenal.00169.2015 C4971893!4971893!26697979     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       Am+J+Physiol+Renal+Physiol 2016 ; 310 (7): F607-20 Nephropedia Template TP {{tp|p=26697979|t=2016. G protein ?12 (G?12) is a negative regulator of kidney injury molecule-1-mediated efferocytosis |pdf=|usr=}}{{26697979}} gab.com Text G protein 12 (G 12) is a negative regulator of kidney injury molecule-1-mediated efferocytosis JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26697979 #FOAvip Kidney injury molecule-1 (KIM-1) is a receptor for the ?eat me? signal, phosphatidylserine, on apoptotic cells. The specific upregulation of KIM-1 by injured tubular epithelial cells (TECs) enables them to clear apoptotic cells (also known as efferocytosis), thereby protecting from acute kidney injury. Recently, we uncovered that KIM-1 binds directly to the ?-subunit of heterotrimeric G12 protein (G?12) and inhibits its activation by reactive oxygen species during renal ischemia-reperfusion injury (Ismail OZ, Zhang X, Wei J, Haig A, Denker BM, Suri RS, Sener A, Gunaratnam L. Am J Pathol 185: 1207?1215, 2015). Here, we investigated the role that G?12 plays in KIM-1-mediated efferocytosis by TECs. We showed that KIM-1 remains bound to G?12 and suppresses its activity during phagocytosis. When we silenced G?12 expression using small interefering RNA, KIM-1-mediated engulfment of apoptotic cells was increased significantly; in contrast overexpression of constitutively active G?12 (QLG?12) resulted in inhibition of efferocytosis. Inhibition of RhoA, a key effector of G?12, using a chemical inhibitor or expression of dominant-negative RhoA, had the same effect as inhibition of G?12 on efferocytosis. Consistent with this, silencing G?12 suppressed active RhoA in KIM-1-expressing cells. Finally, using primary TECs from Kim-1+/+ and Kim-1?/? mice, we confirmed that engulfment of apoptotic cells requires KIM-1 expression and that silencing G?12 enhanced efferocytosis by primary TECs. Our data reveal a previously unknown role for G?12 in regulating efferocytosis and that renal TECs require KIM-1 to mediate this process. These results may have therapeutic implications given the known harmful role of G?12 in acute kidney injury. Twit Text FOAVip G protein 12 (G 12) is a negative regulator of kidney injury molecule-1-mediated efferocytosis ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26697979 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26697979 #FOAvip English Wikipedia <ref>{{Cite pmid|26697979}}</ref> G protein ?12 (G?12) is a negative regulator of kidney injury molecule-1-mediated efferocytosis #MMPMID26697979 Ismail OZ; Zhang X; Bonventre JV; Gunaratnam L Am J Physiol Renal Physiol 2016[Apr]; 310 (7): F607-20 PMID26697979show ga Kidney injury molecule-1 (KIM-1) is a receptor for the ?eat me? signal, phosphatidylserine, on apoptotic cells. The specific upregulation of KIM-1 by injured tubular epithelial cells (TECs) enables them to clear apoptotic cells (also known as efferocytosis), thereby protecting from acute kidney injury. Recently, we uncovered that KIM-1 binds directly to the ?-subunit of heterotrimeric G12 protein (G?12) and inhibits its activation by reactive oxygen species during renal ischemia-reperfusion injury (Ismail OZ, Zhang X, Wei J, Haig A, Denker BM, Suri RS, Sener A, Gunaratnam L. Am J Pathol 185: 1207?1215, 2015). Here, we investigated the role that G?12 plays in KIM-1-mediated efferocytosis by TECs. We showed that KIM-1 remains bound to G?12 and suppresses its activity during phagocytosis. When we silenced G?12 expression using small interefering RNA, KIM-1-mediated engulfment of apoptotic cells was increased significantly; in contrast overexpression of constitutively active G?12 (QLG?12) resulted in inhibition of efferocytosis. Inhibition of RhoA, a key effector of G?12, using a chemical inhibitor or expression of dominant-negative RhoA, had the same effect as inhibition of G?12 on efferocytosis. Consistent with this, silencing G?12 suppressed active RhoA in KIM-1-expressing cells. Finally, using primary TECs from Kim-1+/+ and Kim-1?/? mice, we confirmed that engulfment of apoptotic cells requires KIM-1 expression and that silencing G?12 enhanced efferocytosis by primary TECs. Our data reveal a previously unknown role for G?12 in regulating efferocytosis and that renal TECs require KIM-1 to mediate this process. These results may have therapeutic implications given the known harmful role of G?12 in acute kidney injury. äG protein ?12 (G?12) is a negative regulator of kidney injury molecule(epmc).pdf DeepDyve Pubget Overpricing