{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T12:14:00Z","timestamp":1791288840141,"version":"4.3.0"},"reference-count":72,"publisher":"The Company of Biologists","license":[{"start":{"date-parts":[[2021,5,18]],"date-time":"2021-05-18T00:00:00Z","timestamp":1621296000000},"content-version":"am","delay-in-days":868,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["NS104083"],"award-info":[{"award-number":["NS104083"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>Endoplasmic Reticulum (ER) stress is a major pathology encountered after hypoxic-ischemic (HI) injury. Accumulation of unfolded proteins triggers the unfolded protein response (UPR) resulting in the activation of pro-apoptotic cascades causing cells to die. Here we identified Bax Inhibitor-1 (BI-1), an evolutionary protein encoded by the Transmembrane Bax inhibitor Motif Containing 6 (TMBIM6) gene, as a novel modulator of ER stress-induced apoptosis after HI brain injury in a neonatal rat pup. The main objective of our study is to overexpress BI-1, via viral-mediated gene delivery of human adenoviral-TMBIM6 (Ad-TMBIM6) vector, to investigate its anti-apoptotic effects as well as to elucidate its signaling pathways in an in vivo neonatal HI rat model and in vitro oxygen-glucose deprivation (OGD) model.<\/jats:p>\n               <jats:p>Ten-day old unsexed Sprague-Daley rat pups underwent right common carotid artery ligation followed by 1.5h of hypoxia. Rat pups injected with Ad-TMBIM6 vector, 48h pre-HI, showed a reduction in percent infarcted area, attenuated neuronal degeneration and improved long-term neurological outcomes. Furthermore, silencing BI-1 or further activating the IRE1\u03b1 branch of the UPR, with CRISPR activation plasmid, showed to reverse BI-1's protective effects. Based on our in vivo and in vitro data, BI-1's protective effects were shown to be mediated via inhibition of IRE1\u03b1 signaling and in part via inhibition of the second stress sensor receptor, PERK. Overall, this study showed a novel role for BI-1 and ER stress in the pathophysiology of HI and could provide a basis for BI-1 as a potential therapeutic target.<\/jats:p>","DOI":"10.1242\/dmm.040352","type":"journal-article","created":{"date-parts":[[2019,10,21]],"date-time":"2019-10-21T13:11:23Z","timestamp":1571663483000},"source":"Crossref","is-referenced-by-count":22,"title":["Adenoviral-TMBIM6 vector attenuates ER stress - induced apoptosis in a neonatal hypoxic-ischemic rat model"],"prefix":"10.1242","author":[{"given":"Desislava","family":"Doycheva","sequence":"first","affiliation":[{"name":"Center for Neuroscience Research, Department of Physiology and Pharmacology, Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ningbo","family":"Xu","sequence":"additional","affiliation":[{"name":"Center for Neuroscience Research, Department of Physiology and Pharmacology, Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA"},{"name":"Department of Interventional Radiology, Zhujiang Hospital, Southern Medical University, Guangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4393-1684","authenticated-orcid":false,"given":"Harpreet","family":"Kaur","sequence":"additional","affiliation":[{"name":"Center for Neuroscience Research, Department of Physiology and Pharmacology, Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay","family":"Malaguit","sequence":"additional","affiliation":[{"name":"Center for Neuroscience Research, Department of Physiology and Pharmacology, Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8988-3353","authenticated-orcid":false,"given":"Devin William","family":"McBride","sequence":"additional","affiliation":[{"name":"The Vivian L. Smith Department of Neurosurgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiping","family":"Tang","sequence":"additional","affiliation":[{"name":"Center for Neuroscience Research, Department of Physiology and Pharmacology, Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4319-4285","authenticated-orcid":false,"given":"John H.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Center for Neuroscience Research, Department of Physiology and Pharmacology, Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA"},{"name":"Departments of Anesthesiology, Neurosurgery and Neurology, Loma Linda University School of Medicine, Loma Linda, CA 92354, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2019,1,1]]},"reference":[{"key":"2021042623041978500_DMM040352C1","doi-asserted-by":"publisher","first-page":"C178","DOI":"10.1152\/ajpcell.00381.2001","article-title":"Role of nitric oxide in the regulation of HIF-1alpha expression during hypoxia","volume":"283","author":"Agani","year":"2002","journal-title":"Am. 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