این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
صفحه اصلی
درباره پایگاه
فهرست سامانه ها
الزامات سامانه ها
فهرست سازمانی
تماس با ما
JCR 2016
جستجوی مقالات
پنجشنبه 20 آذر 1404
Iranian Journal of Public Health
، جلد ۵۲، شماره ۳، صفحات ۵۶۳-۵۷۴
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
Serum Exosome-Derived MiR-7 Exacerbates Chronic Obstructive Pulmonary Disease by Regulating Macrophage Differentiation
چکیده انگلیسی مقاله
Background: Polarization of macrophages and miR-7 have been reported to greatly influence the progress of chronic obstructive pulmonary disease (COPD). However, the interaction is unclear. We aimed to investigate the role of miR-7 in the serum exosome of COPD, thus further revealing the underlying mechanism of COPD. Methods: The study was conducted in 2022 in The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, China. COPD mouse model was established. Macrophages were sorted by flow cytometry assay. ELISA kits were used to detect the levels of TNF-α and IL-6. Exosomes were identified by confocal microscopy and PKH67 staining. RT-qPCR and western blot assay were performed to determine the mRNA and protein expressions. H&E staining assay was used to assess the tissue injury. CCK-8 assay was applied to evaluate cell viability. Luciferase reporter assay was used to confirm the binding between PIM1 and miR-7. Results: The exosomes derived from the COPD mice serum exerted high level of miR-7, which induced M1 differentiation of macrophages and increased the secretion of proinflammatory factors in vivo and in vitro. The effects of exosomes from COPD mice could be inhibited by miR-7 inhibitor. Bioinformatic prediction, luciferase reporter assay, and western blot assay showed an interaction between miR-7 and PIM1. Further examination showed that miR-7 regulated macrophage activation and differentiation to M1 via PIM1 in vitro. Conclusions: miR-7 from serum exosomes might exacerbate COPD by stimulating macrophage differentiation to M1, supplying a potential therapeutic target for COPD treatment.
کلیدواژههای انگلیسی مقاله
نویسندگان مقاله
| Yiming Jiang
Department of Emergency, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, 213003, China
| Jinhai Wang
Department of Emergency, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, 213003, China
| He Zhang
Department of Emergency, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, 213003, China
| Yeping Min
Department of Emergency, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, 213003, China
| Tijun Gu
Department of Emergency, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou, 213003, China
نشانی اینترنتی
https://ijph.tums.ac.ir/index.php/ijph/article/view/29596
فایل مقاله
فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده
برگشت به:
صفحه اول پایگاه
|
نسخه مرتبط
|
نشریه مرتبط
|
فهرست نشریات