{"doi":"10.1073/pnas.0507604103","title":"Proapoptotic Bid is required for pulmonary fibrosis","abstract":"<jats:p>\n                    The molecular mechanisms of pulmonary fibrosis are poorly understood. Previous reports indicate that activation of TGF-β1 is essential for the development of pulmonary fibrosis. Here, we report that the proapoptotic Bcl-2 family member Bid is required for the development of pulmonary fibrosis after the intratracheal instillation of bleomycin. Mice lacking Bid exhibited significantly less pulmonary fibrosis in response to bleomycin compared with WT mice. The attenuation in pulmonary fibrosis was observed despite similar levels of inflammation, lung injury, and active TGF-β1 in bronchoalveolar lavage fluid 5 days after the administration of bleomycin in mice lacking Bid and in WT controls. Bleomycin induced similar levels cell death\n                    <jats:italic>in vitro</jats:italic>\n                    in alveolar epithelial cells isolated from WT and\n                    <jats:italic>bid</jats:italic>\n                    <jats:sup>−/−</jats:sup>\n                    mice. By contrast, alveolar epithelial cells from\n                    <jats:italic>bid</jats:italic>\n                    <jats:sup>−/−</jats:sup>\n                    mice were resistant to TGF-β1-induced cell death. These results indicate that Bcl-2 family members are critical regulators for the development of pulmonary fibrosis downstream of TGF-β1 activation.\n                  </jats:p>","journal":"Proceedings of the National Academy of Sciences","year":2006,"id":593130,"datarank":4.513930629183204,"base_score":4.77912349311153,"endowment":4.77912349311153,"self_citation_contribution":0.7168685239667295,"citation_network_contribution":3.797062105216475,"self_endowment_contribution":0.7168685239667295,"citer_contribution":3.797062105216475,"corpus_percentile":null,"corpus_rank":null,"citation_count":118,"citer_count":73,"citers_with_citation_signal":72,"citers_with_endowment":72,"datacite_reuse_total":18,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":625428,"name":"Gökhan M. 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Scott Budinger","orcid":"0000-0002-3114-5208","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Proapoptotic Bid is required for pulmonary fibrosis","abstract":"<jats:p>\n                    The molecular mechanisms of pulmonary fibrosis are poorly understood. Previous reports indicate that activation of TGF-β1 is essential for the development of pulmonary fibrosis. Here, we report that the proapoptotic Bcl-2 family member Bid is required for the development of pulmonary fibrosis after the intratracheal instillation of bleomycin. Mice lacking Bid exhibited significantly less pulmonary fibrosis in response to bleomycin compared with WT mice. The attenuation in pulmonary fibrosis was observed despite similar levels of inflammation, lung injury, and active TGF-β1 in bronchoalveolar lavage fluid 5 days after the administration of bleomycin in mice lacking Bid and in WT controls. Bleomycin induced similar levels cell death\n                    <jats:italic>in vitro</jats:italic>\n                    in alveolar epithelial cells isolated from WT and\n                    <jats:italic>bid</jats:italic>\n                    <jats:sup>−/−</jats:sup>\n                    mice. By contrast, alveolar epithelial cells from\n                    <jats:italic>bid</jats:italic>\n                    <jats:sup>−/−</jats:sup>\n                    mice were resistant to TGF-β1-induced cell death. These results indicate that Bcl-2 family members are critical regulators for the development of pulmonary fibrosis downstream of TGF-β1 activation.\n                  </jats:p>","is_dataset_classified":null,"base_score":4.77912349311153,"endowment":4.77912349311153,"datacite_reuse_total":18,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"16537427","pmcid":"PMC1401229","openalex_id":"https://openalex.org/W2121729413","authors":[],"funders":[{"funder_name":"NHLBI NIH HHS","grant_id":"1P01 HL 071643-01A1","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"5K08 HL 067835-05","title":null},{"funder_name":"NIGMS NIH HHS","grant_id":"R01 GM060472","title":null},{"funder_name":"NHLBI NIH HHS","grant_id":"K08 HL067835","title":null},{"funder_name":"NIGMS NIH HHS","grant_id":"GM 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Lung Diseases and Idiopathic Pulmonary Fibrosis","Inhalation and Respiratory Drug Delivery","Cardiac electrophysiology and arrhythmias","Animals","Apoptosis","BH3 Interacting Domain Death Agonist Protein","Bleomycin","Bronchoalveolar Lavage Fluid","Epithelial Cells","Fibroblasts","Lung","Mice","Mice, Mutant Strains","Pulmonary Fibrosis","Transforming Growth Factor beta","Transforming Growth Factor beta1"],"mesh_terms":["Animals","Bleomycin","Bronchoalveolar Lavage Fluid","Epithelial Cells","Fibroblasts","Lung","Mice, Mutant Strains","Pulmonary Fibrosis","Transforming Growth Factor beta","Apoptosis","BH3 Interacting Domain Death Agonist Protein","Mice","Transforming Growth Factor beta1"],"keywords":["Bleomycin","Pulmonary fibrosis","Fibrosis","Lung","Bronchoalveolar lavage","Medicine","Transforming growth factor","Idiopathic pulmonary fibrosis","Pathology","Apoptosis","Inflammation","Immunology","Cancer research","Internal 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