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10.1111/jcmm.13448 http://scihub22266oqcxt.onion/10.1111/jcmm.13448 C5824371!5824371 !29193726     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29193726 &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       J+Cell+Mol+Med 2018 ; 22 (3 ): 2028-2032 Nephropedia Template TP {{tp|p=29193726 |t=2018. Dihydroartemisinin up-regulates VE-cadherin expression in human renal glomerular endothelial cells |pdf=|usr=}}{{29193726 }} gab.com Text Dihydroartemisinin up-regulates VE-cadherin expression in human renal glomerular endothelial cells JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29193726 #FOAvip The antimalarial agent dihydroartemisinin (DHA) has been shown to be anti-inflammatory. In this study, we found that DHA increased the expression of the junctional protein vascular endothelial (VE)-cadherin in human renal glomerular endothelial cells. In addition, DHA inhibited TGF-? RI-Smad2/3 signalling and its downstream effectors SNAIL and SLUG, which repress VE-cadherin gene transcription. Correspondingly, DHA decreased the binding of SNAIL and SLUG to the VE-cadherin promoter. Together, our results suggest an effect of DHA in regulating glomerular permeability by elevation of VE-cadherin expression. Twit Text FOAVip Dihydroartemisinin up-regulates VE-cadherin expression in human renal glomerular endothelial cells ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29193726 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29193726 #FOAvip English Wikipedia <ref>{{Cite pmid|29193726 }}</ref> Dihydroartemisinin up-regulates VE-cadherin expression in human renal glomerular endothelial cells #MMPMID29193726 Li L ; Chen X ; Dong F ; Liu Q ; Zhang C ; Xu D ; Allen TD ; Liu J J Cell Mol Med 2018[Mar]; 22 (3 ): 2028-2032 PMID29193726 show ga The antimalarial agent dihydroartemisinin (DHA) has been shown to be anti-inflammatory. In this study, we found that DHA increased the expression of the junctional protein vascular endothelial (VE)-cadherin in human renal glomerular endothelial cells. In addition, DHA inhibited TGF-? RI-Smad2/3 signalling and its downstream effectors SNAIL and SLUG, which repress VE-cadherin gene transcription. Correspondingly, DHA decreased the binding of SNAIL and SLUG to the VE-cadherin promoter. Together, our results suggest an effect of DHA in regulating glomerular permeability by elevation of VE-cadherin expression. |Anti-Inflammatory Agents, Non-Steroidal/*pharmacology [MESH] |Antigens, CD/*genetics/metabolism [MESH] |Antimalarials/pharmacology [MESH] |Artemisinins/*pharmacology [MESH] |Cadherins/agonists/*genetics/metabolism [MESH] |Cell Line [MESH] |Drug Repositioning [MESH] |Endothelial Cells/cytology/*drug effects/metabolism [MESH] |Gene Expression Regulation [MESH] |Humans [MESH] |Kidney Glomerulus/cytology/drug effects/metabolism [MESH] |Promoter Regions, Genetic [MESH] |Protein Binding [MESH] |Signal Transduction [MESH] |Smad2 Protein/antagonists & inhibitors/*genetics/metabolism [MESH] |Smad3 Protein/genetics/metabolism [MESH] |Snail Family Transcription Factors/genetics/metabolism [MESH]Dihydroartemisinin up-regulates VE-cadherin expression in human renal (epmc).pdf DeepDyve Pubget Overpricing