Protective role of microRNA-29a in denatured dermis and skin fibroblast cells after thermal injury

• Main Authors: Jie Zhou, Xipeng Zhang, Pengfei Liang, Licheng Ren, Jizhang Zeng, Minghua Zhang, Pihong Zhang, Xiaoyuan Huang
• Format: Article
• Language: English
• Published: The Company of Biologists 2016-03-01
• Series: Biology Open
• Subjects: Denatured dermis; Fibroblast cells; MicroRNA-29a; Thermal injury; Wound healing
• Online Access: http://bio.biologists.org/content/5/3/211

Our previous study has suggested that downregulated microRNA (miR)-29a in denatured dermis might be involved in burn wound healing. However, the exact role of miR-29a in healing of burn injury still remains unclear. Here, we found that expression of miR-29a was notably upregulated in denatured dermis tissues and skin fibroblast cells after thermal injury, and thereafter gradually downregulated compared with control group. By contrast, the expression of collagen, type I, alpha 2 (COL1A2) and vascular endothelial growth factor (VEGF-A) were first reduced and subsequently upregulated in denatured dermis tissues and skin fibroblast cells after thermal injury. We further identified COL1A2 as a novel target of miR-29a, which is involved in type I collagen synthesis, and showed that miR-29a negatively regulated the expression level of COL1A2 in skin fibroblast cells. In addition, VEGF-A, another target gene of miR-29a, was also negatively mediated by miR-29a in skin fibroblast cells. Inhibition of miR-29a expression significantly promoted the proliferation and migration of skin fibroblast cells after thermal injury, and knockdown of COL1A2 and VEGF-A reversed the effects of miR-29a on the proliferation and migration of skin fibroblast cells. Furthermore, we found that Notch2/Jagged2 signaling was involved in miR-29a response to burn wound healing. Our findings suggest that downregulated miR-29a in denatured dermis may help burn wound healing in the later phase, probably via upregulation of COL1A2 and VEGF-A expression, which can further enhance type I collagen synthesis and angiogenesis.