دورية أكاديمية
Caveolin-1-Derived Peptide Reduces ER Stress and Enhances Gelatinolytic Activity in IPF Fibroblasts
العنوان: | Caveolin-1-Derived Peptide Reduces ER Stress and Enhances Gelatinolytic Activity in IPF Fibroblasts |
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المؤلفون: | Komatsu, Satoshi, Fan, Liang, Idell, Steven, Shetty, Sreerama, Ikebe, Mitsuo |
المصدر: | Cellular and Molecular Biology Faculty Publications and Presentations |
بيانات النشر: | Scholar Works at UT Tyler |
سنة النشر: | 2022 |
المجموعة: | Scholar Works at UT Tyler (University of Texas at Tyler) |
مصطلحات موضوعية: | idiopathic pulmonary fibrosis, endoplasmic reticulum stress, caveolin-1 scaffolding domain peptide, matrix metalloproteinases, Medicine and Health Sciences |
الوصف: | Idiopathic pulmonary fibrosis (IPF) is a fatal disease characterized by an excess deposition of extracellular matrix in the pulmonary interstitium. Caveolin-1 scaffolding domain peptide (CSP) has been found to mitigate pulmonary fibrosis in several animal models. However, its pathophysiological role in IPF is obscure, and it remains critical to understand the mechanism by which CSP protects against pulmonary fibrosis. We first studied the delivery of CSP into cells and found that it is internalized and accumulated in the Endoplasmic Reticulum (ER). Furthermore, CSP reduced ER stress via suppression of inositol requiring enzyme1α (IRE1α) in transforming growth factor β (TGFβ)-treated human IPF lung fibroblasts (hIPF-Lfs). Moreover, we found that CSP enhanced the gelatinolytic activity of TGFβ-treated hIPF-Lfs. The IRE1α inhibitor; 4µ8C also augmented the gelatinolytic activity of TGFβ-treated hIPF-Lfs, supporting the concept that CSP induced inhibition of the IRE1α pathway. Furthermore, CSP significantly elevated expression of MMPs in TGFβ-treated hIPF-Lfs, but conversely decreased the secretion of collagen 1. Similar results were observed in two preclinical murine models of PF, bleomycin (BLM)- and adenovirus expressing constitutively active TGFβ (Ad-TGFβ)-induced PF. Our findings provide new insights into the mechanism by which lung fibroblasts contribute to CSP dependent protection against lung fibrosis. |
نوع الوثيقة: | text |
وصف الملف: | application/pdf |
اللغة: | unknown |
العلاقة: | https://scholarworks.uttyler.edu/cmb_fac/4Test; https://scholarworks.uttyler.edu/context/cmb_fac/article/1004/viewcontent/Caveolin1Derived_Peptide_Reduces_ER_Stress_and_Enhances_Gelatinolytic_Activity_in_IPF_FibroblastsInternational_Journal_of_Molecular_Sciences.pdfTest |
الإتاحة: | https://scholarworks.uttyler.edu/cmb_fac/4Test https://scholarworks.uttyler.edu/context/cmb_fac/article/1004/viewcontent/Caveolin1Derived_Peptide_Reduces_ER_Stress_and_Enhances_Gelatinolytic_Activity_in_IPF_FibroblastsInternational_Journal_of_Molecular_Sciences.pdfTest |
رقم الانضمام: | edsbas.29D1B43A |
قاعدة البيانات: | BASE |
الوصف غير متاح. |