Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1371/journal.pone.0123724 http://scihub22266oqcxt.onion/10.1371/journal.pone.0123724 C4397085!4397085 !25874449     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25874449 &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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25874449 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+One 2015 ; 10 (4 ): e0123724 Nephropedia Template TP {{tp|p=25874449 |t=2015. Rosiglitzone suppresses angiotensin II-induced production of KLF5 and cell proliferation in rat vascular smooth muscle cells |pdf=|usr=}}{{25874449 }} gab.com Text Rosiglitzone suppresses angiotensin II-induced production of KLF5 and cell proliferation in rat vascular smooth muscle cells JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25874449 #FOAvip Krüppel-like factor (KLF) 5, which initiates vascular smooth muscle cell (VSMC) proliferation, also participates in Angiotensin (Ang) II-induced vascular remodeling. The protective effect of rosiglitazone on vascular remodeling may be due to their impact on VSMC proliferation. However, the underlying mechanisms involved remain unclear. This study was designed to investigate whether the antiproliferation effects of rosiglitazone are mediated by regulating Ang II/KLF5 response. We found that, in aortas of Ang II-infused rats, vascular remodeling and KLF5 expression were markedly increased, and its target gene cyclin D1 was overexpressed. Co-treatment with rosiglitazone diminished these changes. In growth-arrested VSMCs, PPAR-? agonists (rosiglitazone and 15d-PGJ2) dose-dependently inhibited Ang II-induced cell proliferation and expression of KLF5 and cyclin D1. Moreover, these effects were attenuated by the PPAR-? antagonists GW9662, bisphenol A diglycidyl ether and PPAR-? specific siRNA. Furthermore, rosiglitazone inhibited Ang II-induced phosphorylation of protein kinase C (PKC) ? and extracellular signal-regulated kinase (ERK) 1/2 and activation of early growth response protein (Egr). In conclusion, in Ang II-stimulated VSMCs, rosiglitazone might have an antiproliferative effect through mechanisms that include reducing KLF5 expression, and a crosstalk between PPAR-? and PKC?/ERK1/2/Egr may be involved in. These findings not only provide a previously unrecognized mechanism by which PPAR-? agonists inhibit VSMC proliferation, but also document a novel evidence for the beneficial vascular effect of PPAR-? activation. Twit Text FOAVip Rosiglitzone suppresses angiotensin II-induced production of KLF5 and cell proliferation in rat vascular smooth muscle cells ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25874449 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25874449 #FOAvip English Wikipedia <ref>{{Cite pmid|25874449 }}</ref> Rosiglitzone suppresses angiotensin II-induced production of KLF5 and cell proliferation in rat vascular smooth muscle cells #MMPMID25874449 Gao D ; Hao G ; Meng Z ; Ning N ; Yang G ; Liu Z ; Dong X ; Niu X PLoS One 2015[]; 10 (4 ): e0123724 PMID25874449 show ga Krüppel-like factor (KLF) 5, which initiates vascular smooth muscle cell (VSMC) proliferation, also participates in Angiotensin (Ang) II-induced vascular remodeling. The protective effect of rosiglitazone on vascular remodeling may be due to their impact on VSMC proliferation. However, the underlying mechanisms involved remain unclear. This study was designed to investigate whether the antiproliferation effects of rosiglitazone are mediated by regulating Ang II/KLF5 response. We found that, in aortas of Ang II-infused rats, vascular remodeling and KLF5 expression were markedly increased, and its target gene cyclin D1 was overexpressed. Co-treatment with rosiglitazone diminished these changes. In growth-arrested VSMCs, PPAR-? agonists (rosiglitazone and 15d-PGJ2) dose-dependently inhibited Ang II-induced cell proliferation and expression of KLF5 and cyclin D1. Moreover, these effects were attenuated by the PPAR-? antagonists GW9662, bisphenol A diglycidyl ether and PPAR-? specific siRNA. Furthermore, rosiglitazone inhibited Ang II-induced phosphorylation of protein kinase C (PKC) ? and extracellular signal-regulated kinase (ERK) 1/2 and activation of early growth response protein (Egr). In conclusion, in Ang II-stimulated VSMCs, rosiglitazone might have an antiproliferative effect through mechanisms that include reducing KLF5 expression, and a crosstalk between PPAR-? and PKC?/ERK1/2/Egr may be involved in. These findings not only provide a previously unrecognized mechanism by which PPAR-? agonists inhibit VSMC proliferation, but also document a novel evidence for the beneficial vascular effect of PPAR-? activation. |Angiotensin II/*pharmacology [MESH] |Anilides/pharmacology [MESH] |Animals [MESH] |Blood Pressure/drug effects [MESH] |Body Weight/drug effects [MESH] |Cell Proliferation/*drug effects [MESH] |Cells, Cultured [MESH] |Cyclin D1/metabolism [MESH] |Gene Expression Regulation/drug effects [MESH] |Hypoglycemic Agents/*pharmacology [MESH] |Kruppel-Like Transcription Factors/genetics/*metabolism [MESH] |Male [MESH] |Mitogen-Activated Protein Kinase 1/metabolism [MESH] |Mitogen-Activated Protein Kinase 3/metabolism [MESH] |Muscle, Smooth, Vascular/cytology/metabolism [MESH] |PPAR gamma/agonists/antagonists & inhibitors/metabolism [MESH] |Phosphorylation/drug effects [MESH] |Prostaglandin D2/analogs & derivatives/pharmacology [MESH] |Protein Kinase C/metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Rosiglitazone [MESH] |Signal Transduction/drug effects [MESH]Rosiglitzone suppresses angiotensin II-induced production of KLF5 and (epmc).pdf DeepDyve Pubget Overpricing