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10.3904/kjim.2016.060 http://scihub22266oqcxt.onion/10.3904/kjim.2016.060 C5668392!5668392 !28192890     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28192890 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Korean+J+Intern+Med 2017 ; 32 (6 ): 1053-1061 Nephropedia Template TP {{tp|p=28192890 |t=2017. Blocking junctional adhesion molecule C promotes the recovery of cisplatin-induced acute kidney injury |pdf=|usr=}}{{28192890 }} gab.com Text Blocking junctional adhesion molecule C promotes the recovery of cisplatin-induced acute kidney injury JO: Korean J Intern Med http://www.kidney.de/pget.php?&tw=1&pmid=28192890 #FOAvip BACKGROUND/AIMS: Recent findings have demonstrated the occurrence of neutrophil transendothelial migration in the reverse direction (reverse TEM) and that endothelial junctional adhesion molecule C (JAM-C) is a negative regulator of reverse TEM. In this study, we tested the effects of a JAM-C blocking antibody on the resolution of kidney injuries and inflammation in a mouse model of cisplatin-induced acute kidney injury (AKI). METHODS: Cisplatin was administered via intraperitoneal injection. A JAM-C blocking antibody or a control immunoglobulin G was administered intraperitoneal at 1.5 mg/kg, with the injection being delayed until day 4 following cisplatin administration to restrict the effect of antibodies on recovery. RESULTS: After cisplatin injection, serum creatinine and histologic injuries peaked on day 4. Treatment with a JAM-C blocking antibody on days 4 and 5 promoted the functional and histologic recovery of cisplatin-induced AKI on days 5 and 6. Facilitating recovery with a JAM-C blocking antibody correlated with significantly increased circulating intercellular adhesion molecule 1+ Tamm-Horsfall protein+ neutrophils and significantly decreased renal neutrophil infiltration, indicating that facilitating reverse the TEM of neutrophils from the kidney to the peripheral circulation partially mediated the resolution of inflammation and recovery. CONCLUSIONS: These results demonstrated that reverse TEM is involved in the resolution of neutrophilic inflammation in cisplatin-induced AKI and that JAM-C is an important regulator of this process. Twit Text FOAVip Blocking junctional adhesion molecule C promotes the recovery of cisplatin-induced acute kidney injury ????Korean J Intern Med http://www.kidney.de/pget.php?&tw=1&pmid=28192890 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28192890 #FOAvip English Wikipedia <ref>{{Cite pmid|28192890 }}</ref> Blocking junctional adhesion molecule C promotes the recovery of cisplatin-induced acute kidney injury #MMPMID28192890 Kim SC ; Ko YS ; Lee HY ; Kim MG ; Jo SK ; Cho WY Korean J Intern Med 2017[Nov]; 32 (6 ): 1053-1061 PMID28192890 show ga BACKGROUND/AIMS: Recent findings have demonstrated the occurrence of neutrophil transendothelial migration in the reverse direction (reverse TEM) and that endothelial junctional adhesion molecule C (JAM-C) is a negative regulator of reverse TEM. In this study, we tested the effects of a JAM-C blocking antibody on the resolution of kidney injuries and inflammation in a mouse model of cisplatin-induced acute kidney injury (AKI). METHODS: Cisplatin was administered via intraperitoneal injection. A JAM-C blocking antibody or a control immunoglobulin G was administered intraperitoneal at 1.5 mg/kg, with the injection being delayed until day 4 following cisplatin administration to restrict the effect of antibodies on recovery. RESULTS: After cisplatin injection, serum creatinine and histologic injuries peaked on day 4. Treatment with a JAM-C blocking antibody on days 4 and 5 promoted the functional and histologic recovery of cisplatin-induced AKI on days 5 and 6. Facilitating recovery with a JAM-C blocking antibody correlated with significantly increased circulating intercellular adhesion molecule 1+ Tamm-Horsfall protein+ neutrophils and significantly decreased renal neutrophil infiltration, indicating that facilitating reverse the TEM of neutrophils from the kidney to the peripheral circulation partially mediated the resolution of inflammation and recovery. CONCLUSIONS: These results demonstrated that reverse TEM is involved in the resolution of neutrophilic inflammation in cisplatin-induced AKI and that JAM-C is an important regulator of this process. |Acute Kidney Injury/chemically induced/*immunology [MESH] |Animals [MESH] |Cisplatin [MESH] |Junctional Adhesion Molecule C/*physiology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH]Blocking junctional adhesion molecule C promotes the recovery of cis(epmc).pdf DeepDyve Pubget Overpricing