Mechanism of long non-coding RNA uc.412 in mediating the autophagy of mesangial cells induced by transforming growth factor-β1

HUANG Chan; WANG Jin; AN Mengru; ZHAO Tangming; ZHANG Aiqing; GAN Weihua

doi:10.3969/j.issn.2096-3882.2021.06.007

Journal of Xuzhou Medical University > 2021 > 41(6): 424-429. > DOI: 10.3969/j.issn.2096-3882.2021.06.007

HUANG Chan, WANG Jin, AN Mengru, ZHAO Tangming, ZHANG Aiqing, GAN Weihua. Mechanism of long non-coding RNA uc.412 in mediating the autophagy of mesangial cells induced by transforming growth factor-β1[J]. Journal of Xuzhou Medical University, 2021, 41(6): 424-429. DOI: 10.3969/j.issn.2096-3882.2021.06.007

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Mechanism of long non-coding RNA uc.412 in mediating the autophagy of mesangial cells induced by transforming growth factor-β1

Department of Pediatric Nephrology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210003, China

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Received Date: April 05, 2021
Revised Date: June 14, 2021

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Abstract

Objective To explore the mechanism of long non-coding RNA uc.412 (LncRNA uc.412) in mediating the autophagy of mesangial cells induced by transforming growth factor-β1 (TGF-β1). Methods Rat mesangial cells were treated with TGF-β1 (10 μg/L). The expression of autophagy markers LC3 and p62 were detected by Western blot. The expression of Lnc RNA uc.412 was detected by Real-time PCR. The mesangial cells infected with over-expressed LncRNA uc.412 lentivirus were used, and the infection efficiency was detected by Real-time PCR. Then, Western blot and Real-time PCR were used to detect the expression of LC3 and p62 at protein and mRNA levels. The mesangial cells were treated with TGF-β1 (10 μg/L) and SIS3, a specific phosphorylation inhibitor of Smad3 (1 μmol). Western blot was used to detect the expression of pSmad3 protein, while Real-time PCR to detect the expression of LncRNA uc.412. Results Compared with the control group, the TGF-β1 group showed an up-regulated ratio of LC3 Ⅱ to LC3Ⅰand increased expression of p62 and LncRNA uc.412 (P<0.05). The levels of LC3 and p62 at protein and mRNA levels were higher in the LncRNA uc.412 over-expression group than those in the control and vector groups (P<0.05). Compared with the control group, the amounts of pSmad3 and LncRNA uc.412 was up-regulated in the TGF-β1 group (P<0.05). Compared with the TGF-β1 group, the amounts of pSmad3 and LncRNA uc.412 was down-regulated in the TGF-β1+SIS3 group (P<0.05). Conclusions LncRNA uc.412 can act as a downstream effector molecule of the TGF/Smad3 pathway to promote mesangial cell autophagy, which provides new thought for the prevention and treatment of chronic kidney disease.
- LncRNA uc.412,
- transforming growth factor-β1,
- mesangial cell,
- autophagy

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Mechanism of long non-coding RNA uc.412 in mediating the autophagy of mesangial cells induced by transforming growth factor-β1

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