{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T22:04:46Z","timestamp":1792101886410,"version":"4.4.0"},"reference-count":70,"publisher":"Wiley","issue":"18","license":[{"start":{"date-parts":[[2013,7,23]],"date-time":"2013-07-23T00:00:00Z","timestamp":1374537600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Key points<\/jats:title>\n                  <jats:p>\n                    <jats:list list-type=\"explicit-label\">\n                      <jats:list-item>\n                        <jats:p>The discovery of microRNAs (miRNAs) has established new mechanisms that control health, but little is known about the regulation of skeletal muscle miRNAs in response to exercise.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          This study investigated components of the miRNA biogenesis pathway (Drosha, Dicer and Exportin\u20105), muscle enriched miRNAs, (miR\u20101, \u2010133a, \u2010133b and 206), and several miRNAs dysregulated in muscle myopathies, and showed that 3 h following an acute exercise bout,\n                          <jats:italic>Drosha<\/jats:italic>\n                          ,\n                          <jats:italic>Dicer<\/jats:italic>\n                          and\n                          <jats:italic>Exportin\u20105<\/jats:italic>\n                          , as well as miR\u20101, \u2010133a, \u2010133\u2010b and miR\u2010181a were all increased, while miR\u20109, \u201023a, \u201023b and \u201031 were decreased.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Short\u2010term training increased miR\u20101 and miR\u201029b, while miR\u201031 remained decreased.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Negative correlations were observed between miR\u20109 and HDAC4 protein, miR\u201031 and HDAC4 protein and between miR\u201031 and NRF1 protein, 3 h after exercise.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>miR\u201031 binding to the HDAC4 and NRF1 3\u2032 untranslated region (UTR) reduced luciferase reporter activity.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Exercise rapidly and transiently regulates several miRNA species potentially involved in the regulation of skeletal muscle regeneration, gene transcription and mitochondrial biogenesis.<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Abstract\u2002<\/jats:bold>\n                    The identification of microRNAs (miRNAs) has established new mechanisms that control skeletal muscle adaptation to exercise. The present study investigated the mRNA regulation of components of the miRNA biogenesis pathway (Drosha, Dicer and Exportin\u20105), muscle enriched miRNAs, (miR\u20101, \u2010133a, \u2010133b and \u2010206), and several miRNAs dysregulated in muscle myopathies (miR\u20109, \u201023, \u201029, \u201031 and \u2010181). Measurements were made in muscle biopsies from nine healthy untrained males at rest, 3 h following an acute bout of moderate\u2010intensity endurance cycling and following 10 days of endurance training. Bioinformatics analysis was used to predict potential miRNA targets. In the 3 h period following the acute exercise bout,\n                    <jats:italic>Drosha<\/jats:italic>\n                    ,\n                    <jats:italic>Dicer<\/jats:italic>\n                    and\n                    <jats:italic>Exportin\u20105<\/jats:italic>\n                    , as well as miR\u20101, \u2010133a, \u2010133\u2010b and \u2010181a were all increased. In contrast miR\u20109, \u201023a, \u201023b and \u201031 were decreased. Short\u2010term training increased miR\u20101 and \u201029b, while miR\u201031 remained decreased. Negative correlations were observed between miR\u20109 and HDAC4 protein (\n                    <jats:italic>r<\/jats:italic>\n                    =\u22120.71;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.04), miR\u201031 and HDAC4 protein (\n                    <jats:italic>r =<\/jats:italic>\n                    \u22120.87;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.026) and miR\u201031 and NRF1 protein (\n                    <jats:italic>r =<\/jats:italic>\n                    \u22120.77;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.01) 3 h following exercise. miR\u201031 binding to the HDAC4 and NRF1 3\u2032 untranslated region (UTR) reduced luciferase reporter activity. Exercise rapidly and transiently regulates several miRNA species in muscle. Several of these miRNAs may be involved in the regulation of skeletal muscle regeneration, gene transcription and mitochondrial biogenesis. Identifying endurance exercise\u2010mediated stress signals regulating skeletal muscle miRNAs, as well as validating their targets and regulatory pathways post exercise, will advance our understanding of their potential role\/s in human health.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2013.255695","type":"journal-article","created":{"date-parts":[[2013,6,24]],"date-time":"2013-06-24T22:26:49Z","timestamp":1372112809000},"page":"4637-4653","source":"Crossref","is-referenced-by-count":241,"title":["Regulation of miRNAs in human skeletal muscle following acute endurance exercise and short\u2010term endurance training"],"prefix":"10.1113","volume":"591","author":[{"given":"Aaron 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