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Functional TRPV4 channels are expressed in mouse skeletal muscle and can modulate resting Ca2+ influx and muscle fatigue
Skeletal muscle contraction is basically controlled by Ca 2+ release and its reuptake into the sarcoplasmic reticulum. However, the long-term maintenance of muscle function requires an additional Ca 2+ influx from extracellular. Several mechanisms seem to contribute to the latter process, such as st...
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Published in: | Pflügers Archiv 2011-01, Vol.461 (1), p.115-122 |
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creator | Pritschow, Bernd W. Lange, Thom Kasch, Joachim Kunert-Keil, Christiane Liedtke, Wolfgang Brinkmeier, Heinrich |
description | Skeletal muscle contraction is basically controlled by Ca
2+
release and its reuptake into the sarcoplasmic reticulum. However, the long-term maintenance of muscle function requires an additional Ca
2+
influx from extracellular. Several mechanisms seem to contribute to the latter process, such as store-operated Ca
2+
entry, stretch-activated Ca
2+
influx and resting Ca
2+
influx. Candidate channels that may control Ca
2+
influx into muscle fibers are the STIM proteins, Orai, and the members of the transient receptor potential (TRP) family of cation channels. Here we show that TRPV4, an osmo-sensitive cation channel of the vanilloid subfamily of TRP channels is functionally expressed in mouse skeletal muscle. Western blot analysis showed the presence of TRPV4-specific bands at about 85 and 100 kDa in all tested muscles. The bands were absent when muscle proteins from TRPV4 deficient mice were analyzed. Using the manganese quench technique, we studied the resting influx of divalent cations into isolated wild-type muscle fibers. The specific TRPV4-channel activator 4α-phorbol-12,13-didecanoate (4α-PDD) stimulated resting influx by about 60% only in wild-type fibers. Electrical stimulation of soleus muscles did not reveal changes in isometric twitch contractions upon application of 4α-PDD, but tetanic contractions (at 120 Hz) were slightly increased by about 15%. When soleus muscles were stimulated with a fatigue protocol, muscle fatigue was significantly attenuated in the presence of 4α-PDD. The latter effect was not observed with muscles from TRPV4
−/−
mice. We conclude that TRPV4 is functionally expressed in mouse skeletal muscle and that TRPV4 activation modulates resting Ca
2+
influx and muscle fatigue. |
doi_str_mv | 10.1007/s00424-010-0883-4 |
format | article |
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2+
release and its reuptake into the sarcoplasmic reticulum. However, the long-term maintenance of muscle function requires an additional Ca
2+
influx from extracellular. Several mechanisms seem to contribute to the latter process, such as store-operated Ca
2+
entry, stretch-activated Ca
2+
influx and resting Ca
2+
influx. Candidate channels that may control Ca
2+
influx into muscle fibers are the STIM proteins, Orai, and the members of the transient receptor potential (TRP) family of cation channels. Here we show that TRPV4, an osmo-sensitive cation channel of the vanilloid subfamily of TRP channels is functionally expressed in mouse skeletal muscle. Western blot analysis showed the presence of TRPV4-specific bands at about 85 and 100 kDa in all tested muscles. The bands were absent when muscle proteins from TRPV4 deficient mice were analyzed. Using the manganese quench technique, we studied the resting influx of divalent cations into isolated wild-type muscle fibers. The specific TRPV4-channel activator 4α-phorbol-12,13-didecanoate (4α-PDD) stimulated resting influx by about 60% only in wild-type fibers. Electrical stimulation of soleus muscles did not reveal changes in isometric twitch contractions upon application of 4α-PDD, but tetanic contractions (at 120 Hz) were slightly increased by about 15%. When soleus muscles were stimulated with a fatigue protocol, muscle fatigue was significantly attenuated in the presence of 4α-PDD. The latter effect was not observed with muscles from TRPV4
−/−
mice. We conclude that TRPV4 is functionally expressed in mouse skeletal muscle and that TRPV4 activation modulates resting Ca
2+
influx and muscle fatigue.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-010-0883-4</identifier><identifier>PMID: 20924600</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Calcium ; Calcium (extracellular) ; Calcium - metabolism ; Calcium influx ; cation channels ; Cell Biology ; Electric Stimulation ; Electrical stimuli ; Fatigue ; Human Physiology ; Manganese ; Mice ; Molecular Medicine ; Muscle contraction ; Muscle Contraction - drug effects ; Muscle Fatigue - drug effects ; Muscle Fatigue - physiology ; Muscle Physiology ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - metabolism ; Neurosciences ; Phorbol Esters - pharmacology ; Receptors ; Sarcoplasmic reticulum ; Skeletal muscle ; transient receptor potential proteins ; TRPV Cation Channels - biosynthesis ; Western blotting</subject><ispartof>Pflügers Archiv, 2011-01, Vol.461 (1), p.115-122</ispartof><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-p184t-9d92a42cb7a00f0d3660e79122530e5d9d87c70a089bb51e37bccd709602663c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20924600$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pritschow, Bernd W.</creatorcontrib><creatorcontrib>Lange, Thom</creatorcontrib><creatorcontrib>Kasch, Joachim</creatorcontrib><creatorcontrib>Kunert-Keil, Christiane</creatorcontrib><creatorcontrib>Liedtke, Wolfgang</creatorcontrib><creatorcontrib>Brinkmeier, Heinrich</creatorcontrib><title>Functional TRPV4 channels are expressed in mouse skeletal muscle and can modulate resting Ca2+ influx and muscle fatigue</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>Skeletal muscle contraction is basically controlled by Ca
2+
release and its reuptake into the sarcoplasmic reticulum. However, the long-term maintenance of muscle function requires an additional Ca
2+
influx from extracellular. Several mechanisms seem to contribute to the latter process, such as store-operated Ca
2+
entry, stretch-activated Ca
2+
influx and resting Ca
2+
influx. Candidate channels that may control Ca
2+
influx into muscle fibers are the STIM proteins, Orai, and the members of the transient receptor potential (TRP) family of cation channels. Here we show that TRPV4, an osmo-sensitive cation channel of the vanilloid subfamily of TRP channels is functionally expressed in mouse skeletal muscle. Western blot analysis showed the presence of TRPV4-specific bands at about 85 and 100 kDa in all tested muscles. The bands were absent when muscle proteins from TRPV4 deficient mice were analyzed. Using the manganese quench technique, we studied the resting influx of divalent cations into isolated wild-type muscle fibers. The specific TRPV4-channel activator 4α-phorbol-12,13-didecanoate (4α-PDD) stimulated resting influx by about 60% only in wild-type fibers. Electrical stimulation of soleus muscles did not reveal changes in isometric twitch contractions upon application of 4α-PDD, but tetanic contractions (at 120 Hz) were slightly increased by about 15%. When soleus muscles were stimulated with a fatigue protocol, muscle fatigue was significantly attenuated in the presence of 4α-PDD. The latter effect was not observed with muscles from TRPV4
−/−
mice. We conclude that TRPV4 is functionally expressed in mouse skeletal muscle and that TRPV4 activation modulates resting Ca
2+
influx and muscle fatigue.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcium</subject><subject>Calcium (extracellular)</subject><subject>Calcium - metabolism</subject><subject>Calcium influx</subject><subject>cation channels</subject><subject>Cell Biology</subject><subject>Electric Stimulation</subject><subject>Electrical stimuli</subject><subject>Fatigue</subject><subject>Human Physiology</subject><subject>Manganese</subject><subject>Mice</subject><subject>Molecular Medicine</subject><subject>Muscle contraction</subject><subject>Muscle Contraction - drug effects</subject><subject>Muscle Fatigue - drug effects</subject><subject>Muscle Fatigue - physiology</subject><subject>Muscle Physiology</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Neurosciences</subject><subject>Phorbol Esters - pharmacology</subject><subject>Receptors</subject><subject>Sarcoplasmic reticulum</subject><subject>Skeletal muscle</subject><subject>transient receptor potential proteins</subject><subject>TRPV Cation Channels - biosynthesis</subject><subject>Western blotting</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNo1kUtPwzAQhC0EgvL4AVyQj0gosH4kTo6o4iUhgRBwtRx7WwKOW-JYKv8el5bTHuab0e4OIacMLhmAuooAkssCGBRQ16KQO2TCpOAFByZ2yQRAsKJSVX1ADmP8BAAua75PDjg0XFYAE7K6TcGO3SIYT19fnt8ltR8mBPSRmgEprpYDxoiOdoH2ixSRxi_0OGa8T9F6pCY4as1adcmbEWk2jF2Y06nhF9k282n1B235mRm7ecJjsjczPuLJdh6Rt9ub1-l98fh09zC9fiyWrJZj0biGG8ltqwzADJyoKkDVMM5LAVi6xtXKKjBQN21bMhSqtdYpaCrgVSWsOCLnm9zlsPhOeTXdd9Gi9yZgvkczYKopS6HqjJ5t0dT26PRy6Hoz_Oj_b2WAb4CYpTDHQX8u0pBft47R60r0phKdK9HrSrQUv7pte-Y</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Pritschow, Bernd W.</creator><creator>Lange, Thom</creator><creator>Kasch, Joachim</creator><creator>Kunert-Keil, Christiane</creator><creator>Liedtke, Wolfgang</creator><creator>Brinkmeier, Heinrich</creator><general>Springer-Verlag</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QP</scope></search><sort><creationdate>20110101</creationdate><title>Functional TRPV4 channels are expressed in mouse skeletal muscle and can modulate resting Ca2+ influx and muscle fatigue</title><author>Pritschow, Bernd W. ; Lange, Thom ; Kasch, Joachim ; Kunert-Keil, Christiane ; Liedtke, Wolfgang ; Brinkmeier, Heinrich</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p184t-9d92a42cb7a00f0d3660e79122530e5d9d87c70a089bb51e37bccd709602663c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcium</topic><topic>Calcium (extracellular)</topic><topic>Calcium - metabolism</topic><topic>Calcium influx</topic><topic>cation channels</topic><topic>Cell Biology</topic><topic>Electric Stimulation</topic><topic>Electrical stimuli</topic><topic>Fatigue</topic><topic>Human Physiology</topic><topic>Manganese</topic><topic>Mice</topic><topic>Molecular Medicine</topic><topic>Muscle contraction</topic><topic>Muscle Contraction - drug effects</topic><topic>Muscle Fatigue - drug effects</topic><topic>Muscle Fatigue - physiology</topic><topic>Muscle Physiology</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Neurosciences</topic><topic>Phorbol Esters - pharmacology</topic><topic>Receptors</topic><topic>Sarcoplasmic reticulum</topic><topic>Skeletal muscle</topic><topic>transient receptor potential proteins</topic><topic>TRPV Cation Channels - biosynthesis</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pritschow, Bernd W.</creatorcontrib><creatorcontrib>Lange, Thom</creatorcontrib><creatorcontrib>Kasch, Joachim</creatorcontrib><creatorcontrib>Kunert-Keil, Christiane</creatorcontrib><creatorcontrib>Liedtke, Wolfgang</creatorcontrib><creatorcontrib>Brinkmeier, Heinrich</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Calcium & Calcified Tissue Abstracts</collection><jtitle>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pritschow, Bernd W.</au><au>Lange, Thom</au><au>Kasch, Joachim</au><au>Kunert-Keil, Christiane</au><au>Liedtke, Wolfgang</au><au>Brinkmeier, Heinrich</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functional TRPV4 channels are expressed in mouse skeletal muscle and can modulate resting Ca2+ influx and muscle fatigue</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>461</volume><issue>1</issue><spage>115</spage><epage>122</epage><pages>115-122</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>Skeletal muscle contraction is basically controlled by Ca
2+
release and its reuptake into the sarcoplasmic reticulum. However, the long-term maintenance of muscle function requires an additional Ca
2+
influx from extracellular. Several mechanisms seem to contribute to the latter process, such as store-operated Ca
2+
entry, stretch-activated Ca
2+
influx and resting Ca
2+
influx. Candidate channels that may control Ca
2+
influx into muscle fibers are the STIM proteins, Orai, and the members of the transient receptor potential (TRP) family of cation channels. Here we show that TRPV4, an osmo-sensitive cation channel of the vanilloid subfamily of TRP channels is functionally expressed in mouse skeletal muscle. Western blot analysis showed the presence of TRPV4-specific bands at about 85 and 100 kDa in all tested muscles. The bands were absent when muscle proteins from TRPV4 deficient mice were analyzed. Using the manganese quench technique, we studied the resting influx of divalent cations into isolated wild-type muscle fibers. The specific TRPV4-channel activator 4α-phorbol-12,13-didecanoate (4α-PDD) stimulated resting influx by about 60% only in wild-type fibers. Electrical stimulation of soleus muscles did not reveal changes in isometric twitch contractions upon application of 4α-PDD, but tetanic contractions (at 120 Hz) were slightly increased by about 15%. When soleus muscles were stimulated with a fatigue protocol, muscle fatigue was significantly attenuated in the presence of 4α-PDD. The latter effect was not observed with muscles from TRPV4
−/−
mice. We conclude that TRPV4 is functionally expressed in mouse skeletal muscle and that TRPV4 activation modulates resting Ca
2+
influx and muscle fatigue.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>20924600</pmid><doi>10.1007/s00424-010-0883-4</doi><tpages>8</tpages></addata></record> |
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source | Springer Nature |
subjects | Animals Biomedical and Life Sciences Biomedicine Calcium Calcium (extracellular) Calcium - metabolism Calcium influx cation channels Cell Biology Electric Stimulation Electrical stimuli Fatigue Human Physiology Manganese Mice Molecular Medicine Muscle contraction Muscle Contraction - drug effects Muscle Fatigue - drug effects Muscle Fatigue - physiology Muscle Physiology Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Neurosciences Phorbol Esters - pharmacology Receptors Sarcoplasmic reticulum Skeletal muscle transient receptor potential proteins TRPV Cation Channels - biosynthesis Western blotting |
title | Functional TRPV4 channels are expressed in mouse skeletal muscle and can modulate resting Ca2+ influx and muscle fatigue |
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