miR‐410 suppresses the expression of interleukin‐6 as well as renal fibrosis in the pathogenesis of lupus nephritis

Li, Dongmei; Zhang, Na; Zhang, Jing; Zhao, Hang; Wang, Xiaofei

doi:10.1111/1440-1681.12576

Cited by 31 publications

(29 citation statements)

References 44 publications

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“…Accumulating evidence has shown that miRNAs as regulators of other signaling pathways are essentially involved in the regulation of extracellular matrix remodeling, mesenchymal stromal cell differentiation and pro-inflammatory mediator releases, which are key factors involved in the progression of osteoarthritis [ 32 ]. It has been reported that abnormal expression of miR-410-3p is present in different kinds of diseases and regulates many important biological processes in inflammation, angiogenesis and tumorigenesis, including cell proliferation, invasion and migration, apoptosis and stem cell differentiation [ 16 , 33 , 34 ]. MiR-410-3p was shown to have protective functions by suppressing cell proliferation and invasion in breast cancer and pancreatic cancer [ 15 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

“…Dysregulation of miR-410-3p has been reported in the progression of breast cancer, pancreatic cancer and prostate cancer [ 13 – 15 ]. For example, miR-410-3p was shown to have protective roles in the pathogenesis of lupus nephritis by suppressing renal fibrosis [ 16 ]. However, the fundamental mechanisms of miRNAs underlying OA remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-410-3p modulates chondrocyte apoptosis and inflammation by targeting high mobility group box 1 (HMGB1) in an osteoarthritis mouse model

Pan

Dai

Wang

et al. 2020

BMC Musculoskelet Disord

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Background: Osteoarthritis (OA) is the most prevalent type of arthritis, which commonly involves inflammation in the articular cartilage in OA pathogenesis. MicroRNAs (miRNAs) play essential roles in the regulation and pathophysiology of various diseases including OA. MiR-410-3p has been demonstrated to mediate inflammatory pathways, however, the regulatory functions of miR-410-3p in OA remain largely unknown. Methods: The regulations of miR-410-3p were investigated in OA. Mouse primary chondrocytes and mouse in vivo models were used. The expression levels of miR-410-3p and HMGB1 were measured by qPCR. The transcription activity of NF-κB was assessed by luciferase reporter assay. MTT assay was performed to assess cellular proliferation. Cell apoptosis was evaluated with the Fluorescein Isothiocyanate (FITC) Annexin V assay. Expression levels of proteins were determined by Western blot. Results: The results demonstrated that miR-410-3p was markedly downregulated in articular cartilage tissues as well as in lipopolysaccharide (LPS)-treated chondrocytes in OA mice. In addition, upregulation of miR-410-3p markedly inhibited LPS-induced apoptosis of chondrocytes. The results also demonstrated that the high mobility group box 1 (HMGB1) was a target of miR-410-3p. LPS-induced upregulated expression of HMGB1 significantly suppressed expression of miR-410-3p. Furthermore, upregulation of miR-410-3p markedly inhibited HMGB1 expression, the nuclear factor (NF)-kB activity and pro-inflammatory cytokines production. Taken together, the results suggested that miR-410-3p targeted HMGB1 and modulated chondrocytes apoptosis and inflammation through the NF-κB signaling pathway. Conclusions: These findings provide insights into the potential of miR-410-3p/ HMGB1 as therapeutic targets for OA treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-410-3p modulates chondrocyte apoptosis and inflammation by targeting high mobility group box 1 (HMGB1) in an osteoarthritis mouse model

Pan

Dai

Wang

et al. 2020

BMC Musculoskelet Disord

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“…miRNAs are able to bind to the 3′-untranslated regions (3′-UTR) of their paired mRNAs to suppress the expression of target genes (10). A number of miRNAs have been reported to participate in the pathogenesis of many diseases, including cancers, autoimmune diseases, cardiovascular diseases and acute and chronic renal disease (10–12). However, the underlying mechanisms of miRNAs in renal diseases require further investigation.…”

Section: Introductionmentioning

confidence: 99%

Quercetin is able to alleviate TGF‑β‑induced fibrosis in renal tubular epithelial cells by suppressing miR‑21

Cao

Jianying

et al. 2018

Exp Ther Med

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Patients with chronic kidney disease (CKD) are characterized by a gradual loss of kidney function over time. A number of studies have indicated that tubule interstitial fibrosis (TIF) is associated with the occurrence and development of CKD. The aim of the present study was to investigate the effect of quercetin treatment on the fibrosis of renal tubular epithelial cells and to determine whether the anti-fibrotic effects of quercetin are achieved via microRNA (miR)-21. Human tubular epithelial HK-2 cells were cultured with transforming growth factor (TGF)-β to induce fibrosis and the expression of fibrotic markers collagen I, fibronectin, α-smooth muscle actin (SMA) and epithelial-cadherin were measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. Cells were treated with 7.5, 15 or 30 mg/ml quercetin, following which fibrosis and miR-21 expression were evaluated. Quercetin-treated cells were transfected with miR-21 mimics and the expression of fibrotic markers was examined using RT-qPCR. Finally, the expression of fibrosis-associated miR-21 target genes, phosphatase and tensin homolog (PTEN) and TIMP Metallopeptidase Inhibitor 3 (TIMP3), was measured in cells treated with quercetin with or without miR-21 mimics using RT-qPCR, western blotting and immunocytochemistry. The results revealed that TGF-β treatment induced a significant increase in the expression of fibrotic markers in HK-2 cells, while quercetin treatment partially inhibited the fibrosis of HK-2 cells. Furthermore, quercetin treatment significantly inhibited TGF-β-induced miR-21 upregulation and transfection with miR-21 mimics reversed the anti-fibrotic effects of quercetin. Quercetin treatment markedly upregulated PTEN and TIMP3 expression, whereas transfection with miR-21 mimics reversed this effect. The results of the present study suggest that quercetin is able to alleviate TGF-β-induced fibrosis in HK-2 cells via suppressing the miR-21 and upregulating PTEN and TIMP3. Quercetin may have potential as an anti-fibrotic treatment for patients with renal fibrosis.

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“…It has been referred to as a tumor suppressor in pancreatic cancer (35) and as an enhancer of tumor invasion in liver and colorectal malignancies (36). A study on systemic lupus erythematosus showed that miR-410 downregulates IL6 and IL10 expression, and its overexpression significantly reduced the expression levels of TGF-b1 in SV40MES13 cells (37). In liver and colorectal tumors, upregulated miR-410 increased the tumor cell growth by silencing FHL1 tissues/cell lines (36).…”

Section: Discussionmentioning

confidence: 99%

Intestinal Expression of miR-130b, miR-410b, and miR-98a in Experimental Canine Echinococcosis by Stem-Loop RT-qPCR

et al. 2020

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Echinococcus granulosus is a zoonotic cestode dwelling in the small intestine of canid definitive hosts. Intermediate hosts are a wide range of domestic and wild ungulates. Human infection with the larval stage causes cystic echinococcosis. Understanding the nature and extent of molecular mechanisms involved in host-parasite interactions helps to answer some very basic questions in the biology of cestode parasites with significant implications in the management and control of cystic echinococcosis. Little is known on the miRNAs expression in the intestinal tissues of dogs infected with E. granulosus. In the present study, expression of a selected profile of miRNAs was evaluated in experimental canine echinococcosis. MiRNAs were extracted from 20 different parts of small intestinal tract of two sibling 3-months-old mix-breed dogs. Complementary DNA was specifically synthesized using an optimized stem-loop system. Intestinal expression of four miRNAs (cfa-let7g, cfa-miR-98, cfamiR-410, cfa-miR-130b) was evaluated using RT-qPCR. The results of the study indicate a significant difference between test and control dogs in cfamiR-130b, cfa-miR-98, and cfa-miR-410 (P ≤ 0.05); however, there was no significant difference for cfa-let7g. The most upregulated miRNAs were cfamiR-130b and cfa-miR-98. An increasing trend for cfa-let7g and a declining trend for cfa-miR-98, cfa-miR-410, and cfamiR-130b were found toward the distal segments of the small intestine. Our study revealed that cfa-miR-98, cfa-miR-410, and cfamiR-130b are involved in the definitive host response in canine echinococcosis. The study provides new information on the molecular basis of interactions between E. granulosus and dogs in terms of miRNA expression and showed that E. granulosus infection could increase the expression of some pro-inflammatory miRNAs at the cellular level in the definitive host.

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miR‐410 suppresses the expression of interleukin‐6 as well as renal fibrosis in the pathogenesis of lupus nephritis

Cited by 31 publications

References 44 publications

MicroRNA-410-3p modulates chondrocyte apoptosis and inflammation by targeting high mobility group box 1 (HMGB1) in an osteoarthritis mouse model

MicroRNA-410-3p modulates chondrocyte apoptosis and inflammation by targeting high mobility group box 1 (HMGB1) in an osteoarthritis mouse model

Quercetin is able to alleviate TGF‑β‑induced fibrosis in renal tubular epithelial cells by suppressing miR‑21

Intestinal Expression of miR-130b, miR-410b, and miR-98a in Experimental Canine Echinococcosis by Stem-Loop RT-qPCR

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