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Murine Excisional Wound Healing Model and Histological Morphometric Wound Analysis
Published on: August 21, 2020
Microplastics impair wound healing via NAT10-mediated epigenetic dysregulation of FASN-PI3K/AKT signaling
Feng-Jie Shen1, Wei-Nan Cao2, Xue-Chun Han1
1Beijing Key Laboratory of Diabetes Research and Care, Department of Endocrinology, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Abstract:
Microplastics (MPs) are environmental pollutants with potential health risks. This study examined the effect of MPs on wound healing in both diabetic and non-diabetic mice. MPs exposure significantly delayed wound healing, particularly in diabetic mice, with reduced epidermal thickness and impaired collagen deposition. Mechanistically, MPs suppressed cell proliferation, angiogenesis, and increased apoptosis. Transcriptomic analysis identified dysregulation of critical wound healing pathways, especially those involved in inflammation, extracellular matrix remodeling, and lipid metabolism. Notably, the PI3K/AKT signaling pathway was inhibited. In vitro experiments using human dermal fibroblasts confirmed that MPs disrupted the PI3K/AKT pathway, reducing cell proliferation and migration. Further investigation revealed that MPs suppressed N-acetyltransferase 10 (NAT10) expression, leading to reduced ac4C-dependent stabilization of Fasn mRNA, which in turn diminished lipid synthesis and further inhibited the PI3K/AKT pathway. Our findings reveal a novel interaction between MPs and diabetes in impairing wound healing and suggest the NAT10-FASN-PI3K/AKT axis as a potential therapeutic target.
Insights
Microplastics (MPs) significantly delay wound healing, especially in diabetic individuals. MPs disrupt cellular processes and the PI3K/AKT pathway, revealing a new link between plastic pollution and impaired healing.
Area of Science:
- Environmental Science
- Toxicology
- Cell Biology
Background:
- Microplastics (MPs) are pervasive environmental pollutants.
- MPs pose potential risks to human health.
- Impaired wound healing is a significant clinical challenge, particularly in diabetic patients.
Purpose of the Study:
- To investigate the impact of microplastic exposure on wound healing in diabetic and non-diabetic mice.
- To elucidate the molecular mechanisms underlying MP-induced impairment of wound healing.
- To identify potential therapeutic targets for mitigating these effects.
Main Methods:
- In vivo studies using diabetic and non-diabetic mouse models with controlled MP exposure.
- Histological analysis of wound tissue, including epidermal thickness and collagen deposition.
- In vitro experiments using human dermal fibroblasts.
- Transcriptomic analysis to identify dysregulated pathways.
- Molecular assays to investigate signaling pathways and gene expression.
Main Results:
- MP exposure significantly delayed wound healing in both groups, with a more pronounced effect in diabetic mice.
- MPs reduced epidermal thickness, impaired collagen deposition, suppressed cell proliferation and angiogenesis, and increased apoptosis.
- Transcriptomic analysis revealed dysregulation of inflammation, ECM remodeling, and lipid metabolism pathways, with notable inhibition of the PI3K/AKT pathway.
- MPs were found to suppress N-acetyltransferase 10 (NAT10) expression, leading to reduced Fasn mRNA stabilization, diminished lipid synthesis, and further inhibition of the PI3K/AKT pathway.
Conclusions:
- Microplastics exacerbate impaired wound healing, particularly in the context of diabetes.
- The NAT10-FASN-PI3K/AKT signaling axis is a critical mediator of MP-induced wound healing defects.
- Targeting the NAT10-FASN-PI3K/AKT pathway may offer a novel therapeutic strategy for managing impaired wound healing associated with microplastic exposure and diabetes.
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