Wnt7a regulates high autophagic and inflammatory response of epidermis in high-glucose environment.
Type 2 diabetes mellitus (T2DM) is an important reason to cause chronic wound healing or even amputation to patients. A common characteristic of T2DM is the presence of hyperglycemia. Autophagy, a cellular pathway which related to protein and organelle degradation, is relevant to many types of cellular homeostasis change and human diseases including diabetes. However, the relationship between high glucose and autophagy in keratinocytes remains unclear. Previously in our research, wnt7a was proved to accelerate healing process by promoting angiogenesis and ameliorating local inflammation, while little is known about its role in epithelial cells, namely keratinocytes. We hypothesized that reduced expression of wnt7a may contribute to the increment of autophagy. We then compared the expression of autophagic markers such as nlrp3, LC3A/B and bip by high glucose-cultured HaCaT cells, with or without wnt7a treatment. Then we examined the expression levels of TNF-α, TLR-4 and p62 to assess inflammatory statement. High glucose induced a significant increasement in the expression of both autophagic markers and inflammatory markers and these elevated protein levels were reversed after the use of wnt7a. Therefore, these results showed that wnt7a regulates overwhelmed autophagy and inflammation promoted under high glucose condition.
['Wang|Wei|W|', 'Zhang|Fang|F|', 'Yan|Xin|X|', 'Tan|Qian|Q|']
D000818:Animals D001343:Autophagy D002460:Cell Line D003921:Diabetes Mellitus, Experimental D003924:Diabetes Mellitus, Type 2 D004817:Epidermis D005947:Glucose D006801:Humans D006943:Hyperglycemia D007249:Inflammation D015603:Keratinocytes D008869:Microtubule-Associated Proteins D000071199:NLR Family, Pyrin Domain-Containing 3 Protein D011518:Proto-Oncogene Proteins D051381:Rats D017207:Rats, Sprague-Dawley D051197:Toll-Like Receptor 4 D014409:Tumor Necrosis Factor-alpha D051153:Wnt Proteins
Wnt7a Autophagy Keratinocytes Inflammation