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10.1186/s12872-015-0103-4 http://scihub22266oqcxt.onion/10.1186/s12872-015-0103-4 C4597385!4597385!26446519     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 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       BMC+Cardiovasc+Disord 2015 ; 15 (ä): ä Nephropedia Template TP {{tp|p=26446519|t=2015. PEP-1-SOD1 fusion proteins block cardiac myofibroblast activation and angiotensin II-induced collagen production |pdf=|usr=}}{{26446519}} gab.com Text PEP-1-SOD1 fusion proteins block cardiac myofibroblast activation and angiotensin II-induced collagen production JO: BMC Cardiovasc Disord http://www.kidney.de/pget.php?&tw=1&pmid=26446519 #FOAvip Background: Oxidative stress is closely associated with cardiac fibrosis. However, the effect of copper, zinc-superoxide dismutase (SOD1) as a therapeutic agent is limited due to the insufficient transduction. This study was aimed to investigate the effect of PEP-1-SOD1 fusion protein on angiotensin II (ANG II)-induced collagen metabolism in rat cardiac myofibroblasts (MCFs). Methods: MCFs were pretreated with SOD1 or PEP-1-SOD1 fusion protein for 2 h followed by incubation with ANG II for 24 h. Cell proliferation was measured by Cell Counting Kit-8. Superoxide anion productions were detected by both fluorescent microscopy and Flow Cytometry. MMP-1 and TIMP-1 were determined by ELISA. Intracellular MDA content and SOD activity were examined by commercial assay kits. Protein expression was analyzed by western blotting. Results: PEP-1-SOD1 fusion protein efficiently transduced into MCF, scavenged intracellular O2?, decreased intracellular MDA content, increased SOD activity, suppressed ANG II-induced proliferation, reduced expression of TGF-?1, ?-SMA, collagen type I and III, restored MMP-1 secretion, and attenuated TIMP-1 secretion. Conclusion: PEP-1-SOD1 suppressed MCF proliferation and differentiation and reduced production of collagen type I and III. Therefore, PEP-1-SOD1 fusion protein may be a potential novel therapeutic agent for cardiac fibrosis. Electronic supplementary material: The online version of this article (doi:10.1186/s12872-015-0103-4) contains supplementary material, which is available to authorized users. Twit Text FOAVip PEP-1-SOD1 fusion proteins block cardiac myofibroblast activation and angiotensin II-induced collagen production ????BMC Cardiovasc Disord http://www.kidney.de/pget.php?&tw=1&pmid=26446519 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26446519 #FOAvip English Wikipedia <ref>{{Cite pmid|26446519}}</ref> PEP-1-SOD1 fusion proteins block cardiac myofibroblast activation and angiotensin II-induced collagen production #MMPMID26446519 Tan LG; Xiao JH; Yu DL; Zhang L; Zheng F; Guo LY; Yang JY; Tang Jm; Chen SY; Wang JN BMC Cardiovasc Disord 2015[]; 15 (ä): ä PMID26446519show ga Background: Oxidative stress is closely associated with cardiac fibrosis. However, the effect of copper, zinc-superoxide dismutase (SOD1) as a therapeutic agent is limited due to the insufficient transduction. This study was aimed to investigate the effect of PEP-1-SOD1 fusion protein on angiotensin II (ANG II)-induced collagen metabolism in rat cardiac myofibroblasts (MCFs). Methods: MCFs were pretreated with SOD1 or PEP-1-SOD1 fusion protein for 2 h followed by incubation with ANG II for 24 h. Cell proliferation was measured by Cell Counting Kit-8. Superoxide anion productions were detected by both fluorescent microscopy and Flow Cytometry. MMP-1 and TIMP-1 were determined by ELISA. Intracellular MDA content and SOD activity were examined by commercial assay kits. Protein expression was analyzed by western blotting. Results: PEP-1-SOD1 fusion protein efficiently transduced into MCF, scavenged intracellular O2?, decreased intracellular MDA content, increased SOD activity, suppressed ANG II-induced proliferation, reduced expression of TGF-?1, ?-SMA, collagen type I and III, restored MMP-1 secretion, and attenuated TIMP-1 secretion. Conclusion: PEP-1-SOD1 suppressed MCF proliferation and differentiation and reduced production of collagen type I and III. Therefore, PEP-1-SOD1 fusion protein may be a potential novel therapeutic agent for cardiac fibrosis. Electronic supplementary material: The online version of this article (doi:10.1186/s12872-015-0103-4) contains supplementary material, which is available to authorized users. äPEP-1-SOD1 fusion proteins block cardiac myofibroblast activation and (epmc).pdf DeepDyve Pubget Overpricing