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Isoform-specific role of Na/K-ATPase α1 in skeletal muscle
The distribution of Na/K-ATPase α-isoforms in skeletal muscle is unique, with α1 as the minor (15%) isoform and α2 comprising the bulk of the Na/K-ATPase pool. The acute and isoform-specific role of α2 in muscle performance and resistance to fatigue is well known, but the isoform-specific role of α1...
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Published in: | American journal of physiology: endocrinology and metabolism 2018-06, Vol.314 (6), p.E620-E629 |
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creator | Kutz, Laura C Mukherji, Shreya T Wang, Xiaoliang Bryant, Amber Larre, Isabel Heiny, Judith A Lingrel, Jerry B Pierre, Sandrine V Xie, Zijian |
description | The distribution of Na/K-ATPase α-isoforms in skeletal muscle is unique, with α1 as the minor (15%) isoform and α2 comprising the bulk of the Na/K-ATPase pool. The acute and isoform-specific role of α2 in muscle performance and resistance to fatigue is well known, but the isoform-specific role of α1 has not been as thoroughly investigated. In vitro, we reported that α1 has a role in promoting cell growth that is not supported by α2. To assess whether α1 serves this isoform-specific trophic role in the skeletal muscle, we used Na/K-ATPase α1-haploinsufficient (α1
) mice. A 30% decrease of Na/K-ATPase α1 protein expression without change in α2 induced a modest yet significant decrease of 10% weight in the oxidative soleus muscle. In contrast, the mixed plantaris and glycolytic extensor digitorum longus weights were not significantly affected, likely because of their very low expression level of α1 compared with the soleus. The soleus mass reduction occurred without change in total Na/K-ATPase activity or glycogen metabolism. Serum analytes including K
, fat tissue mass, and exercise capacity were not altered in α1
mice. The impact of α1 content on soleus muscle mass is consistent with a Na/K-ATPase α1-specific role in skeletal muscle growth that cannot be fulfilled by α2. The preserved running capacity in α1
is in sharp contrast with previously reported consequences of genetic manipulation of α2. Taken together, these results lend further support to the concept of distinct isoform-specific functions of Na/K-ATPase α1 and α2 in skeletal muscle. |
doi_str_mv | 10.1152/AJPENDO.00275.2017 |
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) mice. A 30% decrease of Na/K-ATPase α1 protein expression without change in α2 induced a modest yet significant decrease of 10% weight in the oxidative soleus muscle. In contrast, the mixed plantaris and glycolytic extensor digitorum longus weights were not significantly affected, likely because of their very low expression level of α1 compared with the soleus. The soleus mass reduction occurred without change in total Na/K-ATPase activity or glycogen metabolism. Serum analytes including K
, fat tissue mass, and exercise capacity were not altered in α1
mice. The impact of α1 content on soleus muscle mass is consistent with a Na/K-ATPase α1-specific role in skeletal muscle growth that cannot be fulfilled by α2. The preserved running capacity in α1
is in sharp contrast with previously reported consequences of genetic manipulation of α2. Taken together, these results lend further support to the concept of distinct isoform-specific functions of Na/K-ATPase α1 and α2 in skeletal muscle.</description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/AJPENDO.00275.2017</identifier><identifier>PMID: 29438630</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Gene Expression Regulation, Enzymologic ; Isoenzymes - genetics ; Isoenzymes - physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle Contraction - physiology ; Muscle, Skeletal - growth & development ; Muscle, Skeletal - metabolism ; Muscle, Skeletal - pathology ; Organ Size - genetics ; Physical Conditioning, Animal ; Sodium-Potassium-Exchanging ATPase - genetics ; Sodium-Potassium-Exchanging ATPase - physiology</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2018-06, Vol.314 (6), p.E620-E629</ispartof><rights>Copyright © 2018 the American Physiological Society 2018 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3177-1818f1da38eda7ce9973a6c98ab63c7949f770b9b752cb93ec7a5e5eac0610d53</citedby><cites>FETCH-LOGICAL-c3177-1818f1da38eda7ce9973a6c98ab63c7949f770b9b752cb93ec7a5e5eac0610d53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29438630$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kutz, Laura C</creatorcontrib><creatorcontrib>Mukherji, Shreya T</creatorcontrib><creatorcontrib>Wang, Xiaoliang</creatorcontrib><creatorcontrib>Bryant, Amber</creatorcontrib><creatorcontrib>Larre, Isabel</creatorcontrib><creatorcontrib>Heiny, Judith A</creatorcontrib><creatorcontrib>Lingrel, Jerry B</creatorcontrib><creatorcontrib>Pierre, Sandrine V</creatorcontrib><creatorcontrib>Xie, Zijian</creatorcontrib><title>Isoform-specific role of Na/K-ATPase α1 in skeletal muscle</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description>The distribution of Na/K-ATPase α-isoforms in skeletal muscle is unique, with α1 as the minor (15%) isoform and α2 comprising the bulk of the Na/K-ATPase pool. The acute and isoform-specific role of α2 in muscle performance and resistance to fatigue is well known, but the isoform-specific role of α1 has not been as thoroughly investigated. In vitro, we reported that α1 has a role in promoting cell growth that is not supported by α2. To assess whether α1 serves this isoform-specific trophic role in the skeletal muscle, we used Na/K-ATPase α1-haploinsufficient (α1
) mice. A 30% decrease of Na/K-ATPase α1 protein expression without change in α2 induced a modest yet significant decrease of 10% weight in the oxidative soleus muscle. In contrast, the mixed plantaris and glycolytic extensor digitorum longus weights were not significantly affected, likely because of their very low expression level of α1 compared with the soleus. The soleus mass reduction occurred without change in total Na/K-ATPase activity or glycogen metabolism. Serum analytes including K
, fat tissue mass, and exercise capacity were not altered in α1
mice. The impact of α1 content on soleus muscle mass is consistent with a Na/K-ATPase α1-specific role in skeletal muscle growth that cannot be fulfilled by α2. The preserved running capacity in α1
is in sharp contrast with previously reported consequences of genetic manipulation of α2. Taken together, these results lend further support to the concept of distinct isoform-specific functions of Na/K-ATPase α1 and α2 in skeletal muscle.</description><subject>Animals</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Isoenzymes - genetics</subject><subject>Isoenzymes - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Muscle Contraction - physiology</subject><subject>Muscle, Skeletal - growth & development</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Organ Size - genetics</subject><subject>Physical Conditioning, Animal</subject><subject>Sodium-Potassium-Exchanging ATPase - genetics</subject><subject>Sodium-Potassium-Exchanging ATPase - physiology</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNpVkMtOwkAUhidGI4i-gAvTpZvCXDqdTkxMCKKiBFjgejKdnmqx7dQONfGxfBGfySJIdHUW_-X8-RA6J7hPCKeD4cNiPLuZ9zGmgvcpJuIAdVuB-oRzfoi6mEjmkyiQHXTi3ApjLHhAj1GHyoBFIcNddDVxNrV14bsKTJZmxqttDp5NvZkePPrD5UI78L4-iZeVnnuFHNY694rGmRxO0VGqcwdnu9tDT7fj5ejen87vJqPh1DeMCNEOIFFKEs0iSLQwIKVgOjQy0nHIjJCBTIXAsYwFpyaWDIzQHDhog0OCE8566HrbWzVxAYmBcl3rXFV1Vuj6Q1mdqf9Kmb2oZ_uuQswoDjcFl7uC2r414NaqyJyBPNcl2MYp2hKkhAoStVa6tZraOldDun9DsNpQV3pVQZlY9UNdbai3oYu_A_eRX8zsG31cfvI</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Kutz, Laura C</creator><creator>Mukherji, Shreya T</creator><creator>Wang, Xiaoliang</creator><creator>Bryant, Amber</creator><creator>Larre, Isabel</creator><creator>Heiny, Judith A</creator><creator>Lingrel, Jerry B</creator><creator>Pierre, Sandrine V</creator><creator>Xie, Zijian</creator><general>American Physiological Society</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><scope>5PM</scope></search><sort><creationdate>20180601</creationdate><title>Isoform-specific role of Na/K-ATPase α1 in skeletal muscle</title><author>Kutz, Laura C ; Mukherji, Shreya T ; Wang, Xiaoliang ; Bryant, Amber ; Larre, Isabel ; Heiny, Judith A ; Lingrel, Jerry B ; Pierre, Sandrine V ; Xie, Zijian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3177-1818f1da38eda7ce9973a6c98ab63c7949f770b9b752cb93ec7a5e5eac0610d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Isoenzymes - genetics</topic><topic>Isoenzymes - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Muscle Contraction - physiology</topic><topic>Muscle, Skeletal - growth & development</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Organ Size - genetics</topic><topic>Physical Conditioning, Animal</topic><topic>Sodium-Potassium-Exchanging ATPase - genetics</topic><topic>Sodium-Potassium-Exchanging ATPase - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kutz, Laura C</creatorcontrib><creatorcontrib>Mukherji, Shreya T</creatorcontrib><creatorcontrib>Wang, Xiaoliang</creatorcontrib><creatorcontrib>Bryant, Amber</creatorcontrib><creatorcontrib>Larre, Isabel</creatorcontrib><creatorcontrib>Heiny, Judith A</creatorcontrib><creatorcontrib>Lingrel, Jerry B</creatorcontrib><creatorcontrib>Pierre, Sandrine V</creatorcontrib><creatorcontrib>Xie, Zijian</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology: endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kutz, Laura C</au><au>Mukherji, Shreya T</au><au>Wang, Xiaoliang</au><au>Bryant, Amber</au><au>Larre, Isabel</au><au>Heiny, Judith A</au><au>Lingrel, Jerry B</au><au>Pierre, Sandrine V</au><au>Xie, Zijian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isoform-specific role of Na/K-ATPase α1 in skeletal muscle</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>314</volume><issue>6</issue><spage>E620</spage><epage>E629</epage><pages>E620-E629</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><abstract>The distribution of Na/K-ATPase α-isoforms in skeletal muscle is unique, with α1 as the minor (15%) isoform and α2 comprising the bulk of the Na/K-ATPase pool. The acute and isoform-specific role of α2 in muscle performance and resistance to fatigue is well known, but the isoform-specific role of α1 has not been as thoroughly investigated. In vitro, we reported that α1 has a role in promoting cell growth that is not supported by α2. To assess whether α1 serves this isoform-specific trophic role in the skeletal muscle, we used Na/K-ATPase α1-haploinsufficient (α1
) mice. A 30% decrease of Na/K-ATPase α1 protein expression without change in α2 induced a modest yet significant decrease of 10% weight in the oxidative soleus muscle. In contrast, the mixed plantaris and glycolytic extensor digitorum longus weights were not significantly affected, likely because of their very low expression level of α1 compared with the soleus. The soleus mass reduction occurred without change in total Na/K-ATPase activity or glycogen metabolism. Serum analytes including K
, fat tissue mass, and exercise capacity were not altered in α1
mice. The impact of α1 content on soleus muscle mass is consistent with a Na/K-ATPase α1-specific role in skeletal muscle growth that cannot be fulfilled by α2. The preserved running capacity in α1
is in sharp contrast with previously reported consequences of genetic manipulation of α2. Taken together, these results lend further support to the concept of distinct isoform-specific functions of Na/K-ATPase α1 and α2 in skeletal muscle.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>29438630</pmid><doi>10.1152/AJPENDO.00275.2017</doi><oa>free_for_read</oa></addata></record> |
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subjects | Animals Gene Expression Regulation, Enzymologic Isoenzymes - genetics Isoenzymes - physiology Male Mice Mice, Inbred C57BL Mice, Transgenic Muscle Contraction - physiology Muscle, Skeletal - growth & development Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Organ Size - genetics Physical Conditioning, Animal Sodium-Potassium-Exchanging ATPase - genetics Sodium-Potassium-Exchanging ATPase - physiology |
title | Isoform-specific role of Na/K-ATPase α1 in skeletal muscle |
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