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Mevastatin Promotes Healing by Targeting Caveolin-1 to Restore EGFR Signaling

ABSTRACT: Mevastatin Promotes Healing by Targeting Caveolin-1 to Restore EGFR Signaling

PROVIDER: PRJNA565444 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10119476.fastq.gz	Fastqsanger.gz
	SRR10119477.fastq.gz	Fastqsanger.gz
	SRR10119478.fastq.gz	Fastqsanger.gz
	SRR10119479.fastq.gz	Fastqsanger.gz
	SRR10119480.fastq.gz	Fastqsanger.gz

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Mevastatin Promotes Healing by Targeting Caveolin-1 to Restore EGFR Signaling

Project description:We performed RNA-seq on primary human keratinocytes treated with mevastatin to identify the molecular mechanisms by which statins promote wound healing. Our results identified a mevastatin gene signature that activated and modulated the EGF signaling to trigger an anti-proliferative and pro-migratory phenotype. In addition, EGFR signaling is downregulated in chronic non-healing wounds and mevastatin was able to restore EGFR signaling by downregulating caveolin proteins, a known inhibitor of EGFR signaling and wound healing. These results demonstrate that statins may have considerable therapeutic potential for patients with chronic wounds that can be rapidly translated to clinical use.

2024-06-30 | GSE137441 | GEO

Mevastatin promotes healing by targeting caveolin-1 to restore EGFR signaling.

Project description:Diabetic foot ulcers (DFUs) are a life-threatening disease that often results in lower limb amputations and a shortened life span. Current treatment options are limited and often not efficacious, raising the need for new therapies. To investigate the therapeutic potential of topical statins to restore healing in patients with DFUs, we performed next-generation sequencing on mevastatin-treated primary human keratinocytes. We found that mevastatin activated and modulated the EGF signaling to trigger an antiproliferative and promigratory phenotype, suggesting that statins may shift DFUs from a hyperproliferative phenotype to a promigratory phenotype in order to stimulate healing. Furthermore, mevastatin induced a migratory phenotype in primary human keratinocytes through EGF-mediated activation of Rac1, resulting in actin cytoskeletal reorganization and lamellipodia formation. Interestingly, the EGF receptor is downregulated in tissue biopsies from patients with DFUs. Mevastatin restored EGF signaling in DFUs through disruption of caveolae to promote keratinocyte migration, which was confirmed by caveolin-1 (Cav1) overexpression studies. We conclude that topical statins may have considerable therapeutic potential as a treatment option for patients with DFUs and offer an effective treatment for chronic wounds that can be rapidly translated to clinical use.

| S-EPMC6962014 | biostudies-literature

SOX2 epidermal overexpression promotes cutaneous wound healing via activation of EGFR/MEK/ERK signaling mediated by EGFR ligands

Project description:We perfomed RNA-seq and wound healing analysis to identify the mechanism how SOX2 promote wound healing. We showed that induction of SOX2 in skin keratinocytes accelerates cutaneous wound healing by promoting keratinocyte migration and proliferation, and enhancement of angiogenesis via the upregulation of EGFR ligands.

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The ambiguous Caveolin-3 G55S sequence variant: Muscle biopsy findings and cell biological analysis

Project description:Caveolins are structural and functional proteins in plasma membrane invaginations called caveolae. Mutations in Caveolin-3 cause myopathies of variable severity. The pathogenicity of the Caveolin-3 variant G55S is still unclear. Here, we report on three patients suffering from mild to moderate myopathy. In all three patients, but also in two seemingly unaffected family members of patient one the G55S variant was found. Histology revealed moderate chronic myopathic changes and reduced sarcolemmal Caveolin-3 immunoreactivity in all three cases. Immunoblots for Caveolin-3 were abnormal in all cases. By electron microscopy, enlarged caveolae were detected in case one and three and vacuolar myopathy in case two. EM studies of RCMH myoblasts transfected with G55S Caveolin-3 revealed autophagic vacuoles. The alterations in Golgi morphology were in line with pathological Caveolin-3 deposits in this organelle detected by immunofluorescence and indicative for activation of autophagy. Phospho-blotting demonstrated that G55S affects EGFR signaling. Proteomic profiling of transfected RCMH myoblasts demonstrated alterations in levels of physiologically relevant proteins which are indicative for antagonization of G55S Caveolin-3 expression. Some proteomic alterations were enhanced by osmotic/mechanical stress. In conclusion, our results suggest that the G55S Caveolin-3 sequence variant can be compensated by cellular defense mechanisms and that additional stress may lead to vulnerability of G55S Caveolin-3 expressing muscle cells.

2018-07-05 | PXD003719 | Pride

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Caveolin-3 Knockout Hearts

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SOX2 epidermal overexpression promotes cutaneous wound healing via activation of EGFR/MEK/ERK signaling mediated by EGFR ligands

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