2. Academic Validation
  3. Accelerating Wound Closure with Metrnl in Normal and Diabetic Mouse Skin

Accelerating Wound Closure with Metrnl in Normal and Diabetic Mouse Skin

  • Diabetes. 2023 Sep 8;db230173. doi: 10.2337/db23-0173.
Lingyu Song 1 2,  Xuebing Chang 1,  Laying Hu 1,  Lu Liu 1,  Guifang Wang 1,  Yali Huang 1,  Lifen Xu 3,  Bangming Jin 4 5,  Jianying Song 6,  Lixin Hu 6,  Tian Zhang 1,  Yuanyuan Wang 1,  Ying Xiao 1,  Fan Zhang 1,  Mingjun Shi 1,  Lingling Liu 1,  Qi Chen 7,  Bing Guo 1 4 5,  Yuxia Zhou 1 4 5
Affiliations

Affiliations

  • 1 Department of Pathophysiology, Guizhou Medical University, Guiyang, 550025, Guizhou, China.
  • 2 Department of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
  • 3 Department of Pathology, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou, China.
  • 4 Guizhou Province Talent Base of Research on the Pathogenesis and Drug Prevention and Treatment for Common Major Diseases, Guizhou Medical University, Guiyang, 550025, Guizhou, China.
  • 5 Guizhou Provincial Key Laboratory of Pathogenesis and Drug Research on Common Chronic Diseases, Guizhou Medical University, Guiyang, 550025, Guizhou, China.
  • 6 School of Nursing, Southwest Medical University, Luzhou, 646000, Sichuan, China.
  • 7 Department of Endocrinology and Metabolism, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, Sichuan, China.
PMID: 37683051 DOI: 10.2337/db23-0173
Abstract

Impaired wound healing and ulcer complications are major causes of morbidity in patients with diabetes. Impaired wound healing is associated with increased inflammation and poor angiogenesis in diabetes patients. Here, we demonstrate that topical administration of a secreted recombinant protein (Meteorin-like, Metrnl) accelerates wound epithelialization and angiogenesis in mice. We observed a significant increase in Metrnl expression during physiological wound healing; however, its expression remained low during diabetic wound healing. Functionally, the recombinant protein Metrnl significantly accelerated wound closure in normal and diabetic mice models including db/db, high-fat diet/streptozotocin (HFD/STZ), and STZ mice. Mechanistically, keratinocytes secrete quantities of Metrnl to promote angiogenesis, increase endothelial cell proliferation, migration and tube formation, and enhance macrophage polarization to the M2 type. Meanwhile, M2 macrophages secrete Metrnl to further stimulate angiogenesis. Moreover, the keratinocyte- and macrophage-produced cytokine Metrnl drives post-injury angiogenesis and re-epithelialization through activation of Akt phosphorylation (S473) in a KIT receptor tyrosine kinase (c-Kit)-dependent manner. In conclusion, our study suggests that Metrnl has a biological activity in accelerating wound closure through c-Kit-dependent angiogenesis and epithelialization.

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