Impact of Mitochondrial Oxidative Phosphorylation Dysfunction in the Patient with Endometriosis

Roya Rozati, Aleem Ahmed Khan, Wajeeda Tabasum, Salwa Sahar Azimi, Vikram Aiman Ayapati, Ayapati Gautam Mehdi, Nasaruddin Khaja, Krishnan Sivaraman, Sripriya Vennamaneni
2024 · doi:10.5281/zenodo.14292090 · W6893205049
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This study found that severe endometriosis is characterized by mitochondrial oxidative phosphorylation dysfunction and epithelial-mesenchymal transition, evidenced by decreased OXPHOS gene expression and increased mesenchymal markers in patient biopsies.

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This study investigates the link between mitochondrial oxidative phosphorylation dysfunction and epithelial-mesenchymal transition in women with severe endometriosis. Researchers analyzed endometrial biopsies using flow cytometry and real-time quantitative PCR to compare gene expression levels among healthy controls, mild cases, and severe disease states. The results demonstrated significantly decreased expression of OXPHOS genes and E-cadherin alongside enhanced markers for mesenchymal stem cells and EMT transcription factors in severe endometriosis samples. These findings indicate that mitochondrial impairment accompanies the cellular shift toward a mesenchymal phenotype, suggesting EMT plays a critical role in the pathogenesis of advanced endometriosis. This paper is centrally about endometriosis — specifically examining mitochondrial dysfunction and its association with epithelial-mesenchymal transition in severe lesions.

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Abstract

Background: Endometriosis is a chronic inflammatory condition where the precise cause of endometriosis is still not unclear. Mitochondrial dysfunction has been reported in severe forms of endometriosis. However, the role of mitochondrial dynamics, mitophagy, and mitochondrial-related complexes in endometriosis and its relation with Epithelial-Mesenchymal Transition (EMT) is not clear.Objective: Therefore, this study aims to elucidate the role of mitochondrial dysfunction and its relation with EMT in the pathogenesis of endometriosis.Material and methods: At present, cell viability, immunophenotypic enrichment using flow cytometry, and gene expression by real-time quantitative PCR were carried out.Results: A significant decrease in the expression of OXPHOS genes, DRP1, Pink-1, Parkin, and E-cadherin in endometrial biopsies collected from women with severe endometriosis compared to biopsies collected both from healthy women and women with mild endometriosis was noted. Enhanced expression of mesenchymal stem cell markers (CD73, CD90, and CD105), N-cadherin, hypoxia-inducible factor-1α, TWIST, SNAIL, and SLUG were severe endometrial forms compared to mild form and controls.Conclusion: Our observations revealed the presence of EMT in severe forms of endometriosis, accompanied by the expression of MSC markers and strongly imply the role of EMT in the pathogenesis of endometriosis. Additional research endeavours are necessary to validate and build upon these discoveries, with the ultimate goal of enhancing care and outcomes for individuals afflicted by endometriosis.
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Background

Endometriosis is a chronic inflammatory condition where the precise cause of endometriosis is still not unclear. Mitochondrial dysfunction has been reported in severe forms of endometriosis. However, the role of mitochondrial dynamics, mitophagy, and mitochondrial-related complexes in endometriosis and its relation with Epithelial-Mesenchymal Transition (EMT) is not clear.

Objective

Therefore, this study aims to elucidate the role of mitochondrial dysfunction and its relation with EMT in the pathogenesis of endometriosis.

Material and methods

At present, cell viability, immunophenotypic enrichment using flow cytometry, and gene expression by real-time quantitative PCR were carried out.

Results

A significant decrease in the expression of OXPHOS genes, DRP1, Pink-1, Parkin, and E-cadherin in endometrial biopsies collected from women with severe endometriosis compared to biopsies collected both from healthy women and women with mild endometriosis was noted. Enhanced expression of mesenchymal stem cell markers (CD73, CD90, and CD105), N-cadherin, hypoxia-inducible factor-1α, TWIST, SNAIL, and SLUG were severe endometrial forms compared to mild form and controls.

Conclusion

Our observations revealed the presence of EMT in severe forms of endometriosis, accompanied by the expression of MSC markers and strongly imply the role of EMT in the pathogenesis of endometriosis. Additional research endeavours are necessary to validate and build upon these discoveries, with the ultimate goal of enhancing care and outcomes for individuals afflicted by endometriosis. Files 32209-M no Q2 accepted file(Roya).pdf Files (1.5 MB) | Name | Size | Download all | |---|---|---| | md5:8d9b712927684f437d2ba4334d90bbc6 | 1.5 MB | Preview Download |

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endometriosis

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