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10.1038/aps.2016.172 http://scihub22266oqcxt.onion/10.1038/aps.2016.172 C5519244!5519244!28414198     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Pharmacol+Sin 2017 ; 38 (7): 1009-23 Nephropedia Template TP {{tp|p=28414198|t=2017. LY333531, a PKC? inhibitor, attenuates glomerular endothelial cell apoptosis in the early stage of mouse diabetic nephropathy via down-regulating swiprosin-1 |pdf=|usr=}}{{28414198}} gab.com Text LY333531, a PKC inhibitor, attenuates glomerular endothelial cell apoptosis in the early stage of mouse diabetic nephropathy via down-regulating swiprosin-1 JO: Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=28414198 #FOAvip Glomerular endothelial cell (GEC) injury plays an important role in the early stage of diabetic nephropathy (DN). Previous studies show that a PKC? inhibitor is effective for treating DN. In the current study we further explored the effects and molecular mechanisms of PKC? inhibitors on GEC apoptosis in DN in streptozotocin-induced diabetic mice in vivo and high glucose- or PMA-treated human renal glomerular endothelial cells (HRGECs) in vitro. In the diabetic mice, hyperglycemia caused aggravated nephropathy and GEC apoptosis accompanied by significantly increased expression of swiprosin-1, a potentally pro-apoptotic protein. Administration of LY333531 (1 mg·kg?1·d?1 for 8 weeks) significantly attenuated both GEC apoptosis and swiprosin-1 upregulation in the diabetic mice. Similar results were observed in high glucose- or PMA-treated HRGECs in vitro. The pro-apoptotic role of swiprosin-1 was further examined using HRGECs treated with lentivirus mediating RNA interference or over-expression and swiprosin-1-knockout mice. Over-expression of swiprosin-1 in HRGECs resulted in increases in apoptosis and in caspase-9, caspase-3 and Bax expression. In contrast, knockdown of swiprosin-1 attenuated high glucose- or PMA-induced HRGECs apoptosis. Furthermore, over-expression of swiprosin-1 promoted interaction between swiprosin-1 and caspase-9 and increased the formation of apoptosomes. In diabetic swiprosin-1?/? mice, the kidney/body weight, urinary albumin, glomerular hypertrophy, mitochondrial apoptotic-associated proteins and GEC apoptosis were significantly attenuated as compared with those in diabetic swiprosin-1+/+ mice. These results demonstrate that swiprosin-1 is up-regulated by PKC? in the early stage of DN, and that PKC? facilitates GEC apoptosis through the mitochondrial-dependent pathway. Twit Text FOAVip LY333531, a PKC inhibitor, attenuates glomerular endothelial cell apoptosis in the early stage of mouse diabetic nephropathy via down-regulating swiprosin-1 ????Acta Pharmacol Sin http://www.kidney.de/pget.php?&tw=1&pmid=28414198 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28414198 #FOAvip English Wikipedia <ref>{{Cite pmid|28414198}}</ref> LY333531, a PKC? inhibitor, attenuates glomerular endothelial cell apoptosis in the early stage of mouse diabetic nephropathy via down-regulating swiprosin-1 #MMPMID28414198 Wang Zb; Zhang S; Li Y; Wang Rm; Tong Lc; Wang Y; Liu Wy; Su Df; Tu Y; Zhang Lc; Li L Acta Pharmacol Sin 2017[Jul]; 38 (7): 1009-23 PMID28414198show ga Glomerular endothelial cell (GEC) injury plays an important role in the early stage of diabetic nephropathy (DN). Previous studies show that a PKC? inhibitor is effective for treating DN. In the current study we further explored the effects and molecular mechanisms of PKC? inhibitors on GEC apoptosis in DN in streptozotocin-induced diabetic mice in vivo and high glucose- or PMA-treated human renal glomerular endothelial cells (HRGECs) in vitro. In the diabetic mice, hyperglycemia caused aggravated nephropathy and GEC apoptosis accompanied by significantly increased expression of swiprosin-1, a potentally pro-apoptotic protein. Administration of LY333531 (1 mg·kg?1·d?1 for 8 weeks) significantly attenuated both GEC apoptosis and swiprosin-1 upregulation in the diabetic mice. Similar results were observed in high glucose- or PMA-treated HRGECs in vitro. The pro-apoptotic role of swiprosin-1 was further examined using HRGECs treated with lentivirus mediating RNA interference or over-expression and swiprosin-1-knockout mice. Over-expression of swiprosin-1 in HRGECs resulted in increases in apoptosis and in caspase-9, caspase-3 and Bax expression. In contrast, knockdown of swiprosin-1 attenuated high glucose- or PMA-induced HRGECs apoptosis. Furthermore, over-expression of swiprosin-1 promoted interaction between swiprosin-1 and caspase-9 and increased the formation of apoptosomes. In diabetic swiprosin-1?/? mice, the kidney/body weight, urinary albumin, glomerular hypertrophy, mitochondrial apoptotic-associated proteins and GEC apoptosis were significantly attenuated as compared with those in diabetic swiprosin-1+/+ mice. These results demonstrate that swiprosin-1 is up-regulated by PKC? in the early stage of DN, and that PKC? facilitates GEC apoptosis through the mitochondrial-dependent pathway. äLY333531, a PKC? inhibitor, attenuates glomerular endothelial cell apo(epmc).pdf DeepDyve Pubget Overpricing