The lncRNA SNHG26 drives the inflammatory-to-proliferative state transition of keratinocyte progenitor cells during wound healing

Dongqing Li (), Zhuang Liu, Letian Zhang, Xiaowei Bian, Jianmin Wu, Li Li, Yongjian Chen, Lihua Luo, Ling Pan, Lingzhuo Kong, Yunting Xiao, Jiating Wang, Xiya Zhang, Wang Wang, Maria Toma, Minna Piipponen, Pehr Sommar and Ning Xu Landén ()
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Dongqing Li: Chinese Academy of Medical Sciences and Peking Union Medical College
Zhuang Liu: Karolinska Institutet
Letian Zhang: Karolinska Institutet
Xiaowei Bian: Karolinska Institutet
Jianmin Wu: Wenzhou Medical University
Li Li: Chinese Academy of Medical Sciences and Peking Union Medical College
Yongjian Chen: Karolinska Institutet
Lihua Luo: Karolinska Institutet
Ling Pan: Chinese Academy of Medical Sciences and Peking Union Medical College
Lingzhuo Kong: Chinese Academy of Medical Sciences and Peking Union Medical College
Yunting Xiao: Chinese Academy of Medical Sciences and Peking Union Medical College
Jiating Wang: Chinese Academy of Medical Sciences and Peking Union Medical College
Xiya Zhang: Chinese Academy of Medical Sciences and Peking Union Medical College
Wang Wang: East China Normal University
Maria Toma: Karolinska Institutet
Minna Piipponen: Karolinska Institutet
Pehr Sommar: Karolinska University Hospital
Ning Xu Landén: Karolinska Institutet

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract The cell transition from an inflammatory phase to a subsequent proliferative phase is crucial for wound healing, yet the driving mechanism remains unclear. By profiling lncRNA expression changes during human skin wound healing and screening lncRNA functions, we identify SNHG26 as a pivotal regulator in keratinocyte progenitors underpinning this phase transition. Snhg26-deficient mice exhibit impaired wound repair characterized by delayed re-epithelization accompanied by exacerbated inflammation. Single-cell transcriptome analysis combined with gain-of-function and loss-of-function of SNHG26 in vitro and ex vivo reveals its specific role in facilitating inflammatory-to-proliferative state transition of keratinocyte progenitors. A mechanistic study unravels that SNHG26 interacts with and relocates the transcription factor ILF2 from inflammatory genomic loci, such as JUN, IL6, IL8, and CCL20, to the genomic locus of LAMB3. Collectively, our findings suggest that lncRNAs play cardinal roles in expediting tissue repair and regeneration and may constitute an invaluable reservoir of therapeutic targets in reparative medicine.

Date: 2024
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DOI: 10.1038/s41467-024-52783-8

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