DACH1, a novel target of miR-218, participates in the regulation of cell viability, apoptosis, inflammatory response, and epithelial-mesenchymal transition process in renal tubule cells treated by high-glucose

Zhang, Yingli; Wang, Jiemin; Yin, Hong; Wang, Shoubao; He, Cailing; Liu, Jing

doi:10.1080/0886022x.2020.1762647

Cited by 15 publications

(11 citation statements)

References 51 publications

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“…Our data show that DACH1 plays a pivotal repressor role in controlling cytokine expression in renal tubule cells. Consistent with our result, a recent report indicated that DACH1 was associated with a proinflammatory phenotype of high glucose-treated cultured renal tubule cells (40). In mechanistic studies, DACH1 antagonizes FOXM1 promoter occupancy and target gene expression (28).…”

Section: Discussionsupporting

confidence: 92%

Transcriptome-wide association analysis identifies DACH1 as a kidney disease risk gene that contributes to fibrosis

Doke¹,

Huang²,

Qiu³

et al. 2021

Journal of Clinical Investigation

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Section: Discussionsupporting

confidence: 92%

Transcriptome-wide association analysis identifies DACH1 as a kidney disease risk gene that contributes to fibrosis

Doke¹,

Huang²,

Qiu³

et al. 2021

Journal of Clinical Investigation

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“…To further explore the specific role of miR-483-5p in DN, we induced HK2 cells by HG as an in vitro study model. This model has been widely used in the study of DN in vitro [23]. Compared with the control group, miR-483-5p levels decreased in a time-dependent manner with the increase of HG induction time (p < 0.05, ▶ Fig.…”

Section: Effects Of Mir-483-5p On Viability Apoptosis and Ros Generation In Hg-induced Hk2 Cellsmentioning

confidence: 99%

miRNA-483–5p Targets HDCA4 to Regulate Renal Tubular Damage in Diabetic Nephropathy

et al. 2021

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This study was designed to evaluate the diagnostic value of miR-483–5p in diabetic nephropathy (DN), and its effect and mechanism on apoptosis and inflammation of human proximal renal tubular cells (HK2) induced by high glucose (HG). Thirty healthy controls, 30 types 2 diabetes mellitus (T2DM) patients, and 28 DN patients were enrolled. miR-483–5p mRNA levels in serum were analyzed by RT-qPCR assays. The receiver operating characteristic curve (ROC) was used to analyze the diagnostic value of miR-483–5p in DN. HK2 cells were induced by HG to establish an in vitro study model. CCK-8 and flow cytometry was used to detect cell viability, apoptosis, and reactive oxygen species (ROS) generation. Inflammation levels were measured by ELISA. Luciferase reporter assay was used to detect target genes of miR-483–5p. miR-483–5p was decreased in DN patients. The decreased level of miR-483–5p was positively correlated with estimated glomerular filtration rate (eGFR) and negatively correlated with proteinuria. miR-483–5p can significantly distinguish DN patients from healthy controls and T2DM and has a high diagnostic value. miR-483–5p decreased in HK2 cells induced by HG, and overexpression of miR-483–5p reversed HG-induced decreased cell activity, increased apoptosis, ROS production, and inflammation. Histone deacetylase 4 (HDCA4) was markedly increased in DN patients and HG-induced HK2 cells. miR-483–5p directly targeted HDCA4, and increasing miR-483–5p inhibited HDCA4 increased in HG-induced HK2. In conclusion, the results indicate that reduction of miR-483–5p has a high diagnostic value in DN, and overexpression of miR-483–5p has a certain protective effect on HK2 cells induced by HG by targeting HDCA4.

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“…Dachshund family transcription factor 1 ( DACH1 ) is a key factor in determining cell fate (47). Studies have indicated that DACH1 is necessary in the occurrence of certain inflammations (48, 49).…”

Section: Discussionmentioning

confidence: 99%

ssc-micorRNA-132 suppresses theClostridium perfringensbeta2 toxin induced inflammation and apoptosis of IPEC-J2 cells via targetingDACH1

Xie

Zhang

Wang

et al. 2020

Preprint

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Clostridium perfringens (C. perfringens) beta2 (CPB2) is the main virulence factor secreted from C. perfringens type C, which caused diarrhea characterized by high mortality in pig, especially newborn piglets. Our previous research found that ssc-miR-132 displayed decreased expression in piglets diarrhea after infected with C. perfringens type C compared with normal piglets. We speculated that ssc-miR-132 may play an important role in the diarrhea. However, the function of ssc-miR-132 in the diarrhea is limited. Thus, we overexpressed and knocked down ssc-miR-132 in intestinal porcine epithelial (IPEC-J2) cells, and then treated the cells with recombinant CPB2 (rCPB2) toxin (20 μg/mL). Our results showed that ssc-miR-132 was significantly decreased after treated with rCPB2 toxin. In addition, overexpression of ssc-miR-132 reduced the expression of lactate dehydrogenase (LDH) and tumor necrosis factor (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8) caused by rCPB2 toxin. The CCK8, Edu and TUNEL staining showed that overexpression of ssc-miR-132 weakened the inhibition of rCPB2 toxin on cell proliferation and reduced the promotion of cell apoptosis; while inhibition of ssc-miR-132 had opposite results. The dual luciferase experiment showed that dachshund family transcription factor 1 (DACH1) was the target gene of ssc-miR-132. Silencing DACH1 was consistent with the results of overexpression of ssc-miR-132, and reversed the apoptosis and inflammation caused by rCPB2 toxin. Overexpression of DACH1 weakened the role of ssc-miR-132 in rCPB2 toxin -induced inflammation and apoptosis. In summary, ssc-miR-132 inhibited rCPB2 toxin-induced apoptosis and inflammation in IPEC-J2 cells by targeting DACH1.

show abstract

DACH1, a novel target of miR-218, participates in the regulation of cell viability, apoptosis, inflammatory response, and epithelial-mesenchymal transition process in renal tubule cells treated by high-glucose

Cited by 15 publications

References 51 publications

Transcriptome-wide association analysis identifies DACH1 as a kidney disease risk gene that contributes to fibrosis

Transcriptome-wide association analysis identifies DACH1 as a kidney disease risk gene that contributes to fibrosis

miRNA-483–5p Targets HDCA4 to Regulate Renal Tubular Damage in Diabetic Nephropathy

ssc-micorRNA-132 suppresses theClostridium perfringensbeta2 toxin induced inflammation and apoptosis of IPEC-J2 cells via targetingDACH1

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