DUSP5 suppresses interleukin-1β-induced chondrocyte inflammation and ameliorates osteoarthritis in rats

Wu, Zhipeng; Xu, Langhai; He, Yuzhe; Xu, Kai; Chen, Zhonggai; Moqbel, Safwat Adel Abdo; Ma, Chiyuan; Jiang, Lifeng; Ran, Jisheng; Wu, Lidong; Zhong, Ying

doi:10.18632/aging.202252

Cited by 19 publications

(17 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…DUSP5 belongs to a dual-specificity phosphatase subfamily. Although a number of cytokines are capable of inducing the expression of DUSP5 in mammalian cells, 31 DUSP5 was found to be implicated in numerous tumors and to affect the prognosis of cancer patients through facilitating tumor growth, invasion, and metastasis. 32,33 For example, Cai et al 34 identified a significant correlation between DUSP5 downregulation and aggressive clinicopathologic features of prostate cancer, as previously observed in gastric and colorectal tumors.…”

Section: Discussionmentioning

confidence: 99%

Silencing of AFAP1‐AS1 lncRNA impairs cell proliferation and migration by epigenetically promoting DUSP5 expression in pre‐eclampsia

Zhang

Zou

Tang

et al. 2021

J of Cellular Biochemistry

View full text Add to dashboard Cite

As a unique and common obstetric complication of pregnant women, pre‐eclampsia (PE) has been the first leading cause of maternal and perinatal morbidity and mortality in the world. Mounting studies have demonstrated that an abnormality of long noncoding RNA (lncRNA) expression was related to the pathological process of PE. Here, we showed that lncRNA AFAP1‐AS1 was markedly downregulated in pre‐eclamptic placentas. We further investigated the mechanism underlying the regulatory role of AFAP1‐AS1 in PE using human trophoblast cells. In vitro functional assays revealed that AFAP1‐AS1 knockdown inhibited trophoblast proliferation, migration, and invasion. Moreover, AFAP1‐AS1 interacts with EZH2 and inhibits DUSP5 expression through modulating H3K27m3 in the DUSP5 promoter of trophoblast cells, thus being involved in PE pathogenesis. Overall, these findings suggest that AFAP1‐AS1 could potentially become a prognostic biomarker as well as a new therapeutic target for PE.

show abstract

Section: Discussionmentioning

confidence: 99%

Silencing of AFAP1‐AS1 lncRNA impairs cell proliferation and migration by epigenetically promoting DUSP5 expression in pre‐eclampsia

Zhang

Zou

Tang

et al. 2021

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…DUSP5 was reported to inhibit interleukin-1β -induced chondrocyte inflammation and to ameliorate osteoarthritis by inhibiting the NF-κB and ERK signaling pathways in rats. 219 Analogously, DUSP5 mediated the protective effects against a high glucose‑induced inflammatory response by reducing the production of ROS and inflammatory cytokines. 220 …”

Section: The Signaling Pathways Regulated By the Protein Phosphatases...mentioning

confidence: 99%

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

Pan

Zhou

Zhang

et al. 2022

Sig Transduct Target Ther

View full text Add to dashboard Cite

Inflammation is the common pathological basis of autoimmune diseases, metabolic diseases, malignant tumors, and other major chronic diseases. Inflammation plays an important role in tissue homeostasis. On one hand, inflammation can sense changes in the tissue environment, induce imbalance of tissue homeostasis, and cause tissue damage. On the other hand, inflammation can also initiate tissue damage repair and maintain normal tissue function by resolving injury and restoring homeostasis. These opposing functions emphasize the significance of accurate regulation of inflammatory homeostasis to ameliorate inflammation-related diseases. Potential mechanisms involve protein phosphorylation modifications by kinases and phosphatases, which have a crucial role in inflammatory homeostasis. The mechanisms by which many kinases resolve inflammation have been well reviewed, whereas a systematic summary of the functions of protein phosphatases in regulating inflammatory homeostasis is lacking. The molecular knowledge of protein phosphatases, and especially the unique biochemical traits of each family member, will be of critical importance for developing drugs that target phosphatases. Here, we provide a comprehensive summary of the structure, the “double-edged sword” function, and the extensive signaling pathways of all protein phosphatases in inflammation-related diseases, as well as their potential inhibitors or activators that can be used in therapeutic interventions in preclinical or clinical trials. We provide an integrated perspective on the current understanding of all the protein phosphatases associated with inflammation-related diseases, with the aim of facilitating the development of drugs that target protein phosphatases for the treatment of inflammation-related diseases.

show abstract

“…The ERK signaling pathway is closely associated with several chronic in ammatory diseases, such as osteoarthritis, RA, and psoriatic arthritis [17,34]. The active form of ERK (p-ERK) can promote the expression of in ammatory genes [35].…”

Section: Discussionmentioning

confidence: 99%

Dual-specificity phosphatase 5 is a novel target gene of miR-216a-3p, inhibits the proliferation and invasion of fibroblast-like synoviocytes

Liu

Song

et al. 2022

Preprint

View full text Add to dashboard Cite

Dual-specificity phosphatase 5 (DUSP5) is a novel anti-inflammatory modulator in many inflammatory diseases. However, the role of DUSP5 in the fibroblast-like synoviocytes (FLS) of Rheumatoid arthritis (RA) remains unknown. In this study, we aimed to explore the biological function and regulation of DUSP5 in FLS. We found that lower DUSP5 expression levels were detected in collagen-induced arthritis (CIA) and synoviocytes MH7A. Overexpression of DUSP5 markedly decreased the proliferation, migration, and invasion of MH7A, which correlated with suppressing the phosphorylation of ERK. Moreover, DUSP5 was identified as a novel target gene of miR-216a-3p, which is upregulated in FLS. Therefore, DUSP5 expression was negatively regulated by miR-216a-3p, and the effect of DUSP5 overexpression on FLS was reversed by miR-216a-3p mimics. Overall, our study demonstrates that DUSP5 is a miR-216a-3p target gene and its anti-inflammatory function in FLS via inactivation of ERK. These results revealed that the miR-216a-3p/DUSP5 pathway may play a crucial role in the malignant behavior of FLS, which may serve as a new target for the treatment of RA.

show abstract

DUSP5 suppresses interleukin-1β-induced chondrocyte inflammation and ameliorates osteoarthritis in rats

Cited by 19 publications

References 55 publications

Silencing of AFAP1‐AS1 lncRNA impairs cell proliferation and migration by epigenetically promoting DUSP5 expression in pre‐eclampsia

Silencing of AFAP1‐AS1 lncRNA impairs cell proliferation and migration by epigenetically promoting DUSP5 expression in pre‐eclampsia

Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy

Dual-specificity phosphatase 5 is a novel target gene of miR-216a-3p, inhibits the proliferation and invasion of fibroblast-like synoviocytes

Contact Info

Product

Resources

About