Tissue & cell · 2025
Role of lncRNA H19 modification (m6A methylation) and YTHDC1 in high glucose induced human microvascular endothelial cell biological behaviors.
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Sun Jingcun, Zhang Zhongyong, Li Huajun, Chi Yuqian, Yang Shuo, Zhang Guiye, Li Zhaozhen, Zhang Hongliang
Аннотация
BACKGROUND: Diabetes could lead to microangiopathy. This study attempts to explore the role of N6-methyladenosine (m6A) of lncRNA H19 in high glucose (HG)-induced changes of dermal microvascular endothelial cell (DMEC) biological behaviors, thereby finding a theoretical basis to reduce cell damage.
METHODS: DMECs were cultured and treated by HG, and then functional assays were conducted to detect cell viability, proliferation, migration and angiogenesis. On the other hand, expression of H19 and YTHDC1 was assessed by RT-qPCR and western blot analysis. H19 was overexpressed in HG-treated DMECs to explore the specific role of H19 in DMEC biological behaviors. Afterwards, total m6A level was analyzed, the enrichment of m6A modification and YTHDC1 on H19 was verified by MeRIP-qPCR, and H19 stability was determined upon actinomycin D treatment. Additionally, rescue experiment was performed to validate the mechanism of YTHDC1 binding to m6A modification of H19 to stabilize H19 expression, so as to modulate human DMEC damage.
RESULTS: HG treatment inhibited DMEC viability, proliferation, migration and angiogenesis, downregulated H19 expression and reduced total m6A content and m6A modification level of H19, while overexpressed H19 promoted cell biological behaviors. YTHDC1 overexpression bound to m6A modification of H19 to stabilize H19 expression, thereby restricting HG-induced DMEC damage, and silencing of H19 counteracted the protective role of YTHDC1 on cell damage.
CONCLUSION: H19 expression was downregulated in HG-induced human DMECs, and YTHDC1 bound to m6A modification on H19 to stabilize H19 expression, thereby reducing DMEC damage.
METHODS: DMECs were cultured and treated by HG, and then functional assays were conducted to detect cell viability, proliferation, migration and angiogenesis. On the other hand, expression of H19 and YTHDC1 was assessed by RT-qPCR and western blot analysis. H19 was overexpressed in HG-treated DMECs to explore the specific role of H19 in DMEC biological behaviors. Afterwards, total m6A level was analyzed, the enrichment of m6A modification and YTHDC1 on H19 was verified by MeRIP-qPCR, and H19 stability was determined upon actinomycin D treatment. Additionally, rescue experiment was performed to validate the mechanism of YTHDC1 binding to m6A modification of H19 to stabilize H19 expression, so as to modulate human DMEC damage.
RESULTS: HG treatment inhibited DMEC viability, proliferation, migration and angiogenesis, downregulated H19 expression and reduced total m6A content and m6A modification level of H19, while overexpressed H19 promoted cell biological behaviors. YTHDC1 overexpression bound to m6A modification of H19 to stabilize H19 expression, thereby restricting HG-induced DMEC damage, and silencing of H19 counteracted the protective role of YTHDC1 on cell damage.
CONCLUSION: H19 expression was downregulated in HG-induced human DMECs, and YTHDC1 bound to m6A modification on H19 to stabilize H19 expression, thereby reducing DMEC damage.