Targeted inhibition of GRK2 kinase domain by CP-25 to reverse fibroblast-like synoviocytes dysfunction and improve collagen-induced arthritis in rats.

Author: Chenchen HAN ¹ ; Yifan LI ¹ ; Yuwen ZHANG ¹ ; Yang WANG ¹ ; Dongqian CUI ¹ ; Tingting LUO ¹ ; Yu ZHANG ¹ ; Qian LIU ¹ ; Hao LI ¹ ; Chun WANG ¹ ; Dexiang XU ² ; Yang MA ¹ ; Wei WEI ¹
Author Information

1. Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immune Medicine (Anhui Medical University), Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, China.
2. Public Health and Preventive Medicine Postdoctoral Research Station of Anhui Medical University, Hefei 230032, China.
Publication Type:Journal Article
Keywords: CP-25; Fibroblast-like synoviocyte; G protein coupled receptor kinase 2; MH7A; Prostaglandin E4 receptor; Rheumatoid arthritis
From: Acta Pharmaceutica Sinica B 2021;11(7):1835-1852
CountryChina
Language:English
Abstract: Rheumatoid arthritis (RA) is an autoimmune disease and is mainly characterized by abnormal proliferation of fibroblast-like synoviocytes (FLS). The up-regulated cellular membrane expression of G protein coupled receptor kinase 2 (GRK2) of FLS plays a critical role in RA progression, the increase of GRK2 translocation activity promotes dysfunctional prostaglandin E4 receptor (EP4) signaling and FLS abnormal proliferation. Recently, although our group found that paeoniflorin-6'-