{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T13:50:33Z","timestamp":1790171433989,"version":"4.1.0"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2013,12,1]],"date-time":"2013-12-01T00:00:00Z","timestamp":1385856000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Asbestos exposure results in pulmonary fibrosis (asbestosis) and malignancies (bronchogenic lung cancer and mesothelioma) by mechanisms that are not fully understood. Alveolar epithelial cell (AEC) apoptosis is important in the development of pulmonary fibrosis after exposure to an array of toxins, including asbestos. An endoplasmic reticulum (ER) stress response and mitochondria-regulated (intrinsic) apoptosis occur in AECs of patients with idiopathic pulmonary fibrosis, a disease with similarities to asbestosis. Asbestos induces AEC intrinsic apoptosis, but the role of the ER is unclear. The objective of this study was to determine whether asbestos causes an AEC ER stress response that promotes apoptosis. Using human A549 and rat primary isolated alveolar type II cells, amosite asbestos fibers increased AEC mRNA and protein expression of ER stress proteins involved in the unfolded protein response, such as inositol-requiring kinase (IRE) 1 and X-box\u2013binding protein-1, as well as ER Ca\u00b22+ release ,as assessed by a FURA-2 assay. Eukarion-134, a superoxide dismutase\/catalase mimetic, as well as overexpression of Bcl-XL in A549 cells each attenuate asbestos-induced AEC ER stress (IRE-1 and X-box\u2013binding protein-1 protein expression; ER Ca\u00b22+ release) and apoptosis. Thapsigargin, a known ER stress inducer, augments AEC apoptosis, and eukarion-134 or Bcl-XL overexpression are protective. Finally, 4-phenylbutyric acid, a chemical chaperone that attenuates ER stress, blocks asbestos- and thapsigargin-induced AEC IRE-1 protein expression, but does not reduce ER Ca\u00b22+ release or apoptosis. These results show that asbestos triggers an AEC ER stress response and subsequent intrinsic apoptosis that is mediated in part by ER Ca\u00b22+ release.<\/jats:p>","DOI":"10.1165\/rcmb.2013-0053oc","type":"journal-article","created":{"date-parts":[[2013,7,25]],"date-time":"2013-07-25T18:49:22Z","timestamp":1374778162000},"page":"892-901","source":"Crossref","is-referenced-by-count":62,"title":["Asbestos-Induced Alveolar Epithelial Cell Apoptosis. The Role of Endoplasmic Reticulum Stress Response"],"prefix":"10.1093","volume":"49","author":[{"given":"David W.","family":"Kamp","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Pulmonary & Critical Care Medicine, Jesse Brown Veterans Affairs Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gang","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Pulmonary & Critical Care Medicine, Jesse Brown Veterans Affairs Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois; and"},{"name":"Clinical Research Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, People\u2019s Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Cheresh","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division 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