Effect of β-arrestin2 deficiency on the function of mouse peritoneal macrophages
Received:August 09, 2021  
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DOI:10. 3969 / j.issn.1005-4847. 2022. 01. 005
KeyWord:β-arrestin2; peritoneal macrophages; inflammatory cytokines; JAK1; STAT1
                          
AuthorInstitution
陈婷婷 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
单杉 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
李南 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
汪子颖 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
杞萌 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
张胜男 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
胡姗姗 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
魏伟 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
孙妩弋 安徽医科大学临床药理研究所,抗炎免疫药物教育部重点实验室,抗炎免疫药物安徽省协同创新中心, 合肥
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Abstract:
       Objective To investigate the effect of β-arrestin2 deficiency on the function of mouse peritoneal macrophages (pMφ). Methods The primary mouse pMφ were isolated from wild type mice and β-arrestin2 gene knockout mice. The migration of pMφ was measured by Transwell assay. Changes in the phagocytosis of pMφ after β-arrestin2 gene knockout were detected by the neutral red phagocytosis test. The expression of CD86 on pMφ was analyzed by flow cytometry. The levels of interleukin-1β ( IL-1β), IL-6 and tumor necrosis factor-α ( TNF-α) in pMφ were detected by ELISA. Protein expression levels of β-arrestin2, JAK1, p-JAK1, STAT1 and p-STAT1 were detected by Western Blot. Results Compared with the control group, β-arrestin2 knockout significantly inhibited the migration ability of pMφ, and significantly enhanced the phagocytosis of pMφ and the expression of CD86. The production of IL-1β, IL-6 and TNF-α was significantly increased in pMφ after β-arrestin2 depletion. The result of Western Blot showed that β-arrestin2 deficiency significantly up-regulated the levels of p-JAK1 and p-STAT1 in pMφ. Conclusions These result indicated that β-arrestin2 plays an important role in regulating the migration, phagocytosis and polarization of pMφ, and these effects appear to be mediated by the JAK1 / STAT1 signaling pathway.
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