Endothelin-1 and fibroblast growth factors stimulate the mitogen-activated protein kinase signaling cascade in cardiac myocytes. The potential role of the cascade in the integration of two signaling pathways leading to myocyte hypertrophy
Maximally effective concentrations of endothelin-1 (ET-1), acidic FGF (aFGF), or 12-O-tetradecanoylphorbol-13-acetate (TPA) activated mitogen-activated protein kinase (MAPK) by 3-4-fold in crude extracts of myocytes cultured from neonatal rat heart ventricles. Maximal activation was achieved after 5...
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| Veröffentlicht in: | The Journal of biological chemistry 1994-01, Vol.269 (2), p.1110-1119 |
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| creator | BOGOYEVITCH, M. A GLENNON, P. E ANDERSSON, M. B CLERK, A LAZOU, A MARSHALL, C. J PARKER, P. J SUGDEN, P. H |
| description | Maximally effective concentrations of endothelin-1 (ET-1), acidic FGF (aFGF), or 12-O-tetradecanoylphorbol-13-acetate (TPA)
activated mitogen-activated protein kinase (MAPK) by 3-4-fold in crude extracts of myocytes cultured from neonatal rat heart
ventricles. Maximal activation was achieved after 5 min. Thereafter, MAPK activity stimulated by ET-1 or aFGF declined to
control values within 1-2 h, whereas activation by TPA was more sustained. Two peaks of MAPK activity (a 42- and a 44-kDa
MAPK) were resolved in cells exposed to ET-1 or aFGF by fast protein liquid chromatography on a Mono Q column. One major and
one minor peak of MAPK kinase (MAPKK) was stimulated by ET-1 or aFGF. Cardiac myocytes expressed protein kinase C (PKC)-alpha,
-delta, -epsilon and -zeta as shown immunoblotting. Exposure to 1 microM TPA for 24 h down-regulated PKC-alpha, -delta, and
-epsilon, but not PKC-zeta. This maneuver wholly abolished the activation of MAPK on re-exposure to TPA but did not affect
the response to aFGF. The effect of ET-1 was partially down-regulated. ET-1 stimulated phospho[3H]inositide hydrolysis 18-fold,
whereas aFGF stimulated by only 30%. Agonists which initially utilize dissimilar signaling pathways may therefore converge
at the level of MAPKK/MAPK and this may be relevant to the hypertrophic response of the heart. |
| doi_str_mv | 10.1016/s0021-9258(17)42228-9 |
| format | Article |
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activated mitogen-activated protein kinase (MAPK) by 3-4-fold in crude extracts of myocytes cultured from neonatal rat heart
ventricles. Maximal activation was achieved after 5 min. Thereafter, MAPK activity stimulated by ET-1 or aFGF declined to
control values within 1-2 h, whereas activation by TPA was more sustained. Two peaks of MAPK activity (a 42- and a 44-kDa
MAPK) were resolved in cells exposed to ET-1 or aFGF by fast protein liquid chromatography on a Mono Q column. One major and
one minor peak of MAPK kinase (MAPKK) was stimulated by ET-1 or aFGF. Cardiac myocytes expressed protein kinase C (PKC)-alpha,
-delta, -epsilon and -zeta as shown immunoblotting. Exposure to 1 microM TPA for 24 h down-regulated PKC-alpha, -delta, and
-epsilon, but not PKC-zeta. This maneuver wholly abolished the activation of MAPK on re-exposure to TPA but did not affect
the response to aFGF. The effect of ET-1 was partially down-regulated. ET-1 stimulated phospho[3H]inositide hydrolysis 18-fold,
whereas aFGF stimulated by only 30%. Agonists which initially utilize dissimilar signaling pathways may therefore converge
at the level of MAPKK/MAPK and this may be relevant to the hypertrophic response of the heart.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/s0021-9258(17)42228-9</identifier><identifier>PMID: 7507104</identifier><identifier>CODEN: JBCHA3</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Biochemistry and Molecular Biology</publisher><subject>Animals ; Animals, Newborn ; Biological and medical sciences ; Calcium-Calmodulin-Dependent Protein Kinases - metabolism ; Cardiomegaly - enzymology ; Cell physiology ; Cells, Cultured ; Endothelins - pharmacology ; Enzyme Activation - drug effects ; Fibroblast Growth Factor 1 - pharmacology ; Fibroblast Growth Factor 2 - pharmacology ; Fundamental and applied biological sciences. Psychology ; In Vitro Techniques ; Isoenzymes - metabolism ; Mitogen-Activated Protein Kinase Kinases ; Molecular and cellular biology ; Myelin Basic Protein - metabolism ; Myocardium - enzymology ; Phosphatidylinositols - metabolism ; Phosphorylation ; Protein Kinase C - physiology ; Protein-Serine-Threonine Kinases - metabolism ; Protein-Tyrosine Kinases - metabolism ; Rats ; Responses to growth factors, tumor promotors, other factors ; Second Messenger Systems ; Signal Transduction ; Tetradecanoylphorbol Acetate - pharmacology</subject><ispartof>The Journal of biological chemistry, 1994-01, Vol.269 (2), p.1110-1119</ispartof><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4199-9a49812011528604258e0805aad0ed99332e62102fd8c9d8d6f1c7f766e96acb3</citedby><cites>FETCH-LOGICAL-c4199-9a49812011528604258e0805aad0ed99332e62102fd8c9d8d6f1c7f766e96acb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3953527$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7507104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BOGOYEVITCH, M. A</creatorcontrib><creatorcontrib>GLENNON, P. E</creatorcontrib><creatorcontrib>ANDERSSON, M. B</creatorcontrib><creatorcontrib>CLERK, A</creatorcontrib><creatorcontrib>LAZOU, A</creatorcontrib><creatorcontrib>MARSHALL, C. J</creatorcontrib><creatorcontrib>PARKER, P. J</creatorcontrib><creatorcontrib>SUGDEN, P. H</creatorcontrib><title>Endothelin-1 and fibroblast growth factors stimulate the mitogen-activated protein kinase signaling cascade in cardiac myocytes. The potential role of the cascade in the integration of two signaling pathways leading to myocyte hypertrophy</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Maximally effective concentrations of endothelin-1 (ET-1), acidic FGF (aFGF), or 12-O-tetradecanoylphorbol-13-acetate (TPA)
activated mitogen-activated protein kinase (MAPK) by 3-4-fold in crude extracts of myocytes cultured from neonatal rat heart
ventricles. Maximal activation was achieved after 5 min. Thereafter, MAPK activity stimulated by ET-1 or aFGF declined to
control values within 1-2 h, whereas activation by TPA was more sustained. Two peaks of MAPK activity (a 42- and a 44-kDa
MAPK) were resolved in cells exposed to ET-1 or aFGF by fast protein liquid chromatography on a Mono Q column. One major and
one minor peak of MAPK kinase (MAPKK) was stimulated by ET-1 or aFGF. Cardiac myocytes expressed protein kinase C (PKC)-alpha,
-delta, -epsilon and -zeta as shown immunoblotting. Exposure to 1 microM TPA for 24 h down-regulated PKC-alpha, -delta, and
-epsilon, but not PKC-zeta. This maneuver wholly abolished the activation of MAPK on re-exposure to TPA but did not affect
the response to aFGF. The effect of ET-1 was partially down-regulated. ET-1 stimulated phospho[3H]inositide hydrolysis 18-fold,
whereas aFGF stimulated by only 30%. Agonists which initially utilize dissimilar signaling pathways may therefore converge
at the level of MAPKK/MAPK and this may be relevant to the hypertrophic response of the heart.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biological and medical sciences</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Cardiomegaly - enzymology</subject><subject>Cell physiology</subject><subject>Cells, Cultured</subject><subject>Endothelins - pharmacology</subject><subject>Enzyme Activation - drug effects</subject><subject>Fibroblast Growth Factor 1 - pharmacology</subject><subject>Fibroblast Growth Factor 2 - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>In Vitro Techniques</subject><subject>Isoenzymes - metabolism</subject><subject>Mitogen-Activated Protein Kinase Kinases</subject><subject>Molecular and cellular biology</subject><subject>Myelin Basic Protein - metabolism</subject><subject>Myocardium - enzymology</subject><subject>Phosphatidylinositols - metabolism</subject><subject>Phosphorylation</subject><subject>Protein Kinase C - physiology</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Rats</subject><subject>Responses to growth factors, tumor promotors, other factors</subject><subject>Second Messenger Systems</subject><subject>Signal Transduction</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkc2KFDEUhQtRxnb0EQaCiOiixiT1m-UwjD8w4MIR3IXbya2qaFVSJmmbemmfwVR320w2ITnfuQfuybIrRq8ZZfWHQClnueBV-44170vOeZuLJ9mG0bbIi4r9eJptzsjz7EUIP2k6pWAX2UVT0YbRcpP9vbPaxQFHY3NGwGrSma132xFCJL13-ziQDlR0PpAQzbQbISJJBjKZ6Hq0eRLNn_SpyexdRGPJL2MhIAmmt5Dm9kRBUKCRJE2B1wYUmRanlojhmjykWXMy2mhgJN6NSFx3SHhkW5_GRuw9ROPsgdi7RxEzxGEPSyAjgl4_ovufQYZlRh-9m4flZfasgzHgq9N9mX3_ePdw-zm___rpy-3Nfa5KJkQuoBQt45Sxirc1LdMGkba0AtAUtRBFwbHmjPJOt0roVtcdU03X1DWKGtS2uMzeHuemnfzeYYhyMkHhOIJFtwuS1Q0tqSgTWB1B5V0IHjs5ezOBXySjcu1ZfltLlGuJkjXy0LMUyXd1CthtJ9Rn16nYpL856esSx86DVSacsUJURcWbhL0-YoPph73xKLfGqQEnyWshuWSM0eIfF37CDA</recordid><startdate>19940114</startdate><enddate>19940114</enddate><creator>BOGOYEVITCH, M. A</creator><creator>GLENNON, P. E</creator><creator>ANDERSSON, M. B</creator><creator>CLERK, A</creator><creator>LAZOU, A</creator><creator>MARSHALL, C. J</creator><creator>PARKER, P. J</creator><creator>SUGDEN, P. H</creator><general>American Society for Biochemistry and Molecular Biology</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>7TO</scope><scope>H94</scope></search><sort><creationdate>19940114</creationdate><title>Endothelin-1 and fibroblast growth factors stimulate the mitogen-activated protein kinase signaling cascade in cardiac myocytes. The potential role of the cascade in the integration of two signaling pathways leading to myocyte hypertrophy</title><author>BOGOYEVITCH, M. A ; GLENNON, P. E ; ANDERSSON, M. B ; CLERK, A ; LAZOU, A ; MARSHALL, C. J ; PARKER, P. J ; SUGDEN, P. 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Psychology</topic><topic>In Vitro Techniques</topic><topic>Isoenzymes - metabolism</topic><topic>Mitogen-Activated Protein Kinase Kinases</topic><topic>Molecular and cellular biology</topic><topic>Myelin Basic Protein - metabolism</topic><topic>Myocardium - enzymology</topic><topic>Phosphatidylinositols - metabolism</topic><topic>Phosphorylation</topic><topic>Protein Kinase C - physiology</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Rats</topic><topic>Responses to growth factors, tumor promotors, other factors</topic><topic>Second Messenger Systems</topic><topic>Signal Transduction</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BOGOYEVITCH, M. A</creatorcontrib><creatorcontrib>GLENNON, P. E</creatorcontrib><creatorcontrib>ANDERSSON, M. B</creatorcontrib><creatorcontrib>CLERK, A</creatorcontrib><creatorcontrib>LAZOU, A</creatorcontrib><creatorcontrib>MARSHALL, C. J</creatorcontrib><creatorcontrib>PARKER, P. J</creatorcontrib><creatorcontrib>SUGDEN, P. H</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BOGOYEVITCH, M. A</au><au>GLENNON, P. E</au><au>ANDERSSON, M. B</au><au>CLERK, A</au><au>LAZOU, A</au><au>MARSHALL, C. J</au><au>PARKER, P. J</au><au>SUGDEN, P. H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelin-1 and fibroblast growth factors stimulate the mitogen-activated protein kinase signaling cascade in cardiac myocytes. The potential role of the cascade in the integration of two signaling pathways leading to myocyte hypertrophy</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1994-01-14</date><risdate>1994</risdate><volume>269</volume><issue>2</issue><spage>1110</spage><epage>1119</epage><pages>1110-1119</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><coden>JBCHA3</coden><abstract>Maximally effective concentrations of endothelin-1 (ET-1), acidic FGF (aFGF), or 12-O-tetradecanoylphorbol-13-acetate (TPA)
activated mitogen-activated protein kinase (MAPK) by 3-4-fold in crude extracts of myocytes cultured from neonatal rat heart
ventricles. Maximal activation was achieved after 5 min. Thereafter, MAPK activity stimulated by ET-1 or aFGF declined to
control values within 1-2 h, whereas activation by TPA was more sustained. Two peaks of MAPK activity (a 42- and a 44-kDa
MAPK) were resolved in cells exposed to ET-1 or aFGF by fast protein liquid chromatography on a Mono Q column. One major and
one minor peak of MAPK kinase (MAPKK) was stimulated by ET-1 or aFGF. Cardiac myocytes expressed protein kinase C (PKC)-alpha,
-delta, -epsilon and -zeta as shown immunoblotting. Exposure to 1 microM TPA for 24 h down-regulated PKC-alpha, -delta, and
-epsilon, but not PKC-zeta. This maneuver wholly abolished the activation of MAPK on re-exposure to TPA but did not affect
the response to aFGF. The effect of ET-1 was partially down-regulated. ET-1 stimulated phospho[3H]inositide hydrolysis 18-fold,
whereas aFGF stimulated by only 30%. Agonists which initially utilize dissimilar signaling pathways may therefore converge
at the level of MAPKK/MAPK and this may be relevant to the hypertrophic response of the heart.</abstract><cop>Bethesda, MD</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>7507104</pmid><doi>10.1016/s0021-9258(17)42228-9</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9258 |
| ispartof | The Journal of biological chemistry, 1994-01, Vol.269 (2), p.1110-1119 |
| issn | 0021-9258 1083-351X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_16704094 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Animals, Newborn Biological and medical sciences Calcium-Calmodulin-Dependent Protein Kinases - metabolism Cardiomegaly - enzymology Cell physiology Cells, Cultured Endothelins - pharmacology Enzyme Activation - drug effects Fibroblast Growth Factor 1 - pharmacology Fibroblast Growth Factor 2 - pharmacology Fundamental and applied biological sciences. Psychology In Vitro Techniques Isoenzymes - metabolism Mitogen-Activated Protein Kinase Kinases Molecular and cellular biology Myelin Basic Protein - metabolism Myocardium - enzymology Phosphatidylinositols - metabolism Phosphorylation Protein Kinase C - physiology Protein-Serine-Threonine Kinases - metabolism Protein-Tyrosine Kinases - metabolism Rats Responses to growth factors, tumor promotors, other factors Second Messenger Systems Signal Transduction Tetradecanoylphorbol Acetate - pharmacology |
| title | Endothelin-1 and fibroblast growth factors stimulate the mitogen-activated protein kinase signaling cascade in cardiac myocytes. The potential role of the cascade in the integration of two signaling pathways leading to myocyte hypertrophy |
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