例如:"lncRNA", "apoptosis", "WRKY"

Pannexin-3 Deficiency Delays Skin Wound Healing in Mice due to Defects in Channel Functionality.

J. Invest. Dermatol.2019 Apr;139(4):909-918. Epub 2018 Oct 30
Peipei Zhang 1 , Masaki Ishikawa 2 , Craig Rhodes 1 , Andrew Doyle 3 , Tomoko Ikeuchi 1 , Kuniyuki Nakamura 1 , Yuta Chiba 1 , Bing He 4 , Yoshihiko Yamada 5
Peipei Zhang 1 , Masaki Ishikawa 2 , Craig Rhodes 1 , Andrew Doyle 3 , Tomoko Ikeuchi 1 , Kuniyuki Nakamura 1 , Yuta Chiba 1 , Bing He 4 , Yoshihiko Yamada 5
+ et al

[No authors listed]

Author information
  • 1 Molecular Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA.
  • 2 Molecular Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA; Division of Operative Dentistry, Tohoku University Graduate School of Dentistry, Sendai, Japan.
  • 3 Cell Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA.
  • 4 Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
  • 5 Molecular Biology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: yyamada@dir.nidcr.nih.gov.

摘要


Pannexin-3 (Panx3) is a gap junction protein that is required for regulating cell cycle exit and the differentiation of osteoblasts and chondrocytes during skeletal development. However, the role of Panx3 in skin tissue regeneration remains unclear. After dorsal skin punch biopsies, Panx3-knockout mice exhibited a significant delay in wound healing with insufficient re-epithelialization, decreased inflammatory reaction, and reduced collagen remodeling. Panx3 expression coincided with inflammatory reactions both in vivo and in vitro. By applying exogenous tumor necrosis factor-α to mimic inflammation in vitro, Panx3 expression was induced in HaCaT cells. In addition, Panx3 depletion reduced epithelial-mesenchymal transition during skin wound healing. A protein essential for signaling in epithelial-mesenchymal transition, transforming growth factor-β interacted with Panx3 by modulating intracellular adenosine triphosphate levels and thereby enhanced HaCaT cell migration ability with Panx3 overexpression. In conclusion, Panx3 plays a key role in the skin wound healing process by controlling keratinocytes and keratinocyte-mesenchyme cross-talk via hemichannel and endoplasmic reticulum Ca2+ channel functions, which differs from another gap junction, connexin 43 (Cx43), during skin wound healing.