دورية أكاديمية
CD5L Deficiency Protects Mice Against Bleomycin-Induced Pulmonary Fibrosis
العنوان: | CD5L Deficiency Protects Mice Against Bleomycin-Induced Pulmonary Fibrosis |
---|---|
المؤلفون: | Yang Guo, Mengyan Zhu, Ruling Shen |
المصدر: | Frontiers in Bioscience-Landmark, Vol 28, Iss 9, p 209 (2023) |
بيانات النشر: | IMR Press, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Biochemistry LCC:Biology (General) |
مصطلحات موضوعية: | cd5l, pulmonary fibrosis, macrophage, Biochemistry, QD415-436, Biology (General), QH301-705.5 |
الوصف: | Background: Pulmonary fibrosis (PF), the most common clinical type of irreversible interstitial lung disease with one of the worse prognoses, has a largely unknown molecular mechanisms that underlies its progression. CD5 molecule-like (CD5L) functions in an indispensable role during inflammatory responses; however, whether CD5L functions in regulating bleomycin (BLM)-induced lung fibrosis is less clear. Methods: Herein, we describe the engineering of Cd5l knockout mice using CRISPR/Cas9 gene editing technology. The BLM-induced model of acute lung injury represents the most widely used experimental rodent model for PF. Results: Taking advantage of this model, we demonstrated that both CD5L mRNA and protein were enriched in the lungs of mice following BLM-induced pulmonary fibrosis. Inhibition of CD5L prevented mice from BLM-induced lung fibrosis and injury. In particular, a lack of CD5L significantly attenuated inflammatory response and promoted M2 polarization in the lung of this pulmonary fibrosis model as well as suppressing macrophage apoptosis. Conclusions: Collectively, our data support that CD5L deficiency can suppress the development of pulmonary fibrosis, and also provides new molecular targets for the use of immunotherapy to treat lung fibrosis. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2768-6701 |
العلاقة: | https://www.imrpress.com/journal/FBL/28/9/10.31083/j.fbl2809209Test; https://doaj.org/toc/2768-6701Test |
DOI: | 10.31083/j.fbl2809209 |
الوصول الحر: | https://doaj.org/article/360b00f8012e4b9bb04ea391791157c9Test |
رقم الانضمام: | edsdoj.360b00f8012e4b9bb04ea391791157c9 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 27686701 |
---|---|
DOI: | 10.31083/j.fbl2809209 |