دورية أكاديمية
أعرض في EDS

Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.

التفاصيل البيبلوغرافية
العنوان: Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.
المؤلفون: Podolsky MJ; Department of Medicine, Weill Cornell Medical College, New York, NY, USA. mip9227@med.cornell.edu., Kheyfets B; Department of Medicine, Weill Cornell Medical College, New York, NY, USA., Pandey M; Department of Medicine, Weill Cornell Medical College, New York, NY, USA., Beigh AH; Department of Medicine, Weill Cornell Medical College, New York, NY, USA., Yang CD; Cardiovascular Research Institute, University of California, San Francisco, CA, USA., Lizama CO; Cardiovascular Research Institute, University of California, San Francisco, CA, USA., Datta R; Cardiovascular Research Institute, University of California, San Francisco, CA, USA., Lin LL; Department of Molecular Physiology and Biological Physics, University of Virginia School of Medicine, Charlottesville, VA, USA., Wang Z; Department of Molecular Physiology and Biological Physics, University of Virginia School of Medicine, Charlottesville, VA, USA., Wolters PJ; Department of Medicine, University of California, San Francisco, CA, USA., McManus MT; Department of Microbiology and Immunology and UCSF Diabetes Center, University of California, San Francisco, CA, USA., Qi L; Department of Molecular Physiology and Biological Physics, University of Virginia School of Medicine, Charlottesville, VA, USA., Atabai K; Cardiovascular Research Institute, University of California, San Francisco, CA, USA. kamran.atabai@ucsf.edu.; Department of Medicine, University of California, San Francisco, CA, USA. kamran.atabai@ucsf.edu.; Lung Biology Center, University of California, San Francisco, CA, USA. kamran.atabai@ucsf.edu.
المصدر: Nature communications [Nat Commun] 2024 Feb 20; Vol. 15 (1), pp. 1531. Date of Electronic Publication: 2024 Feb 20.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Collagen*/metabolism , Extracellular Matrix*/metabolism, Animals ; Humans ; Fibrosis ; Proteolysis ; Lung/pathology ; Mammals/metabolism ; Proteins/metabolism
مستخلص: Accumulating evidence has implicated impaired extracellular matrix (ECM) clearance as a key factor in fibrotic disease. Despite decades of research elucidating the effectors of ECM clearance, relatively little is understood regarding the upstream regulation of this process. Collagen is the most abundant constituent of normal and fibrotic ECM in mammalian tissues. Its catabolism occurs through extracellular proteolysis and cell-mediated uptake of collagen fragments for intracellular degradation. Given the paucity of information regarding the regulation of this latter process, here we execute unbiased genome-wide screens to understand the molecular underpinnings of cell-mediated collagen clearance. Using this approach, we discover a mechanism through which collagen biosynthesis is sensed by cells internally and directly regulates clearance of extracellular collagen. The sensing mechanism appears to be dependent on endoplasmic reticulum-resident protein SEL1L and occurs via a noncanonical function of this protein. This pathway functions as a homeostatic negative feedback loop that limits collagen accumulation in tissues. In human fibrotic lung disease, the induction of this collagen clearance pathway by collagen synthesis is impaired, thereby contributing to the pathological accumulation of collagen in lung tissue. Thus, we describe cell-autonomous, rheostatic collagen clearance as an important pathway of tissue homeostasis.
(© 2024. The Author(s).)
التعليقات: Update of: bioRxiv. 2023 Sep 24;:. (PMID: 36711851)
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معلومات مُعتمدة: P30 DK063720 United States DK NIDDK NIH HHS; K08 HL145015 United States HL NHLBI NIH HHS; S10 OD025102 United States OD NIH HHS; S10 OD021822 United States OD NIH HHS; R01 HL136377 United States HL NHLBI NIH HHS; R01 DK132786 United States DK NIDDK NIH HHS; R35 GM130292 United States GM NIGMS NIH HHS
المشرفين على المادة: 9007-34-5 (Collagen)
0 (SEL1L protein, human)
0 (Proteins)
تواريخ الأحداث: Date Created: 20240220 Date Completed: 20240222 Latest Revision: 20240304
رمز التحديث: 20240304
مُعرف محوري في PubMed: PMC10879544
DOI: 10.1038/s41467-024-45817-8
PMID: 38378719
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-024-45817-8