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Silencing of METTL3 prevents the proliferation, migration, epithelial-mesenchymal transition, and renal fibrosis of high glucose-induced HK2 cells by mediating WISP1 in m6A-dependent manner.
Chen, Yuanzhen; Li, Ping; Lin, Mei; Jiang, Ying; Tan, Guiping; Huang, Lianfang; Song, Dan.
Afiliación
  • Chen Y; Department of Nephrology, Shenzhen Guangming District People’s Hospital, Guangming, Shenzhen 518000, China.
  • Li P; Department of Nephrology, Shenzhen Guangming District People’s Hospital, Guangming, Shenzhen 518000, China.
  • Lin M; Department of Nephrology, Shenzhen Guangming District People’s Hospital, Guangming, Shenzhen 518000, China.
  • Jiang Y; Department of Nephrology, Shenzhen Guangming District People’s Hospital, Guangming, Shenzhen 518000, China.
  • Tan G; Department of Nephrology, Shenzhen Guangming District People’s Hospital, Guangming, Shenzhen 518000, China.
  • Huang L; Department of Nephrology, Shenzhen Guangming District People’s Hospital, Guangming, Shenzhen 518000, China.
  • Song D; Department of Nephrology, Shenzhen Guangming District People’s Hospital, Guangming, Shenzhen 518000, China.
Aging (Albany NY) ; 16(2): 1237-1248, 2024 01 29.
Article en En | MEDLINE | ID: mdl-38289593
ABSTRACT
Diabetic nephropathy (DN) is one of the most serious complications in diabetic patients. And m6A modifications mediated by METTL3 are involved multiple biological processes. However, the specific function and mechanism of METTL3 in DN remains unclear. DN model mice were first established with streptozotocin, and WISP1 expression was confirmed by qRT-PCR. Then the influences of WISP1 or/and METTL3 on the proliferation, migration, and epithelial-mesenchymal transition (EMT) and fibrosis-related proteins of high glucose (HG)-induced HK2 cells or HK2 cells were tested through CCK-8, wound healing, and western blot. We first revealed that WISP1 was highly expressed in renal tissues of DN model mice and HG-induced HK2 cells. Functionally, WISP1 or METTL3 silencing could weaken the proliferation, migration, EMT, and fibrosis of HG-treated HK2 cells, and WISP1 or METTL3 overexpression could induce the proliferation, migration, EMT, and fibrosis of HK2 cells. Additionally, METTL3 silencing could decrease WISP1 m6A modification, and silencing of METTL3 also could notably suppress the biological functions of HG-induced HK2 cells by downregulating WISP1. Silencing of METTL3 prevents DN development process by decreasing WISP1 with m6A modification pattern. Therefore, we suggest that METTL3/WISP1 axis might be a novel therapeutic target for DN.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nefropatías Diabéticas / Proteínas CCN de Señalización Intercelular / Transición Epitelial-Mesenquimal / Metiltransferasas Límite: Animals / Humans Idioma: En Revista: Aging (Albany NY) Asunto de la revista: GERIATRIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nefropatías Diabéticas / Proteínas CCN de Señalización Intercelular / Transición Epitelial-Mesenquimal / Metiltransferasas Límite: Animals / Humans Idioma: En Revista: Aging (Albany NY) Asunto de la revista: GERIATRIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos