Abstract
Aberrant expression of miRNAs is significantly correlated with the occurrence of immune thrombocytopenic purpura (ITP). The immune imbalance of M1/M2 macrophage contributes to the development of ITP. However, the role of miR-148b-3p in macrophage phenotype imbalance remains unknown in ITP. In this study, we aimed to explore whether miR-148b-3p inhibits M2 macrophage polarization in ITP and to investigate the underlying mechanism. Peripheral blood from 22 ITP patients were collected, and real-time PCR confirmed that miR-148b-3p was up-regulated and Western blot analyses detected the expression of SOCS3 was down-regulated. Subsequent dual-luciferase reporter gene assay indicated that miR-148b-3p could bind to SOCS3. Furthermore, we found significant correlation between miR-148b-3p expression and platelet count. Applying gain and lose the function experiments of miR-148b-3p and SOCS3, we demonstrated that suppression of miR-148b-3p or up-regulation of SOCS3 promoted macrophage M2 polarization by inhibiting JAK2/STAT3 pathway. Together, our findings demonstrate that that miR-148b-3p targeting SOCS3 inhibits M2 macrophage polarization via JAK2/STAT3 signaling in ITP.
Highlights
Immune thrombocytopenic purpura (ITP) is a common autoimmune disease, which is resulted in a low platelet count and bleeding in the majority of patients
Results miR-148b-3p is up-regulated in peripheral blood of patients with ITP Previous studies reported that the dysregulation of miRNAs is important in the development of ITP, especially in monocytes
These results indicated that upregulation of miR-148b-3p could is significantly correlated with ITP by regulating M2 macrophages
Summary
Immune thrombocytopenic purpura (ITP) is a common autoimmune disease, which is resulted in a low platelet count and bleeding in the majority of patients. The main mechanisms include decreased platelet production and autoantibody-against platelet demolition (Cines et al, 2009). During this process, T cell dysfunction, such as regulatory T cells (Treg) imbalance, and abnormal activation of cytotoxic T cells are considered to play a prominent role (Yu et al, 2015). Accumulating evidence indicates that the aberrant differentiation and function of macrophage are essential in the pathogenesis of ITP (Chi et al, 2019). Macrophages are highly heterogeneous cells that can be activated by environmental stimuli and polarized to functionally different phenotypes. Macrophages can mainly differentiate into two subsets, classically activated M1 or alternatively activated M2 phenotype macrophages (Wang et al, 2014, Cui et al, 2018). M1 polarization is characterized by their ability to produce relatively high levels of proinflammatory cytokines, such as interleukin-1 (IL-1), IL-6, IL-12 and tumor necrosis factor-α (TNF-α), and promote an inflammatory response (Joshi et al, 2010, Batra et al, 2018)
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