{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T12:57:44Z","timestamp":1788872264688,"version":"build-2803163510"},"reference-count":42,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,6,6]],"date-time":"2014-06-06T00:00:00Z","timestamp":1402012800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001700","name":"The Ministry of Education, culture, Sports, Science and Technology, Japan","doi-asserted-by":"crossref","award":["21591907"],"award-info":[{"award-number":["21591907"]}],"id":[{"id":"10.13039\/501100001700","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    After traumatic spinal cord injury (\n                    <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>\n                    ), endoplasmic reticulum (\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    ) stress exacerbates secondary injury, leading to expansion of demyelination and reduced remyelination due to oligodendrocyte precursor cell (\n                    <jats:styled-content style=\"fixed-case\">OPC<\/jats:styled-content>\n                    ) apoptosis. Although recent studies have revealed that amiloride controls\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    stress and leads to improvement in several neurological disorders including\n                    <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>\n                    , its mechanism is not completely understood. Here, we used a rat\n                    <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>\n                    model to assess the effects of amiloride on functional recovery, secondary damage expansion,\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    stress\u2010induced cell death and\n                    <jats:styled-content style=\"fixed-case\">OPC<\/jats:styled-content>\n                    survival. Hindlimb function in rats with spinal cord contusion significantly improved after amiloride administration. Amiloride significantly decreased the expression of the pro\u2010apoptotic transcription factor\n                    <jats:styled-content style=\"fixed-case\">CHOP<\/jats:styled-content>\n                    in the injured spinal cord and significantly increased the expression of the\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    chaperone\n                    <jats:styled-content style=\"fixed-case\">GRP<\/jats:styled-content>\n                    78, which protects cells against\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    stress. In addition, amiloride treatment led to a significant decrease in\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    stress\u2010induced apoptosis and a significant increase of\n                    <jats:styled-content style=\"fixed-case\">NG<\/jats:styled-content>\n                    2\u2010positive\n                    <jats:styled-content style=\"fixed-case\">OPC<\/jats:styled-content>\n                    s in the injured spinal cord. Furthermore,\n                    <jats:italic>in vitro<\/jats:italic>\n                    experiments performed to investigate the direct effect of amiloride on\n                    <jats:styled-content style=\"fixed-case\">OPC<\/jats:styled-content>\n                    s revealed that amiloride reduced\n                    <jats:styled-content style=\"fixed-case\">CHOP<\/jats:styled-content>\n                    expression in\n                    <jats:styled-content style=\"fixed-case\">OPC<\/jats:styled-content>\n                    s cultured under\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    stress. These results suggest that amiloride controls\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    stress in\n                    <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>\n                    and inhibits cellular apoptosis, contributing to\n                    <jats:styled-content style=\"fixed-case\">OPC<\/jats:styled-content>\n                    survival. The present study suggests that amiloride may be an effective treatment to reduce\n                    <jats:styled-content style=\"fixed-case\">ER<\/jats:styled-content>\n                    stress\u2010induced cell death in the acute phase of\n                    <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/ejn.12647","type":"journal-article","created":{"date-parts":[[2014,6,6]],"date-time":"2014-06-06T06:38:44Z","timestamp":1402036724000},"page":"3120-3127","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Effect of amiloride on endoplasmic reticulum stress response in the injured spinal cord of rats"],"prefix":"10.1111","volume":"40","author":[{"given":"Masahiro","family":"Kuroiwa","sequence":"first","affiliation":[{"name":"Department of Orthopaedic Surgery, Surgical Science Tokai University School of Medicine 143 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