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Adiponectin receptor agonist AdipoRon blocks skin inflamm-ageing by regulating mitochondrial dynamics
Jiachen Sun1, Xinzhu Liu1, Chuan'an Shen1
1Department of Burns and Plastic Surgery, The Fourth Medical Center of Chinese PLA General Hospital, Beijing, China.
Introduction:
Skin is susceptible to senescence-associated secretory phenotype (SASP) and inflamm-ageing partly owing to the degeneration of mitochondria. AdipoRon (AR) has protective effects on mitochondria in metabolic diseases such as diabetes. We explored the role of AR on mitochondria damage induced by skin inflamm-ageing and its underlying mechanism.
Methods:
Western blot, immunofluorescence and TUNEL staining were used to detect inflammatory factors and apoptosis during skin ageing. Transmission electron microscopy, ATP determination kit, CellLight Mitochondria GFP (Mito-GFP), mitochondrial stress test, MitoSOX and JC-1 staining were used to detect mitochondrial changes. Western blot was applied to explore the underlying mechanism. Flow cytometry, scratch test, Sulforhodamine B assay and wound healing test were used to detect the effects of AR on cell apoptosis, migration and proliferation.
Results:
AR attenuated inflammatory factors and apoptosis that increased in aged skin, and improved mitochondrial morphology and function. This process at least partly depended on the suppression of dynamin-related protein 1 (Drp1)-mediated excessive mitochondrial division. More specifically, AR up-regulated the phosphorylation of Drp1 at Serine 637 by activating AMP-activated protein kinase (AMPK), thereby inhibiting the mitochondrial translocation of Drp1. Moreover, AR reduced mitochondrial fragmentation and the production of superoxide, preserved the membrane potential and permeability of mitochondria and accelerated wound healing in aged skin.
Conclusion:
AR rescues the mitochondria in aged skin by suppressing its excessive division mediated by Drp1.
Insights
AdipoRon (AR) protects aged skin mitochondria by inhibiting excessive division, a key factor in inflamm-ageing. This improves mitochondrial function and accelerates skin repair.
Area of Science:
- Dermatology
- Cell Biology
- Mitochondrial Biology
Background:
- Skin ageing involves senescence-associated secretory phenotype (SASP) and inflamm-ageing, driven by mitochondrial damage.
- AdipoRon (AR) demonstrates protective effects on mitochondria in metabolic diseases like diabetes.
Purpose of the Study:
- To investigate the role of AdipoRon (AR) in mitigating mitochondria damage associated with skin inflamm-ageing.
- To elucidate the underlying molecular mechanisms of AR's protective effects on skin mitochondria.
Main Methods:
- Assessed inflammatory factors and apoptosis using Western blot, immunofluorescence, and TUNEL staining.
- Evaluated mitochondrial morphology and function via transmission electron microscopy, ATP assays, Mito-GFP, stress tests, MitoSOX, and JC-1 staining.
- Determined AR's impact on cell apoptosis, migration, and proliferation using flow cytometry, scratch, and wound healing assays.
Main Results:
- AR reduced elevated inflammatory factors and apoptosis in aged skin, enhancing mitochondrial morphology and function.
- AR suppressed excessive mitochondrial division mediated by dynamin-related protein 1 (Drp1).
- AR activated AMP-activated protein kinase (AMPK), increasing Drp1 phosphorylation and inhibiting its mitochondrial translocation, thereby reducing fragmentation and superoxide production.
Conclusions:
- AdipoRon (AR) effectively rescues mitochondria in aged skin.
- AR's protective mechanism involves suppressing Drp1-mediated excessive mitochondrial division.
- AR treatment preserves mitochondrial function and promotes wound healing in aged skin.
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