KIND1 Loss Sensitizes Keratinocytes to UV-Induced Inflammatory Response and DNA Damage
作者: Xiaoling ZhangSuju LuoJoseph WuLong ZhangWen-hui WangSimone DeganDetlev ErdmannRussell HallJennifer Y. Zhang
作者单位: 1Department of Dermatology, Duke University Medical Center, Durham, North Carolina, USA
2Department of Dermatology, Tianjin Medical University General Hospital, Tianjin, PR China
3Department of Dermatology, Peking University Third Hospital, Beijing, PR China
4Department of Interventional Radiology and Vascular Surgery, Peking University Third Hospital, Beijing, PR China
5Center of Molecular and Biomolecular Imaging, Duke University, Durham, North Carolina, USA
6Department of Surgery, Division of Plastic, Reconstructive, Maxillofacial and Oral Surgery, Duke University Medical Center, Durham, North Carolina, USA
刊名: Journal of Investigative Dermatology, 2017, Vol.137 (2), pp.475-483
来源数据库: Elsevier Journal
DOI: 10.1016/j.jid.2016.09.023
英文摘要: Loss of function of KIND1, a cytoskeletal protein involved in β1-integrin function, causes Kindler syndrome, a genetic disease characterized by skin fragility, photosensitivity, and increased risk of squamous cell carcinoma. Dysregulation of β1-integrin underlies Kindler syndrome skin fragility. However, the mechanisms underlying squamous cell carcinoma susceptibility are unclear. Here, we demonstrate that gene silencing of KIND1 decreased keratinocyte proliferation and increased apoptosis in vitro and in skin grafts regenerated on mice, which was correlated with reduced cyclinB1. In addition, KIND1 loss sensitized keratinocytes to cytokine and UV-induced NF-κB and c-Jun N-terminal kinase activation and upregulation of CXCL10 and tumor necrosis factor-α. Moreover, KIND1 loss impaired DNA...
全文获取路径: Elsevier  (合作)
影响因子:6.193 (2012)

  • DNA Deoxyribonucleic Acid