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  3. The stress-responsive gene ATF3 drives fibroblast activation and collagen production through transcriptionally activating TGF-β receptor Ⅱ in skin wound healing

The stress-responsive gene ATF3 drives fibroblast activation and collagen production through transcriptionally activating TGF-β receptor Ⅱ in skin wound healing

  • Arch Biochem Biophys. 2024 Oct:760:110134. doi: 10.1016/j.abb.2024.110134.
Peng Luo 1,  Fulong Wang 1,  Jialun Li 1,  Gaoyu Liu 1,  Qin Xiong 1,  Benhuang Yan 1,  Xiaohui Cao 1,  Bao Liu 2,  Yang Wang 1,  Gang Wu 3,  Chunmeng Shi 4
Affiliations

Affiliations

  • 1 Institute of Rocket Force Medicine, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing, 400038, China.
  • 2 Institute of Medicine and Equipment for High Altitude Region, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Army Medical University, Chongqing, 400038, China.
  • 3 Institute of Rocket Force Medicine, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing, 400038, China; Institute of Medicine and Equipment for High Altitude Region, Key Laboratory of Extreme Environmental Medicine of Ministry of Education, Army Medical University, Chongqing, 400038, China. Electronic address: wugang1990@tmmu.edu.cn.
  • 4 Institute of Rocket Force Medicine, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing, 400038, China. Electronic address: shicm@tmmu.edu.cn.
PMID: 39181381 DOI: 10.1016/j.abb.2024.110134
Abstract

Skin wound is an emerging health challenge on account of the high-frequency trauma, surgery and chronic refractory ulcer. Further study on the disease biology will help to develop new effective approaches for wound healing. Here, we identified a wound-stress responsive gene, activating transcription factor 3 (ATF3), and then investigated its biological action and mechanism in wound healing. In the full-thickness skin wound model, ATF3 was found to promote fibroblast activation and collagen production, resulted in accelerated wound healing. Mechanically, ATF3 transcriptionally activated TGF-β Receptor Ⅱ via directly binding to its specific promoter motif, followed by the enhanced TGF-β/Smad pathway in fibroblasts. Moreover, the increased ATF3 upon skin injury was partly resulted from hypoxia stimulation with HIF-1α dependent manner. Altogether, this work gives novel insights into the biology and mechanism of stress-responsive gene ATF3 in wound healing, and provides a potential therapeutic target for treatment.

Keywords

Activating transcription factor 3; Collagen; Fibroblast; Skin wound healing; TGF-β receptor Ⅱ.

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