Pharmacologically Preconditioned Skeletal Myoblasts Are Resistant to Oxidative Stress and Promote Angiomyogenesis via Release of Paracrine Factors in the Infarcted Heart
Strategies to enhance skeletal myoblast (SkM) survival after transplantation in the ischemic heart have achieved little success. We posit that preconditioned (PC) SkMs show improved survival and promote repair of the infarcted myocardium via paracrine signaling after transplantation. SkMs from male...
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| Veröffentlicht in: | Circulation research 2007-03, Vol.100 (4), p.545-555 |
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| description | Strategies to enhance skeletal myoblast (SkM) survival after transplantation in the ischemic heart have achieved little success. We posit that preconditioned (PC) SkMs show improved survival and promote repair of the infarcted myocardium via paracrine signaling after transplantation. SkMs from male Fischer-344 rats (rSkMs) were PC for 30 minutes with 200 μmol/L diazoxide. Treatment of PC rSkMs with 100 μmol/L H2O2 for 2 hours resulted in significantly reduced cell injury, as shown by lactate dehydrogenase–release assay, and prevented apoptosis, as demonstrated by cytochrome c translocation, TUNEL, annexin V staining, and preservation of mitochondrial membrane potential. PC rSkMs expressed elevated phospho-Akt (1.85-fold), basic fibroblast growth factor (1.44-fold), hepatocyte growth factor (2.26-fold), and cyclooxygenase-2 (1.33-fold) as compared with non-PC rSkMs. For in vivo studies, female Fischer-344 rats after permanent coronary artery ligation were grouped (n=12/group) to receive 80 μL of basal medium without rSkMs (group 1) or containing 1.5×10 non-PC (group 2) or PC (group 3) rSkMs. Real-time PCR for sry gene 4 days after transplantation (n=4/group) showed 1.93-fold higher survival of rSkMs in group 3 as compared with group 2. Four weeks later, echocardiography revealed improved indices of left ventricular function, including ejection fraction and fractional shortening in group 3 (P |
| doi_str_mv | 10.1161/01.RES.0000258460.41160.ef |
| format | Article |
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We posit that preconditioned (PC) SkMs show improved survival and promote repair of the infarcted myocardium via paracrine signaling after transplantation. SkMs from male Fischer-344 rats (rSkMs) were PC for 30 minutes with 200 μmol/L diazoxide. Treatment of PC rSkMs with 100 μmol/L H2O2 for 2 hours resulted in significantly reduced cell injury, as shown by lactate dehydrogenase–release assay, and prevented apoptosis, as demonstrated by cytochrome c translocation, TUNEL, annexin V staining, and preservation of mitochondrial membrane potential. PC rSkMs expressed elevated phospho-Akt (1.85-fold), basic fibroblast growth factor (1.44-fold), hepatocyte growth factor (2.26-fold), and cyclooxygenase-2 (1.33-fold) as compared with non-PC rSkMs. For in vivo studies, female Fischer-344 rats after permanent coronary artery ligation were grouped (n=12/group) to receive 80 μL of basal medium without rSkMs (group 1) or containing 1.5×10 non-PC (group 2) or PC (group 3) rSkMs. Real-time PCR for sry gene 4 days after transplantation (n=4/group) showed 1.93-fold higher survival of rSkMs in group 3 as compared with group 2. Four weeks later, echocardiography revealed improved indices of left ventricular function, including ejection fraction and fractional shortening in group 3 (P<0.02) as compared with groups 1 and 2. Blood vessel count per surface area (at ×400 magnification) was highest in scar and periscar areas in group 3 as compared with the other groups (P<0.05). We conclude that activation of signaling pathways of preconditioning in SkMs promoted their survival by release of paracrine factors to promote angiomyogenesis in the infarcted heart. Transplantation of PC SkMs for heart cell therapy is an innovative approach in the clinical perspective.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.0000258460.41160.ef</identifier><identifier>PMID: 17234963</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Cell Survival - drug effects ; Cell Survival - physiology ; Cell Transplantation - methods ; Coronary heart disease ; Diazoxide - pharmacology ; Fundamental and applied biological sciences. Psychology ; Heart ; Intercellular Signaling Peptides and Proteins - secretion ; Male ; Medical sciences ; Myoblasts, Skeletal - drug effects ; Myoblasts, Skeletal - physiology ; Myoblasts, Skeletal - transplantation ; Myocardial Infarction - physiopathology ; Myocardial Infarction - prevention & control ; Myocardial Infarction - surgery ; Myocarditis. Cardiomyopathies ; Neovascularization, Physiologic - drug effects ; Neovascularization, Physiologic - physiology ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Rats ; Rats, Inbred F344 ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 2007-03, Vol.100 (4), p.545-555</ispartof><rights>2007 American Heart Association, Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5474-44931cd4e922e711379148fb388193f886b6fc84702fde656df53a5d8709bfb23</citedby><cites>FETCH-LOGICAL-c5474-44931cd4e922e711379148fb388193f886b6fc84702fde656df53a5d8709bfb23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18565522$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17234963$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Niagara, Muhammad Idris</creatorcontrib><creatorcontrib>Haider, Husnain Kh</creatorcontrib><creatorcontrib>Jiang, Shujia</creatorcontrib><creatorcontrib>Ashraf, Muhammad</creatorcontrib><title>Pharmacologically Preconditioned Skeletal Myoblasts Are Resistant to Oxidative Stress and Promote Angiomyogenesis via Release of Paracrine Factors in the Infarcted Heart</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Strategies to enhance skeletal myoblast (SkM) survival after transplantation in the ischemic heart have achieved little success. We posit that preconditioned (PC) SkMs show improved survival and promote repair of the infarcted myocardium via paracrine signaling after transplantation. SkMs from male Fischer-344 rats (rSkMs) were PC for 30 minutes with 200 μmol/L diazoxide. Treatment of PC rSkMs with 100 μmol/L H2O2 for 2 hours resulted in significantly reduced cell injury, as shown by lactate dehydrogenase–release assay, and prevented apoptosis, as demonstrated by cytochrome c translocation, TUNEL, annexin V staining, and preservation of mitochondrial membrane potential. PC rSkMs expressed elevated phospho-Akt (1.85-fold), basic fibroblast growth factor (1.44-fold), hepatocyte growth factor (2.26-fold), and cyclooxygenase-2 (1.33-fold) as compared with non-PC rSkMs. For in vivo studies, female Fischer-344 rats after permanent coronary artery ligation were grouped (n=12/group) to receive 80 μL of basal medium without rSkMs (group 1) or containing 1.5×10 non-PC (group 2) or PC (group 3) rSkMs. Real-time PCR for sry gene 4 days after transplantation (n=4/group) showed 1.93-fold higher survival of rSkMs in group 3 as compared with group 2. Four weeks later, echocardiography revealed improved indices of left ventricular function, including ejection fraction and fractional shortening in group 3 (P<0.02) as compared with groups 1 and 2. Blood vessel count per surface area (at ×400 magnification) was highest in scar and periscar areas in group 3 as compared with the other groups (P<0.05). We conclude that activation of signaling pathways of preconditioning in SkMs promoted their survival by release of paracrine factors to promote angiomyogenesis in the infarcted heart. Transplantation of PC SkMs for heart cell therapy is an innovative approach in the clinical perspective.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - physiology</subject><subject>Cell Transplantation - methods</subject><subject>Coronary heart disease</subject><subject>Diazoxide - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart</subject><subject>Intercellular Signaling Peptides and Proteins - secretion</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myoblasts, Skeletal - drug effects</subject><subject>Myoblasts, Skeletal - physiology</subject><subject>Myoblasts, Skeletal - transplantation</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial Infarction - prevention & control</subject><subject>Myocardial Infarction - surgery</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkttuEzEQhlcIREPhFZCFBHcbfNoTd1HV0kpFjRq4tma948TUuy6205JH4i1xDlJ9Y8v6_pmxPhfFJ0bnjNXsK2Xz-8vVnObFq1bWdC7zPZ2jeVXMWMVlKauGvS5mGejKRgh6VryL8TelTArevS3OWMOF7GoxK_4tNxBG0N75tdXg3I4sA2o_DTZZP-FAVg_oMIEjP3a-dxBTJIuA5B6jjQmmRJInd3_tAMk-IVmlgDESmIZcx48-IVlMa-vHnV_jtM-QJws57RAiEm_IEgLoYCckV6CTD5HYiaQNkpvJQNApj3CNENL74o0BF_HDaT8vfl1d_ry4Lm_vvt9cLG5LXckmP112gulBYsc5NoyJpmOyNb1oW9YJ07Z1XxvdyoZyM2Bd1YOpBFRD29CuNz0X58WXY93H4P9sMSY12qjROZjQb6PKQUGpaDP47Qjq4GMMaNRjsCOEnWJU7UUpylQWpV5EqYMohSaHP566bPsRh5foyUwGPp8AiNmLCTBpG1-4tqqriu_HlUfu2buEIT647TMGtUFwaXNoLSjjJae0ySdOS3r4Bv8BqAavKg</recordid><startdate>20070302</startdate><enddate>20070302</enddate><creator>Niagara, Muhammad Idris</creator><creator>Haider, Husnain Kh</creator><creator>Jiang, Shujia</creator><creator>Ashraf, Muhammad</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070302</creationdate><title>Pharmacologically Preconditioned Skeletal Myoblasts Are Resistant to Oxidative Stress and Promote Angiomyogenesis via Release of Paracrine Factors in the Infarcted Heart</title><author>Niagara, Muhammad Idris ; Haider, Husnain Kh ; Jiang, Shujia ; Ashraf, Muhammad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5474-44931cd4e922e711379148fb388193f886b6fc84702fde656df53a5d8709bfb23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - physiology</topic><topic>Cell Transplantation - methods</topic><topic>Coronary heart disease</topic><topic>Diazoxide - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart</topic><topic>Intercellular Signaling Peptides and Proteins - secretion</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myoblasts, Skeletal - drug effects</topic><topic>Myoblasts, Skeletal - physiology</topic><topic>Myoblasts, Skeletal - transplantation</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial Infarction - prevention & control</topic><topic>Myocardial Infarction - surgery</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Niagara, Muhammad Idris</creatorcontrib><creatorcontrib>Haider, Husnain Kh</creatorcontrib><creatorcontrib>Jiang, Shujia</creatorcontrib><creatorcontrib>Ashraf, Muhammad</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Niagara, Muhammad Idris</au><au>Haider, Husnain Kh</au><au>Jiang, Shujia</au><au>Ashraf, Muhammad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacologically Preconditioned Skeletal Myoblasts Are Resistant to Oxidative Stress and Promote Angiomyogenesis via Release of Paracrine Factors in the Infarcted Heart</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2007-03-02</date><risdate>2007</risdate><volume>100</volume><issue>4</issue><spage>545</spage><epage>555</epage><pages>545-555</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Strategies to enhance skeletal myoblast (SkM) survival after transplantation in the ischemic heart have achieved little success. We posit that preconditioned (PC) SkMs show improved survival and promote repair of the infarcted myocardium via paracrine signaling after transplantation. SkMs from male Fischer-344 rats (rSkMs) were PC for 30 minutes with 200 μmol/L diazoxide. Treatment of PC rSkMs with 100 μmol/L H2O2 for 2 hours resulted in significantly reduced cell injury, as shown by lactate dehydrogenase–release assay, and prevented apoptosis, as demonstrated by cytochrome c translocation, TUNEL, annexin V staining, and preservation of mitochondrial membrane potential. PC rSkMs expressed elevated phospho-Akt (1.85-fold), basic fibroblast growth factor (1.44-fold), hepatocyte growth factor (2.26-fold), and cyclooxygenase-2 (1.33-fold) as compared with non-PC rSkMs. For in vivo studies, female Fischer-344 rats after permanent coronary artery ligation were grouped (n=12/group) to receive 80 μL of basal medium without rSkMs (group 1) or containing 1.5×10 non-PC (group 2) or PC (group 3) rSkMs. Real-time PCR for sry gene 4 days after transplantation (n=4/group) showed 1.93-fold higher survival of rSkMs in group 3 as compared with group 2. Four weeks later, echocardiography revealed improved indices of left ventricular function, including ejection fraction and fractional shortening in group 3 (P<0.02) as compared with groups 1 and 2. Blood vessel count per surface area (at ×400 magnification) was highest in scar and periscar areas in group 3 as compared with the other groups (P<0.05). We conclude that activation of signaling pathways of preconditioning in SkMs promoted their survival by release of paracrine factors to promote angiomyogenesis in the infarcted heart. Transplantation of PC SkMs for heart cell therapy is an innovative approach in the clinical perspective.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>17234963</pmid><doi>10.1161/01.RES.0000258460.41160.ef</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Cardiology. Vascular system Cell Survival - drug effects Cell Survival - physiology Cell Transplantation - methods Coronary heart disease Diazoxide - pharmacology Fundamental and applied biological sciences. Psychology Heart Intercellular Signaling Peptides and Proteins - secretion Male Medical sciences Myoblasts, Skeletal - drug effects Myoblasts, Skeletal - physiology Myoblasts, Skeletal - transplantation Myocardial Infarction - physiopathology Myocardial Infarction - prevention & control Myocardial Infarction - surgery Myocarditis. Cardiomyopathies Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - physiology Oxidative Stress - drug effects Oxidative Stress - physiology Rats Rats, Inbred F344 Vertebrates: cardiovascular system |
| title | Pharmacologically Preconditioned Skeletal Myoblasts Are Resistant to Oxidative Stress and Promote Angiomyogenesis via Release of Paracrine Factors in the Infarcted Heart |
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