MiR-155 promotes cell proliferation and inhibits apoptosis by PTEN signaling pathway in the psoriasis

Diosgenin Glucoside Protects against Spinal Cord Injury by Regulating Autophagy and Alleviating Apoptosis

“…MicroRNAs have gained extensive attention, and could become a novel therapeutic target for the treatment of SCI. A large number of studies have shown that miR-155 is a broad regulator of inflammatory mediators, and plays a key regulatory role in immune and inflammatory disorders [34,35,36,37]. The development of neurodegenerative diseases is closely correlated with immunity and inflammation, suggesting that miR-155 may be a novel target for its treatment.…”

MiR‐126 correlates with increased disease severity and promotes keratinocytes proliferation and inflammation while suppresses cells' apoptosis in psoriasis

“…MicroRNAs (miRNAs) are a class of small noncoding RNAs that play crucial roles in the regulation of biological processes in signal transduction, cells' proliferation, differentiation, and apoptosis . Accumulating studies disclose that dysregulation of miRNAs including miR‐31, miR‐155, and miR‐26b is involved in the pathological processes of a variety of immune diseases including psoriasis . MiR‐126, located on human chromosome 9q34.3, has been reported to participate in the development and progression of multiple immune diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD) .…”

“…[9][10][11][12] Accumulating studies disclose that dysregulation of miRNAs including miR-31, miR-155, and miR-26b is involved in the pathological processes of a variety of immune diseases including psoriasis. [13][14][15] MiR-126, located on human chromosome 9q34.3, has been reported to participate in the development and progression of multiple immune diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD). [16][17][18] However, to the best of our knowledge, the role of miR-126 in the etiology of psoriasis has not been reported.…”

The contribution of feedback loops between miRNAs, cytokines and growth factors to the pathogenesis of psoriasis

“…Through targeting PTEN, which inhibits PI3K to AKT signalling, miR‐155 enhances its own effect and creates a positive feedback loop regulation . Taken together, we can see a positive/positive mode of feedback loop, in which pro‐inflammatory cytokines like TNF‐α and IFN‐γ increase miR‐155, while miR‐155 targets SOCS1 and PTEN, which are negative regulators of cytokine signalling. In this way, miR‐155 contributes to inflammation maintenance in psoriasis (Figure ).…”

“…MiR‐155 expression is enhanced by NFκB and its promoter has three NFκB binding sites . MiR‐155 is upregulated in psoriatic lesions . MiR‐155 may promote differentiation towards a Th1 phenotype by limiting the expression of IL‐4, a cytokine whose expression characterizes the Th2 phenotype.…”