Role of protein phosphatases in hypoxic preconditioning
Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen, Germany To find a protein kinase C (PKC)-independent preconditioning mechanism, hypoxic preconditioning (HP; i.e., 10-min anoxia and 10-min reoxygenation) was applied to isolated rat hearts before 60-min global ischemia. HP led to...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2002-09, Vol.283 (3), p.H1092-H1098 |
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| container_issue | 3 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 283 |
| creator | Ladilov, Yury Maxeiner, Hagen Wolf, Christopher Schafer, Claudia Meuter, Karsten Piper, H. Michael |
| description | Physiologisches Institut, Justus-Liebig-Universität,
D-35392 Giessen, Germany
To find a protein kinase C
(PKC)-independent preconditioning mechanism, hypoxic preconditioning
(HP; i.e., 10-min anoxia and 10-min reoxygenation) was applied to
isolated rat hearts before 60-min global ischemia. HP led to
improved recovery of developed pressure and reduced end-diastolic
pressure in the left ventricle during reperfusion. Protection was
unaffected by the PKC inhibitor bisindolylmaleimide (BIM; 1 µmol/l).
It was abolished by the inhibitor of protein phosphatases 1 and 2A
cantharidin (20 or 5 µmol/l) and partially enhanced by the inhibitor
of protein phosphatase 2A okadaic acid (5 nmol/l). In adult rat
cardiomyocytes treated with BIM and exposed to 60-min simulated
ischemia (anoxia, extracellular pH 6.4), HP led to attenuation
of anoxic Na + /Ca 2+ overload and of
hypercontracture, which developed on reoxygenation. This protection was
prevented by treatment with cantharidin but not with okadaic acid. In
conclusion, HP exerts PKC-independent protection on
ischemic-reperfused rat hearts and cardiomyocytes. Protein
phosphatase 1 seems a mediator of this protective mechanism.
cellular calcium; heart function; ischemia; reperfusion |
| doi_str_mv | 10.1152/ajpheart.00318.2001 |
| format | Article |
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D-35392 Giessen, Germany
To find a protein kinase C
(PKC)-independent preconditioning mechanism, hypoxic preconditioning
(HP; i.e., 10-min anoxia and 10-min reoxygenation) was applied to
isolated rat hearts before 60-min global ischemia. HP led to
improved recovery of developed pressure and reduced end-diastolic
pressure in the left ventricle during reperfusion. Protection was
unaffected by the PKC inhibitor bisindolylmaleimide (BIM; 1 µmol/l).
It was abolished by the inhibitor of protein phosphatases 1 and 2A
cantharidin (20 or 5 µmol/l) and partially enhanced by the inhibitor
of protein phosphatase 2A okadaic acid (5 nmol/l). In adult rat
cardiomyocytes treated with BIM and exposed to 60-min simulated
ischemia (anoxia, extracellular pH 6.4), HP led to attenuation
of anoxic Na + /Ca 2+ overload and of
hypercontracture, which developed on reoxygenation. This protection was
prevented by treatment with cantharidin but not with okadaic acid. In
conclusion, HP exerts PKC-independent protection on
ischemic-reperfused rat hearts and cardiomyocytes. Protein
phosphatase 1 seems a mediator of this protective mechanism.
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D-35392 Giessen, Germany
To find a protein kinase C
(PKC)-independent preconditioning mechanism, hypoxic preconditioning
(HP; i.e., 10-min anoxia and 10-min reoxygenation) was applied to
isolated rat hearts before 60-min global ischemia. HP led to
improved recovery of developed pressure and reduced end-diastolic
pressure in the left ventricle during reperfusion. Protection was
unaffected by the PKC inhibitor bisindolylmaleimide (BIM; 1 µmol/l).
It was abolished by the inhibitor of protein phosphatases 1 and 2A
cantharidin (20 or 5 µmol/l) and partially enhanced by the inhibitor
of protein phosphatase 2A okadaic acid (5 nmol/l). In adult rat
cardiomyocytes treated with BIM and exposed to 60-min simulated
ischemia (anoxia, extracellular pH 6.4), HP led to attenuation
of anoxic Na + /Ca 2+ overload and of
hypercontracture, which developed on reoxygenation. This protection was
prevented by treatment with cantharidin but not with okadaic acid. In
conclusion, HP exerts PKC-independent protection on
ischemic-reperfused rat hearts and cardiomyocytes. Protein
phosphatase 1 seems a mediator of this protective mechanism.
cellular calcium; heart function; ischemia; reperfusion</description><subject>Animals</subject><subject>Cantharidin - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Hypoxia - metabolism</subject><subject>In Vitro Techniques</subject><subject>Indoles - pharmacology</subject><subject>Ischemic Preconditioning</subject><subject>Male</subject><subject>Maleimides - pharmacology</subject><subject>Muscle Fibers, Skeletal - enzymology</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardium - cytology</subject><subject>Myocardium - enzymology</subject><subject>Okadaic Acid - pharmacology</subject><subject>Phosphoprotein Phosphatases - metabolism</subject><subject>Protein Phosphatase 1</subject><subject>Protein Phosphatase 2</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Ventricular Pressure</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kN1KAzEQhYMotlafQJB9gW2TzGZ_8EqKtUJBkHod8rfdlO0mbLbYvr1bW6s3Xg3DOd9h5iB0T_CYEEYnYu0rI9pujDGQfEwxJhdo2Cs0JgyKSzTEkEKcEmADdBPCGmPMshSu0YBQkhMCxRBl7642kSsj37rO2CbylQu-Ep0IJkT9Xu2921nV60a5RtvOusY2q1t0VYo6mLvTHKGP2fNyOo8Xby-v06dFrKCALk5lhg0TLC0To7SUUicgSaIYlhK0oSBSpYokywsmBKE0p6CVyLUpIRFYYxghOOaq1oXQmpL71m5Eu-cE80MN_KcG_l0DP9TQUw9Hym_lxuhf5vR3b3g8Giq7qj5ta7iv9sG62q32fLat66XZdedomgMHPie4oNzrsqcn_9Pne_5Q8AW4vYKK</recordid><startdate>20020901</startdate><enddate>20020901</enddate><creator>Ladilov, Yury</creator><creator>Maxeiner, Hagen</creator><creator>Wolf, Christopher</creator><creator>Schafer, Claudia</creator><creator>Meuter, Karsten</creator><creator>Piper, H. Michael</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20020901</creationdate><title>Role of protein phosphatases in hypoxic preconditioning</title><author>Ladilov, Yury ; Maxeiner, Hagen ; Wolf, Christopher ; Schafer, Claudia ; Meuter, Karsten ; Piper, H. Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-6b70e5a56f4ecdbbbd43b14c50bb3de23a6cc947895aa122823dca8def34a0d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Cantharidin - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Hypoxia - metabolism</topic><topic>In Vitro Techniques</topic><topic>Indoles - pharmacology</topic><topic>Ischemic Preconditioning</topic><topic>Male</topic><topic>Maleimides - pharmacology</topic><topic>Muscle Fibers, Skeletal - enzymology</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardium - cytology</topic><topic>Myocardium - enzymology</topic><topic>Okadaic Acid - pharmacology</topic><topic>Phosphoprotein Phosphatases - metabolism</topic><topic>Protein Phosphatase 1</topic><topic>Protein Phosphatase 2</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Ventricular Pressure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ladilov, Yury</creatorcontrib><creatorcontrib>Maxeiner, Hagen</creatorcontrib><creatorcontrib>Wolf, Christopher</creatorcontrib><creatorcontrib>Schafer, Claudia</creatorcontrib><creatorcontrib>Meuter, Karsten</creatorcontrib><creatorcontrib>Piper, H. Michael</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ladilov, Yury</au><au>Maxeiner, Hagen</au><au>Wolf, Christopher</au><au>Schafer, Claudia</au><au>Meuter, Karsten</au><au>Piper, H. Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of protein phosphatases in hypoxic preconditioning</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2002-09-01</date><risdate>2002</risdate><volume>283</volume><issue>3</issue><spage>H1092</spage><epage>H1098</epage><pages>H1092-H1098</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Physiologisches Institut, Justus-Liebig-Universität,
D-35392 Giessen, Germany
To find a protein kinase C
(PKC)-independent preconditioning mechanism, hypoxic preconditioning
(HP; i.e., 10-min anoxia and 10-min reoxygenation) was applied to
isolated rat hearts before 60-min global ischemia. HP led to
improved recovery of developed pressure and reduced end-diastolic
pressure in the left ventricle during reperfusion. Protection was
unaffected by the PKC inhibitor bisindolylmaleimide (BIM; 1 µmol/l).
It was abolished by the inhibitor of protein phosphatases 1 and 2A
cantharidin (20 or 5 µmol/l) and partially enhanced by the inhibitor
of protein phosphatase 2A okadaic acid (5 nmol/l). In adult rat
cardiomyocytes treated with BIM and exposed to 60-min simulated
ischemia (anoxia, extracellular pH 6.4), HP led to attenuation
of anoxic Na + /Ca 2+ overload and of
hypercontracture, which developed on reoxygenation. This protection was
prevented by treatment with cantharidin but not with okadaic acid. In
conclusion, HP exerts PKC-independent protection on
ischemic-reperfused rat hearts and cardiomyocytes. Protein
phosphatase 1 seems a mediator of this protective mechanism.
cellular calcium; heart function; ischemia; reperfusion</abstract><cop>United States</cop><pmid>12181139</pmid><doi>10.1152/ajpheart.00318.2001</doi></addata></record> |
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| source | MEDLINE; American Physiological Society Paid; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Cantharidin - pharmacology Enzyme Inhibitors - pharmacology Hypoxia - metabolism In Vitro Techniques Indoles - pharmacology Ischemic Preconditioning Male Maleimides - pharmacology Muscle Fibers, Skeletal - enzymology Myocardial Reperfusion Injury - metabolism Myocardium - cytology Myocardium - enzymology Okadaic Acid - pharmacology Phosphoprotein Phosphatases - metabolism Protein Phosphatase 1 Protein Phosphatase 2 Rats Rats, Wistar Ventricular Pressure |
| title | Role of protein phosphatases in hypoxic preconditioning |
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