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. 2022 Jan 25:2022:2279072.
doi: 10.1155/2022/2279072. eCollection 2022.

"V体育官网入口" lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis

Hongtu Zhao  1 , Yuanyuan Cui  2 , Fuqing Dong  3 , Wencong Li  4
Affiliations

lncRNA MSC-AS1 Aggravates Diabetic Nephropathy by Regulating the miR-325/CCNG1 Axis

Hongtu Zhao et al. J Healthc Eng. .

Retraction in

Abstract

Background: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes and has become the second leading cause of end-stage renal disease in the world. This study aims to clarify the regulatory mechanism of the lncRNA MSC-AS1/miR-325/cyclin G1 (CCNG1) axis in DN VSports手机版. .

Methods: The regulatory mechanism of lncRNA MSC-AS1/miR-325/CCNG1 was evaluated by RT-qPCR, CCK-8 assay, flow cytometry assay, RNA pull-down assay, ELISA, and western blot assay. V体育安卓版.

Results: Upregulation of lncRNA MSC-AS1 was detected in DN patients and HRMC cells treated with high glucose (HG). Knockdown of lncRNA MSC-AS1 reduced the proliferation, fibrosis, and inflammation of HRMC cells induced by HG. In addition, lncRNA MSC-AS1 acts as a miR-325 sponge in the DN. CCNG1 is the direct target of miR-325, which can be positively regulated by lncRNA MSC-AS1 in DN. More importantly, downregulation of miR-325 and upregulation of CCNG1 can attenuate the protective effect of lncRNA MSC-AS1 knockdown on DN V体育ios版. .

Conclusion: lncRNA MSC-AS1 aggravates DN by downregulating miR-325 and upregulating CCNG1. VSports最新版本.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

V体育官网入口 - Figures

Figure 1
Figure 1
LncRNA MSC-AS1 knockdown alleviates HG-induced proliferation, fibrosis, and inflammation of HRMC cells. (a) The expression of MSC-AS1 in serum samples from DN patients and normal subjects (n = 30). (b) The expression of MSC-AS1 in HG- and NG-treated HRMC cells. (c) The expression of MSC-AS1 in HG-treated HRMC cells with its siRNA. (d, e) Cell proliferation and apoptosis were detected in the NG, HG, and HG + si-MSC-AS1 groups. (f) Cell fibrosis was assessed by the levels of FN, Col IV, and Col I in the NG, HG, and HG + si-MSC-AS1 groups. (g) The release of TNF-α, IL-6, and IL-1β was examined in the NG, HG, and HG + si-MSC-AS1 groups. ∗P < 0.05∗∗P < 0.01.
Figure 2
Figure 2
lncRNA MSC-AS1 functions as a miR-325 sponge. (a) The binding sites between MSC-AS1 and miR-325. (b) The relationship between MSC-AS1 and miR-325 was verified by pull-down assay. (c) MiR-325 expression was detected in HG-treated HRMC cells with MSC-AS1 siRNA and vector. (d) MSC-AS1 expression was measured in HG-treated HRMC cells containing miR-325 mimics or inhibitors. (e) MiR-325 expression was detected in DN patients and normal subjects (n = 30). (f) A negative correlation between MSC-AS1 and miR-325 expression was found in DN patients (n = 30). ∗P < 0.05, ∗∗P < 0.01.
Figure 3
Figure 3
CCNG1 is a direct target of miR-325. (a) The binding sites between miR-325 and CCNG1. (b) The relationship between miR-325 and CCNG1 was confirmed by pull-down assay. (c) CCNG1 expression was measured in HG-treated HRMC cells containing miR-325 mimics or inhibitors. (d) CCNG1 expression was detected in DN patients and normal subjects. (e) A negative correlation between CCNG1 and miR-325 expression was identified in DN patients (n = 30). (f) A positive correlation between MSC-AS1 and CCNG1 expression was detected in DN patients (n = 30). (g) CCNG1 expression was assessed in HG-treated HRMC cells with MSC-AS1 siRNA and vector. ∗P < 0.05, ∗∗P < 0.01.
Figure 4
Figure 4
lncRNA MSC-AS1 aggravates DN by downregulating miR-325 and upregulating CCNG1. (a) The expression of MSC-AS1 was detected in HG, HG + si-MSC-AS1, HG + si-MSC-AS1+miR-325 inhibitor, and HG + si-MSC-AS1+CCNG1 vector groups. (b, c) Cell proliferation and apoptosis were detected in HG, HG + si-MSC-AS1, HG + si-MSC-AS1+miR-325 inhibitor, and HG + si-MSC-AS1+CCNG1 vector groups. (d) The levels of FN, Col IV, and Col I were measured in HG, HG + si-MSC-AS1, HG + si-MSC-AS1+miR-325 inhibitor, and HG + si-MSC-AS1+CCNG1 vector groups. (e) TNF-α, IL-6, and IL-1β levels were examined in HG, HG + si-MSC-AS1, HG + si-MSC-AS1+miR-325 inhibitor, and HG + si-MSC-AS1+CCNG1 vector groups. ∗P < 0.05, ∗∗P < 0.01.
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