{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T21:29:36Z","timestamp":1788557376363,"version":"build-2803163510"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2024,4,1]],"date-time":"2024-04-01T00:00:00Z","timestamp":1711929600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>BCL-2 family members are known to be implicated in survival in numerous biological settings. Here, we provide evidence that in injury and repair processes in lungs, BCL-2 mainly acts to attenuate endoplasmic reticulum (ER) stress and limit extracellular matrix accumulation. Days after an intratracheal bleomycin challenge, mice lose a fraction of their alveolar type II epithelium from terminal ER stress driven by activation of the critical ER sensor and stress effector IRE1\u03b1. This fraction is dramatically increased by BCL-2 inhibition, because IRE1\u03b1 activation is dependent on its physical association with the BCL-2\u2013proapoptotic family member BAX, and we found BCL-2 to disrupt this association in vitro. In vivo, navitoclax (a BCL-2\/BCL-xL inhibitor) given 15\u201321\u2009days after bleomycin challenge evoked strong activation of IRE-1\u03b1 in mesenchymal cells and markers of ER stress, but not apoptosis. Remarkably, after BCL-2 inhibition, bleomycin-exposed mice demonstrated persistent collagen accumulation at Day 42, compared with resolution in controls. Enhanced fibrosis proved to be due to the RNAase activity of IRE1\u03b1 downregulating MRC2 mRNA and protein, a mediator of collagen turnover. The critical role of MRC2 was confirmed in precision-cut lung slice cultures of Day-42 lungs from bleomycin-exposed wild-type and MRC2 null mice. Soluble and tissue collagen accumulated in precision-cut lung slice cultures from navitoclax-treated, bleomycin-challenged mice compared with controls, in a manner nearly identical to that of challenged but untreated MRC2 null mice. Thus, apart from mitochondrial-based antiapoptosis, BCL-2 functions to attenuate ER stress responses, fostering tissue homeostasis and injury repair.<\/jats:p>","DOI":"10.1165\/rcmb.2023-0109oc","type":"journal-article","created":{"date-parts":[[2023,12,20]],"date-time":"2023-12-20T10:26:00Z","timestamp":1703067960000},"page":"247-258","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":17,"title":["BCL-2 Modulates IRE1\u03b1 Activation to Attenuate Endoplasmic Reticulum Stress and Pulmonary Fibrosis"],"prefix":"10.1093","volume":"70","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6041-2870","authenticated-orcid":false,"given":"Claude Jourdan","family":"Le Saux","sequence":"first","affiliation":[{"name":"Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tsung Che","family":"Ho","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexis M.","family":"Brumwell","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaymin J.","family":"Kathiriya","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, Department of Medicine, University of California San Francisco, San Francisco, California; 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