What do the Transcriptome and Proteome of Menstrual Blood-derived Mesenchymal Stem Cells Tell us about Endometriosis?

Letícia Bruna Corrêa Penariol, Carolina Hassibe Thomé, Patrícia A. Tozetti, Carlos Roberto Koscky Paier, Fabiana O. Buono, Kamila Chagas Peronni, Maristela Delgado Orellana, Dimas Tadeu Covas, Maria Elisabete Amaral de Moraes, Wilson A. Silva, Júlio César Rosa e Silva, Rui Alberto Ferriani, Vítor M. Faça, Omero Benedicto Poli‐Neto, Daniel Guimarães Tiezzi, Juliana Meola
2022 · doi:10.20944/preprints202209.0180.v1 · W4295804368
preprint OA: green CC0 ⤵ 9 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study integrated transcriptome and proteome data from menstrual blood-derived mesenchymal stem cells to identify differentially expressed genes and proteins associated with endometriosis, revealing modulated signaling pathways related to inflammation and tissue remodeling.

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Abstract

Given the importance of menstrual blood in the pathogenesis of endometriosis and the multifunctional roles of menstrual mesenchymal stem cells (MenSCs) in regenerative medicine, this issue has gained prominence in the scientific community. Moreover, recent reviews highlight how robust the integrated assessment of omics data is for endometriosis. To our knowledge, no study has applied the multi-omics approaches to endometriosis MenSCs. It is a case-control study at a university-affiliated hospital. MenSCs transcriptome and proteome data were obtained by RNA-seq and UHPLC-MS/MS detection. Among the differentially expressed proteins and genes, we emphasize ATF3, ID1, ID3, FOSB, SNAI1, NR4A1, EGR1, LAMC3, and ZFP36 genes and MT2A, TYMP, COL1A1, COL6A2, and NID2 proteins that were already reported in the endometriosis. Our functional enrichment analysis reveals integrated modulating signaling pathways such as epithelial-mesenchymal transition (↑) and PI3K signaling via AKT to mTORC1 (↓in proteome), mTORC1 signaling, TGF beta signaling, TNFA signaling via NFkB, and response to hypoxia via HIF1A targets (↑in transcriptome). Our findings highlight primary changes in the endometriosis MenSCs, suggesting that the chronic inflammatory endometrial microenvironment can modulate these cells, providing opportunities for endometriosis etiopathogenesis. Moreover, they identify challenges for future research leveraging knowledge for regenerative and precision medicine in endometriosis.

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endometriosis

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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