Protection of neonatal rat cardiac myocytes against radiation-induced damage with agonists of growth hormone-releasing hormone
[Display omitted] Despite the great clinical significance of radiation-induced cardiac damage, experimental investigation of its mechanisms is an unmet need in medicine. Beneficial effects of growth hormone-releasing hormone (GHRH) agonists in regeneration of the heart have been demonstrated. The ai...
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| Veröffentlicht in: | Pharmacological research 2016-09, Vol.111, p.859-866 |
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| creator | Kiscsatári, Laura Varga, Zoltán Schally, Andrew V. Gáspár, Renáta Nagy, Csilla Terézia Giricz, Zoltán Ferdinandy, Péter Fábián, Gabriella Kahán, Zsuzsanna Görbe, Anikó |
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Despite the great clinical significance of radiation-induced cardiac damage, experimental investigation of its mechanisms is an unmet need in medicine. Beneficial effects of growth hormone-releasing hormone (GHRH) agonists in regeneration of the heart have been demonstrated. The aim of this study was the evaluation of the potential of modern GHRH agonistic analogs in prevention of radiation damage in an in vitro cardiac myocyte-based model.
Cultures of cardiac myocytes isolated from newborn rats (NRVM) were exposed to a radiation dose of 10Gy. The effects of the agonistic analogs, JI-34 and MR-356, of human GHRH on cell viability, proliferation, their mechanism of action and the protein expression of the GHRH/SV1 receptors were studied.
JI-34 and MR-356, had no effect on cell viability or proliferation in unirradiated cultures. However, in irradiated cells JI-34 showed protective effects on cell viability at concentrations of 10 and 100nM, and MR-356 at 500nM; but no such protective effect was detected on cell proliferation. Both agonistic analogs decreased radiation-induced ROS level and JI-34 interfered with the activation of SAFE/RISK pathways. Using Western blot analysis, a 52kDa protein isoform of GHRHR was detected in the samples in both irradiated and unirradiated cells.
Since GHRH agonistic analogs, JI-34 and MR-356 alleviated radiation-induced damage of cardiac myocytes, they should be tested in vivo as potential protective agents against radiogenic heart damage. |
| doi_str_mv | 10.1016/j.phrs.2016.07.036 |
| format | Article |
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Despite the great clinical significance of radiation-induced cardiac damage, experimental investigation of its mechanisms is an unmet need in medicine. Beneficial effects of growth hormone-releasing hormone (GHRH) agonists in regeneration of the heart have been demonstrated. The aim of this study was the evaluation of the potential of modern GHRH agonistic analogs in prevention of radiation damage in an in vitro cardiac myocyte-based model.
Cultures of cardiac myocytes isolated from newborn rats (NRVM) were exposed to a radiation dose of 10Gy. The effects of the agonistic analogs, JI-34 and MR-356, of human GHRH on cell viability, proliferation, their mechanism of action and the protein expression of the GHRH/SV1 receptors were studied.
JI-34 and MR-356, had no effect on cell viability or proliferation in unirradiated cultures. However, in irradiated cells JI-34 showed protective effects on cell viability at concentrations of 10 and 100nM, and MR-356 at 500nM; but no such protective effect was detected on cell proliferation. Both agonistic analogs decreased radiation-induced ROS level and JI-34 interfered with the activation of SAFE/RISK pathways. Using Western blot analysis, a 52kDa protein isoform of GHRHR was detected in the samples in both irradiated and unirradiated cells.
Since GHRH agonistic analogs, JI-34 and MR-356 alleviated radiation-induced damage of cardiac myocytes, they should be tested in vivo as potential protective agents against radiogenic heart damage.</description><identifier>ISSN: 1043-6618</identifier><identifier>EISSN: 1096-1186</identifier><identifier>DOI: 10.1016/j.phrs.2016.07.036</identifier><identifier>PMID: 27480202</identifier><language>eng</language><publisher>Netherlands: Elsevier Ltd</publisher><subject>Alprostadil - analogs & derivatives ; Alprostadil - pharmacology ; Animals ; Animals, Newborn ; Cardiac myocytes ; Cardioprotection ; Cardiotoxicity ; Cell Proliferation - drug effects ; Cell Proliferation - radiation effects ; Cell Survival - drug effects ; Cell Survival - radiation effects ; Cells, Cultured ; Cytoprotection ; Dose-Response Relationship, Drug ; GHRH agonists ; GHRH/SV1 receptors ; Growth Hormone-Releasing Hormone - agonists ; Growth Hormone-Releasing Hormone - analogs & derivatives ; Growth Hormone-Releasing Hormone - metabolism ; Growth Hormone-Releasing Hormone - pharmacology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Myocytes, Cardiac - radiation effects ; Peptide Fragments - pharmacology ; Radiation damage ; Radiation-Protective Agents - pharmacology ; Rats, Wistar ; Reactive Oxygen Species - metabolism ; Receptors, Neuropeptide - agonists ; Receptors, Neuropeptide - metabolism ; Receptors, Pituitary Hormone-Regulating Hormone - agonists ; Receptors, Pituitary Hormone-Regulating Hormone - metabolism ; Signal Transduction - drug effects ; Signal Transduction - radiation effects</subject><ispartof>Pharmacological research, 2016-09, Vol.111, p.859-866</ispartof><rights>2016 Elsevier Ltd</rights><rights>Copyright © 2016 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-6ba2383ee2ad7c1060916e2f05c3c13834a819031c30a7ef5b7eb5ebb927abbf3</citedby><cites>FETCH-LOGICAL-c470t-6ba2383ee2ad7c1060916e2f05c3c13834a819031c30a7ef5b7eb5ebb927abbf3</cites><orcidid>0000-0002-1680-9256</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.phrs.2016.07.036$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27480202$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kiscsatári, Laura</creatorcontrib><creatorcontrib>Varga, Zoltán</creatorcontrib><creatorcontrib>Schally, Andrew V.</creatorcontrib><creatorcontrib>Gáspár, Renáta</creatorcontrib><creatorcontrib>Nagy, Csilla Terézia</creatorcontrib><creatorcontrib>Giricz, Zoltán</creatorcontrib><creatorcontrib>Ferdinandy, Péter</creatorcontrib><creatorcontrib>Fábián, Gabriella</creatorcontrib><creatorcontrib>Kahán, Zsuzsanna</creatorcontrib><creatorcontrib>Görbe, Anikó</creatorcontrib><title>Protection of neonatal rat cardiac myocytes against radiation-induced damage with agonists of growth hormone-releasing hormone</title><title>Pharmacological research</title><addtitle>Pharmacol Res</addtitle><description>[Display omitted]
Despite the great clinical significance of radiation-induced cardiac damage, experimental investigation of its mechanisms is an unmet need in medicine. Beneficial effects of growth hormone-releasing hormone (GHRH) agonists in regeneration of the heart have been demonstrated. The aim of this study was the evaluation of the potential of modern GHRH agonistic analogs in prevention of radiation damage in an in vitro cardiac myocyte-based model.
Cultures of cardiac myocytes isolated from newborn rats (NRVM) were exposed to a radiation dose of 10Gy. The effects of the agonistic analogs, JI-34 and MR-356, of human GHRH on cell viability, proliferation, their mechanism of action and the protein expression of the GHRH/SV1 receptors were studied.
JI-34 and MR-356, had no effect on cell viability or proliferation in unirradiated cultures. However, in irradiated cells JI-34 showed protective effects on cell viability at concentrations of 10 and 100nM, and MR-356 at 500nM; but no such protective effect was detected on cell proliferation. Both agonistic analogs decreased radiation-induced ROS level and JI-34 interfered with the activation of SAFE/RISK pathways. Using Western blot analysis, a 52kDa protein isoform of GHRHR was detected in the samples in both irradiated and unirradiated cells.
Since GHRH agonistic analogs, JI-34 and MR-356 alleviated radiation-induced damage of cardiac myocytes, they should be tested in vivo as potential protective agents against radiogenic heart damage.</description><subject>Alprostadil - analogs & derivatives</subject><subject>Alprostadil - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Cardiac myocytes</subject><subject>Cardioprotection</subject><subject>Cardiotoxicity</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Proliferation - radiation effects</subject><subject>Cell Survival - drug effects</subject><subject>Cell Survival - radiation effects</subject><subject>Cells, Cultured</subject><subject>Cytoprotection</subject><subject>Dose-Response Relationship, Drug</subject><subject>GHRH agonists</subject><subject>GHRH/SV1 receptors</subject><subject>Growth Hormone-Releasing Hormone - agonists</subject><subject>Growth Hormone-Releasing Hormone - analogs & derivatives</subject><subject>Growth Hormone-Releasing Hormone - metabolism</subject><subject>Growth Hormone-Releasing Hormone - pharmacology</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Myocytes, Cardiac - radiation effects</subject><subject>Peptide Fragments - pharmacology</subject><subject>Radiation damage</subject><subject>Radiation-Protective Agents - pharmacology</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, Neuropeptide - agonists</subject><subject>Receptors, Neuropeptide - metabolism</subject><subject>Receptors, Pituitary Hormone-Regulating Hormone - agonists</subject><subject>Receptors, Pituitary Hormone-Regulating Hormone - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - radiation effects</subject><issn>1043-6618</issn><issn>1096-1186</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFr3DAQhUVp6Kab_oEeio-92B3JtmxDLyUkaSHQHJKzGMvjXS22tJW0CXvJb4_MJjn2NMOb9x7Mx9hXDgUHLn_siv3Wh0KkvYCmgFJ-YOccOplz3sqPy16VuZS8XbHPIewAoKs4fGIr0VQtCBDn7PnOu0g6GmczN2aWnMWIU-YxZhr9YFBn89HpY6SQ4QaNDTEdk75EcmOHg6YhG3DGDWVPJm6Ty1kTYlj6Nt49JWnr_Ows5Z4mwmDs5k25YGcjToG-vM41e7i-ur_8nd_-vflz-es211UDMZc9irItiQQOjeYgoeOSxAi1LjVPlwpb3kHJdQnY0Fj3DfU19X0nGuz7sVyz76fevXf_DhSimk3QNE2YPj4ExVsBdSc7qJNVnKzauxA8jWrvzYz-qDiohbvaqYW7WrgraFTinkLfXvsP_UzDe-QNdDL8PBkoffloyKugDdnEzviEXw3O_K__BcP7l2Y</recordid><startdate>201609</startdate><enddate>201609</enddate><creator>Kiscsatári, Laura</creator><creator>Varga, Zoltán</creator><creator>Schally, Andrew V.</creator><creator>Gáspár, Renáta</creator><creator>Nagy, Csilla Terézia</creator><creator>Giricz, Zoltán</creator><creator>Ferdinandy, Péter</creator><creator>Fábián, Gabriella</creator><creator>Kahán, Zsuzsanna</creator><creator>Görbe, Anikó</creator><general>Elsevier Ltd</general><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><orcidid>https://orcid.org/0000-0002-1680-9256</orcidid></search><sort><creationdate>201609</creationdate><title>Protection of neonatal rat cardiac myocytes against radiation-induced damage with agonists of growth hormone-releasing hormone</title><author>Kiscsatári, Laura ; Varga, Zoltán ; Schally, Andrew V. ; Gáspár, Renáta ; Nagy, Csilla Terézia ; Giricz, Zoltán ; Ferdinandy, Péter ; Fábián, Gabriella ; Kahán, Zsuzsanna ; Görbe, Anikó</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-6ba2383ee2ad7c1060916e2f05c3c13834a819031c30a7ef5b7eb5ebb927abbf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alprostadil - analogs & derivatives</topic><topic>Alprostadil - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Cardiac myocytes</topic><topic>Cardioprotection</topic><topic>Cardiotoxicity</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Proliferation - radiation effects</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - radiation effects</topic><topic>Cells, Cultured</topic><topic>Cytoprotection</topic><topic>Dose-Response Relationship, Drug</topic><topic>GHRH agonists</topic><topic>GHRH/SV1 receptors</topic><topic>Growth Hormone-Releasing Hormone - agonists</topic><topic>Growth Hormone-Releasing Hormone - analogs & derivatives</topic><topic>Growth Hormone-Releasing Hormone - metabolism</topic><topic>Growth Hormone-Releasing Hormone - pharmacology</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Myocytes, Cardiac - radiation effects</topic><topic>Peptide Fragments - pharmacology</topic><topic>Radiation damage</topic><topic>Radiation-Protective Agents - pharmacology</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, Neuropeptide - agonists</topic><topic>Receptors, Neuropeptide - metabolism</topic><topic>Receptors, Pituitary Hormone-Regulating Hormone - agonists</topic><topic>Receptors, Pituitary Hormone-Regulating Hormone - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - radiation effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kiscsatári, Laura</creatorcontrib><creatorcontrib>Varga, Zoltán</creatorcontrib><creatorcontrib>Schally, Andrew V.</creatorcontrib><creatorcontrib>Gáspár, Renáta</creatorcontrib><creatorcontrib>Nagy, Csilla Terézia</creatorcontrib><creatorcontrib>Giricz, Zoltán</creatorcontrib><creatorcontrib>Ferdinandy, Péter</creatorcontrib><creatorcontrib>Fábián, Gabriella</creatorcontrib><creatorcontrib>Kahán, Zsuzsanna</creatorcontrib><creatorcontrib>Görbe, Anikó</creatorcontrib><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>Pharmacological research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kiscsatári, Laura</au><au>Varga, Zoltán</au><au>Schally, Andrew V.</au><au>Gáspár, Renáta</au><au>Nagy, Csilla Terézia</au><au>Giricz, Zoltán</au><au>Ferdinandy, Péter</au><au>Fábián, Gabriella</au><au>Kahán, Zsuzsanna</au><au>Görbe, Anikó</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protection of neonatal rat cardiac myocytes against radiation-induced damage with agonists of growth hormone-releasing hormone</atitle><jtitle>Pharmacological research</jtitle><addtitle>Pharmacol Res</addtitle><date>2016-09</date><risdate>2016</risdate><volume>111</volume><spage>859</spage><epage>866</epage><pages>859-866</pages><issn>1043-6618</issn><eissn>1096-1186</eissn><abstract>[Display omitted]
Despite the great clinical significance of radiation-induced cardiac damage, experimental investigation of its mechanisms is an unmet need in medicine. Beneficial effects of growth hormone-releasing hormone (GHRH) agonists in regeneration of the heart have been demonstrated. The aim of this study was the evaluation of the potential of modern GHRH agonistic analogs in prevention of radiation damage in an in vitro cardiac myocyte-based model.
Cultures of cardiac myocytes isolated from newborn rats (NRVM) were exposed to a radiation dose of 10Gy. The effects of the agonistic analogs, JI-34 and MR-356, of human GHRH on cell viability, proliferation, their mechanism of action and the protein expression of the GHRH/SV1 receptors were studied.
JI-34 and MR-356, had no effect on cell viability or proliferation in unirradiated cultures. However, in irradiated cells JI-34 showed protective effects on cell viability at concentrations of 10 and 100nM, and MR-356 at 500nM; but no such protective effect was detected on cell proliferation. Both agonistic analogs decreased radiation-induced ROS level and JI-34 interfered with the activation of SAFE/RISK pathways. Using Western blot analysis, a 52kDa protein isoform of GHRHR was detected in the samples in both irradiated and unirradiated cells.
Since GHRH agonistic analogs, JI-34 and MR-356 alleviated radiation-induced damage of cardiac myocytes, they should be tested in vivo as potential protective agents against radiogenic heart damage.</abstract><cop>Netherlands</cop><pub>Elsevier Ltd</pub><pmid>27480202</pmid><doi>10.1016/j.phrs.2016.07.036</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-1680-9256</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Pharmacological research, 2016-09, Vol.111, p.859-866 |
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| subjects | Alprostadil - analogs & derivatives Alprostadil - pharmacology Animals Animals, Newborn Cardiac myocytes Cardioprotection Cardiotoxicity Cell Proliferation - drug effects Cell Proliferation - radiation effects Cell Survival - drug effects Cell Survival - radiation effects Cells, Cultured Cytoprotection Dose-Response Relationship, Drug GHRH agonists GHRH/SV1 receptors Growth Hormone-Releasing Hormone - agonists Growth Hormone-Releasing Hormone - analogs & derivatives Growth Hormone-Releasing Hormone - metabolism Growth Hormone-Releasing Hormone - pharmacology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Myocytes, Cardiac - radiation effects Peptide Fragments - pharmacology Radiation damage Radiation-Protective Agents - pharmacology Rats, Wistar Reactive Oxygen Species - metabolism Receptors, Neuropeptide - agonists Receptors, Neuropeptide - metabolism Receptors, Pituitary Hormone-Regulating Hormone - agonists Receptors, Pituitary Hormone-Regulating Hormone - metabolism Signal Transduction - drug effects Signal Transduction - radiation effects |
| title | Protection of neonatal rat cardiac myocytes against radiation-induced damage with agonists of growth hormone-releasing hormone |
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