دورية أكاديمية
أعرض في EDS

Overexpression of Aquaporin 1 in Synovium Aggravates Rat Collagen-Induced Arthritis Through Regulating β-Catenin Signaling: An in vivo and in vitro Study.

التفاصيل البيبلوغرافية
العنوان: Overexpression of Aquaporin 1 in Synovium Aggravates Rat Collagen-Induced Arthritis Through Regulating β-Catenin Signaling: An in vivo and in vitro Study.
المؤلفون: Mu YR; School of Pharmacy, Anhui Medical University, Hefei, Anhui Province, People's Republic of China.; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Hefei, People's Republic of China., Zhou MY; School of Pharmacy, Anhui Medical University, Hefei, Anhui Province, People's Republic of China.; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Hefei, People's Republic of China., Cai L; Department of Pathology, School of Basic Medicine, Anhui Medical University, Hefei, Anhui Province, People's Republic of China., Liu MM; School of Pharmacy, Anhui Medical University, Hefei, Anhui Province, People's Republic of China.; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Hefei, People's Republic of China., Li R; School of Pharmacy, Anhui Medical University, Hefei, Anhui Province, People's Republic of China.; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Hefei, People's Republic of China.
المصدر: Journal of inflammation research [J Inflamm Res] 2020 Oct 08; Vol. 13, pp. 701-712. Date of Electronic Publication: 2020 Oct 08 (Print Publication: 2020).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Dove Medical Press Country of Publication: New Zealand NLM ID: 101512684 Publication Model: eCollection Cited Medium: Print ISSN: 1178-7031 (Print) Linking ISSN: 11787031 NLM ISO Abbreviation: J Inflamm Res Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Auckland, N.Z.] : Dove Medical Press
مستخلص: Introduction: Previous studies have confirmed that aquaporin 1 (AQP1) is up-regulated in synovium of rheumatoid arthritis (RA), but its exact pathogenic mechanisms in RA are unclear. This study revealed the pathogenic role of AQP1 in rat collagen-induced arthritis (CIA) and the underlying mechanisms related to β-catenin signaling.
Materials and Methods: Secondary paw swelling and pathological changes of ankle joints were used to evaluate the severity of rat CIA. Synovial AQP1 and β-catenin expression were measured by immunohistochemistry (IHC) and Western blot assay. AQP1 siRNA was applied to knockdown AQP1 in cultured CIA fibroblast-like synoviocyte (FLS). Assays of MTT, PCNA immunofluorescence and transwell were performed to detect cell proliferation, migration and invasion. The protein levels of β-catenin pathway members and ratio of TOP/FOP luciferase activity were also measured.
Results: In vivo, we revealed that synovial AQP1 and β-catenin expressions in CIA rats were higher than normal rats, and synovial AQP1 expression of CIA rats increased in parallel with secondary paw swelling and total pathological score on joint damage. Correlation analysis of IHC results indicated that synovial AQP1 expression positively correlated with β-catenin expression in CIA rat. In vitro, AQP1 siRNA apparently reduced the proliferation, migration and invasion of CIA FLS by inhibiting β-catenin signaling pathway. As an activator of β-catenin signaling, lithium chloride (an inhibitor of GSK-3β) reversed the inhibitory effects of AQP1 siRNA on the cultured CIA FLS.
Conclusion: We concluded that the overexpression of synovial AQP1 aggravated rat CIA by promoting the activation of FLS through β-catenin signaling pathway.
Competing Interests: The authors declare that they have no conflicts of interest for this work.
(© 2020 Mu et al.)
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فهرسة مساهمة: Keywords: aquaporin 1; collagen-induced arthritis; fibroblast-like synoviocyte; rheumatoid arthritis; β-catenin signaling
تواريخ الأحداث: Date Created: 20201029 Latest Revision: 20220417
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC7550268
DOI: 10.2147/JIR.S271664
PMID: 33116749
قاعدة البيانات: MEDLINE
الوصف
تدمد:1178-7031
DOI:10.2147/JIR.S271664