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. 2025 Jun 13;162(1):103.
doi: 10.1186/s41065-025-00468-7.

MiR-106b-5p improving the progression of chronic kidney disease by inhibiting the TGF-β/Smad pathway

Qihao Ma  1 , Li Xu  2 , Peng Zhou  1 , Bo Yang  1 , Yong Li  2 , Danan Sun  3
Affiliations

MiR-106b-5p improving the progression of chronic kidney disease by inhibiting the TGF-β/Smad pathway

Qihao Ma et al. Hereditas. .

Abstract

Background: Chronic Kidney Disease (CKD) is a progressive disorder marked by renal impairment and declining kidney function.

Aims: To investigate the expression of miR-106b-5p in CKD and its regulatory relationship with the TGF-β/Smad pathway.

Methods: A total of 150 cases of CKD patients were selected as the observation group, while 100 healthy individuals served as the control group. Lipopolysaccharide (LPS) was utilized to induce damage to HK-2 cells. Real-time fluorescence PCR was used to detect the expression of genes. The CCK - 8 assay was utilized to evaluate cell proliferation, while flow cytometry was applied to measure the cell apoptosis rate.

Results: miR-106b-5p is notably downregulated in CKD and exhibits a significant positive correlation with the eGFR in affected patients. Additionally, miR-106b-5p demonstrates a strong association with the levels of inflammatory factors in individuals with CKD. Furthermore, the expression of miR-106b-5p is reduced in LPS-induced HK-2 cells. Upregulation of miR-106b-5p can improve the inhibitory effect of LPS on the viability of HK-2 cells, reduce the apoptosis rate of cells, and alleviate the inflammatory response. miR-106b-5p serves as a negative regulatory factor within the TGF-β/Smad signaling pathway by directly targeting the pivotal receptor TGFBR2 and the downstream effectors SMAD2/3 within the TGF-β signaling cascade.

Conclusions: miR-106b-5p ameliorates CKD progression by suppressing the TGF - β/Smad signaling pathway and could potentially be a therapeutic target for CKD.

Keywords: CKD; HK-2 cell; TGF-β/Smad; miR-106b-5p.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: The study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of The Second Affiliated Hospital of Heilongjiang, University of Chinese Medicine before the study began. The written informed consent has been obtained from the participants involved. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests. Clinical trial number: Not applicable.

Figures

Fig. 1
Fig. 1
Analysis of the expression level of miR-106b-5p and TGF-β1 in CKD patients. The eGFR of CKD patients was significantly lower, reaching its lowest level in the G4-G5 stage, compared to the control group (p < 0.001) (A). The expression of serum miR-106b-5p in CKD patients decreases with increasing CKD stage and reaches its lowest level in stages G4-G5 (p < 0.001) (B). miR-106b-5p is positively correlated with the level of eGFR in patients with CKD (r = 0.832, p < 0.001) (C).The serum TGF-β1 levels in patients with CKD in the G1-G5 stages showed a gradually increasing trend (p < 0.001) (D). The TGF-β1 level in CKD patients is significantly negatively correlated with the eGFR level (r = 0.852, p < 0.001) (E). Additionally, the TGF-β1 level is negatively correlated with the expression level of miR-106b-5p (r = 0.802, p < 0.001) (F). ** p < 0.01, *** p < 0.001
Fig. 2
Fig. 2
Correlation Between miR-106b-5p and Inflammatory Factor Levels in CKD Patients. As CKD progresses, there is a significant increase in the levels of IL-6, TNF-α and IL-1β (p < 0.001) (A-C). The level of IL-10 increased in patients during the G1-G2 stage, but decreased during the G3-G5 stage (p < 0.05) (D). The Pearson correlation analysis revealed that in CKD patients, miR-106b-5p was significantly negatively correlated with inflammatory factors IL-6, TNF-α and IL-1β (E-G), while it was significantly positively correlated with the anti-inflammatory factor IL-10 (H). * p < 0.05, *** p < 0.001
Fig. 3
Fig. 3
Effect of miR-106b-5p on LPS-induced HK-2 cells. RT-qPCR was used to determine the expression of miR-106b-5p in LPS-induced HK-2 cells (A-B). The CCK-8 assay was used to determine the effect of LPS on the viability of HK-2 cells (C-D). The expression of miR-106b-5p was determined by RT-qPCR as a confirmation of the transfection efficiency of the cells (E). miR-106b-5p can ameliorate the inhibitory effect of LPS on the viability of HK-2 cells, reduce the apoptosis rate of cells (F-G). miR-106b-5p can alleviate the pro-inflammatory effect of LPS on HK-2 cells (H-J). * p < 0.05, ** p < 0.01, *** p < 0.001
Fig. 4
Fig. 4
miR-106b − 5p targets and inhibits the TGF-β/SMAD pathway. The potential binding sites of miR-106b-5p with the targeted genes TGFBR2, SMAD2 and SMAD3 (A). Dual luciferase reporter gene assay was used to verify the targeted relationship (B-D). The overexpression of miR-106b-5p can inhibit the increase in the mRNA levels of TGFBR2, SMAD2 and SMAD3 induced by LPS (E-G). ELISA method was used to determine the effect of miR-106b-5p on the total secretion of TGF-β1 in the cell culture supernatant (H). * p < 0.05, ** p < 0.01, *** p < 0.001
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