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10.1681/ASN.2016070709 http://scihub22266oqcxt.onion/10.1681/ASN.2016070709 C5407726!5407726!27920156     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       J+Am+Soc+Nephrol 2017 ; 28 (5): 1475-90 Nephropedia Template TP {{tp|p=27920156|t=2017. NF?B-Induced Periostin Activates Integrin-?3 Signaling to Promote Renal Injury in GN |pdf=|usr=}}{{27920156}} gab.com Text NF B-Induced Periostin Activates Integrin- 3 Signaling to Promote Renal Injury in GN JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27920156 #FOAvip De novo expression in the kidney of periostin, a protein involved in odontogenesis and osteogenesis, has been suggested as a biomarker of renal disease. In this study, we investigated the mechanism(s) of induction and the role of periostin in renal disease. Using a combination of bioinformatics, reporter assay, and chromatin immunoprecipitation analyses, we found that NF?B and other proinflammatory transcription factors induce periostin expression in vitro and that binding of these factors on the periostin promoter is enriched in glomeruli during experimental GN. Mice lacking expression of periostin displayed preserved renal function and structure during GN. Furthermore, delayed administration of periostin antisense oligonucleotides in wild-type animals with GN reversed already established proteinuria, diminished tissue inflammation, and improved renal structure. Lack of periostin expression also blunted the de novo renal expression of integrin-?3 and phosphorylation of focal adhesion kinase and AKT, known mediators of integrin-?3 signaling that affect cell motility and survival, observed during GN in wild-type animals. In vitro, recombinant periostin increased the expression of integrin-?3 and the concomitant phosphorylation of focal adhesion kinase and AKT in podocytes. Notably, periostin and integrin-?3 were highly colocalized in biopsy specimens from patients with inflammatory GN. These results demonstrate that interplay between periostin and renal inflammation orchestrates inflammatory and fibrotic responses, driving podocyte damage through downstream activation of integrin-?3 signaling. Targeting periostin may be a novel therapeutic strategy for treating CKD. Twit Text FOAVip NF B-Induced Periostin Activates Integrin- 3 Signaling to Promote Renal Injury in GN ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27920156 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27920156 #FOAvip English Wikipedia <ref>{{Cite pmid|27920156}}</ref> NF?B-Induced Periostin Activates Integrin-?3 Signaling to Promote Renal Injury in GN #MMPMID27920156 Prakoura N; Kavvadas P; Kormann R; Dussaule JC; Chadjichristos CE; Chatziantoniou C J Am Soc Nephrol 2017[May]; 28 (5): 1475-90 PMID27920156show ga De novo expression in the kidney of periostin, a protein involved in odontogenesis and osteogenesis, has been suggested as a biomarker of renal disease. In this study, we investigated the mechanism(s) of induction and the role of periostin in renal disease. Using a combination of bioinformatics, reporter assay, and chromatin immunoprecipitation analyses, we found that NF?B and other proinflammatory transcription factors induce periostin expression in vitro and that binding of these factors on the periostin promoter is enriched in glomeruli during experimental GN. Mice lacking expression of periostin displayed preserved renal function and structure during GN. Furthermore, delayed administration of periostin antisense oligonucleotides in wild-type animals with GN reversed already established proteinuria, diminished tissue inflammation, and improved renal structure. Lack of periostin expression also blunted the de novo renal expression of integrin-?3 and phosphorylation of focal adhesion kinase and AKT, known mediators of integrin-?3 signaling that affect cell motility and survival, observed during GN in wild-type animals. In vitro, recombinant periostin increased the expression of integrin-?3 and the concomitant phosphorylation of focal adhesion kinase and AKT in podocytes. Notably, periostin and integrin-?3 were highly colocalized in biopsy specimens from patients with inflammatory GN. These results demonstrate that interplay between periostin and renal inflammation orchestrates inflammatory and fibrotic responses, driving podocyte damage through downstream activation of integrin-?3 signaling. Targeting periostin may be a novel therapeutic strategy for treating CKD. äNF?B-Induced Periostin Activates Integrin-?3 Signaling to Promote Rena(epmc).pdf DeepDyve Pubget Overpricing