{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T03:53:24Z","timestamp":1790049204833,"version":"4.0.1"},"reference-count":32,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2024,1,10]],"date-time":"2024-01-10T00:00:00Z","timestamp":1704844800000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Neuromuscular Diseases"],"published-print":{"date-parts":[[2024,3,5]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>\n                      Amyotrophic lateral sclerosis (ALS) is characterized by progressive loss of muscle mass and muscle function. Previous work from our lab demonstrated that skeletal muscles from a mouse model of ALS show elevated intracellular calcium (Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ) levels and heightened endoplasmic reticulum (ER) stress.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>\n                      To investigate whether overexpression of sarcoplasmic reticulum (SR) Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ATPase 1 (SERCA1) in skeletal muscle would improve intracellular Ca\n                      <jats:sup>2+<\/jats:sup>\n                      handling, attenuate ER stress, and improve motor function ALS transgenic mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      B6SJL-Tg (SOD1*G93A)1Gur\/J (ALS-Tg) mice were bred with skeletal muscle \u03b1-actinin SERCA1 overexpressing mice to generate wild type (WT), SERCA1 overexpression (WT\/+SERCA1), ALS-Tg, and SERCA1 overexpressing ALS-Tg (ALS-Tg\/+SERCA1) mice. Motor function (grip test) was assessed weekly and skeletal muscles were harvested at 16 weeks of age to evaluate muscle mass, SR-Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ATPase activity, levels of SERCA1 and ER stress proteins - protein disulfide isomerase (PDI), Grp78\/BiP, and C\/EBP homologous protein (CHOP). Single muscle fibers were also isolated from the flexor digitorum brevis muscle to assess changes in resting and peak Fura-2 ratios.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      ALS-Tg\/+SERCA1 mice showed improved motor function, delayed onset of disease, and improved muscle mass compared to ALS-Tg. Further, ALS-Tg\/+SERCA1 mice returned levels of SERCA1 protein and SR-Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ATPase activity back to levels in WT mice. Unexpectedly, SERCA-1 overexpression increased levels of the ER stress maker Grp78\/BiP in both WT and ALS-Tg mice, while not altering protein levels of PDI or CHOP. Lastly, single muscle fibers from ALS-Tg\/+SERCA1 had similar resting but lower peak Fura-2 levels (at 30\u200aHz and 100\u200aHz) compared to ALS-Tg mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>\n                      These data indicate that SERCA1 overexpression attenuates the progressive loss of muscle mass and maintains motor function in ALS-Tg mice while not lowering resting Ca\n                      <jats:sup>2+<\/jats:sup>\n                      levels or ER stress.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jnd-230123","type":"journal-article","created":{"date-parts":[[2024,1,12]],"date-time":"2024-01-12T12:25:10Z","timestamp":1705062310000},"page":"315-326","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":11,"title":["SERCA1 Overexpression in Skeletal Muscle Attenuates Muscle Atrophy and Improves Motor Function in a Mouse Model of ALS"],"prefix":"10.1177","volume":"11","author":[{"given":"Davi A.G.","family":"M\u00e1zala","sequence":"first","affiliation":[{"name":"Department of Kinesiology, School of Public Health, University of Maryland, College Park, MD, USA"},{"name":"Department of Kinesiology, College of Health Professions, Towson University, Towson, MD, USA"},{"name":"Center for Genetic Medicine Research, Children\u2019s National Research Institute, Children\u2019s National Hospital, Washington, DC, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dapeng","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, School of Public Health, University of Maryland, College Park, MD, USA"},{"name":"Zeteo Tech, Inc., Sykesville, MD, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva R.","family":"Chin","sequence":"additional","affiliation":[{"name":"Department of Kinesiology, School of Public Health, University of Maryland, College Park, MD, USA"},{"name":"Solve FSHD, Vancouver, British Columbia, 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