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10.1152/ajprenal.00083.2008 http://scihub22266oqcxt.onion/10.1152/ajprenal.00083.2008 C5504389!5504389!18495803     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18495803&cmd=llinks): Failed to open stream: HTTP request failed! 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Tamm-Horsfall protein protects the kidney from ischemic injury by decreasing inflammation and altering TLR4 expression |pdf=|usr=}}{{18495803}} gab.com Text Tamm-Horsfall protein protects the kidney from ischemic injury by decreasing inflammation and altering TLR4 expression JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=18495803 #FOAvip Tamm-Horsfall protein (THP) is a glycoprotein with unclear functions expressed exclusively in thick ascending limbs (TAL) of the kidney. Its role in ischemic acute kidney injury is uncertain, with previous data suggesting a possible negative effect by enhancing cast formation and promoting inflammation. Using a recently characterized THP knockout mouse (THP?/?), we investigated the role of THP in renal ischemia-reperfusion injury (IRI). In wild-type mice (THP+/+), THP expression was increased by injury. THP?/? mice developed more functional and histological renal damage after IRI compared with THP+/+. THP?/? kidneys showed more inflammation and tubular necrosis. Cast formation correlated with the severity of injury and was independent of THP presence. THP absence was associated with a more necrotic, rather than apoptotic, phenotype of cell death. The outer medulla was predominantly affected, where significant interstitial neutrophil infiltration was detected in proximity to injured S3 proximal tubular segments and TAL. This coincided with an enhanced expression of the innate immunity receptor Toll-like receptor 4 (TLR4) in S3 segments of THP?/? compared with THP+/+ mice. Specifically, a basolateral S3 expression of TLR4 was more evident in THP?/? kidneys compared with a more apical distribution in THP+/+. Such basolateral location for TLR4 allows a greater interaction with proinflammatory ligands present in the interstitium during ischemia. In conclusion, we are showing a completely novel role for a very old protein in the setting of renal injury. Our data suggest that THP stabilizes the outer medulla in the face of injury by decreasing inflammation, possibly through an effect on TLR4. Twit Text FOAVip Tamm-Horsfall protein protects the kidney from ischemic injury by decreasing inflammation and altering TLR4 expression ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=18495803 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18495803 #FOAvip English Wikipedia <ref>{{Cite pmid|18495803}}</ref> Tamm-Horsfall protein protects the kidney from ischemic injury by decreasing inflammation and altering TLR4 expression #MMPMID18495803 El-Achkar TM; Wu XR; Rauchman M; McCracken R; Kiefer S; Dagher PC Am J Physiol Renal Physiol 2008[Aug]; 295 (2): F534-44 PMID18495803show ga Tamm-Horsfall protein (THP) is a glycoprotein with unclear functions expressed exclusively in thick ascending limbs (TAL) of the kidney. Its role in ischemic acute kidney injury is uncertain, with previous data suggesting a possible negative effect by enhancing cast formation and promoting inflammation. Using a recently characterized THP knockout mouse (THP?/?), we investigated the role of THP in renal ischemia-reperfusion injury (IRI). In wild-type mice (THP+/+), THP expression was increased by injury. THP?/? mice developed more functional and histological renal damage after IRI compared with THP+/+. THP?/? kidneys showed more inflammation and tubular necrosis. Cast formation correlated with the severity of injury and was independent of THP presence. THP absence was associated with a more necrotic, rather than apoptotic, phenotype of cell death. The outer medulla was predominantly affected, where significant interstitial neutrophil infiltration was detected in proximity to injured S3 proximal tubular segments and TAL. This coincided with an enhanced expression of the innate immunity receptor Toll-like receptor 4 (TLR4) in S3 segments of THP?/? compared with THP+/+ mice. Specifically, a basolateral S3 expression of TLR4 was more evident in THP?/? kidneys compared with a more apical distribution in THP+/+. Such basolateral location for TLR4 allows a greater interaction with proinflammatory ligands present in the interstitium during ischemia. In conclusion, we are showing a completely novel role for a very old protein in the setting of renal injury. Our data suggest that THP stabilizes the outer medulla in the face of injury by decreasing inflammation, possibly through an effect on TLR4. äTamm-Horsfall protein protects the kidney from ischemic injury by decr(epmc).pdf DeepDyve Pubget Overpricing