MicroRNA-99 family targets AKT/mTOR signaling pathway in dermal wound healing.
MicroRNA-99 family targets AKT/mTOR signaling pathway in dermal wound healing.
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DOI：
10.1371/journal.pone.0064434
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Zhou X
中科院分区：
文献类型：
--
作者：
Jin Y;Tymen SD;Chen D;Fang ZJ;Zhao Y;Dragas D;Dai Y;Marucha PT;Zhou X
Recent studies suggest that microRNAs play important roles in dermal wound healing and microRNA deregulation has been linked with impaired wound repair. Here, using a mouse experimental wound healing model, we identified a panel of 63 differentially expressed microRNAs during dermal wound healing, including members of miR-99 family (miR-99a, miR-99b, miR-100). We further demonstrated that miR-99 family members regulate cell proliferation, cell migration, and AKT/mTOR signaling. Combined experimental and bioinformatics analyses revealed that miR-99 family members regulate AKT/mTOR signaling by targeting multiple genes, including known target genes (e.g., IGF1R, mTOR) and a new target (AKT1). The effects of miR-99 family members on the expression of IGF1R, mTOR and AKT1 were validated at both the mRNA and protein levels. Two adjacent miR-99 family targeting sites were identified in the 3′-UTR of the AKT1 mRNA. The direct interaction of miR-100 with these targeting sites was confirmed using luciferase reporter assays. The microRNA-100-directed recruitment of AKT1 mRNA to the RNAi-induced silencing complex (RISC) was confirmed by a ribonucleoprotein-IP assay. In summary, we identified a panel of differentially expressed microRNAs which may play important roles in wound healing. We provide evidence that miR-99 family members contribute to wound healing by regulating the AKT/mTOR signaling.
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影响因子：
4.1
作者：
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通讯作者：
Stadler PF
影响因子：
2.6
作者：
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DOI：
10.1161/atvbaha.112.248583
发表时间：
2012-06
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Chan YC;Roy S;Khanna S;Sen CK
通讯作者：
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影响因子：
11.2
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Doghman M;El Wakil A;Cardinaud B;Thomas E;Wang J;Zhao W;Peralta-Del Valle MH;Figueiredo BC;Zambetti GP;Lalli E
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3.7
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Lerman G;Avivi C;Mardoukh C;Barzilai A;Tessone A;Gradus B;Pavlotsky F;Barshack I;Polak-Charcon S;Orenstein A;Hornstein E;Sidi Y;Avni D
通讯作者：
Avni D