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

Letícia Bruna Corrêa Penariol, Penariol LBC, Carolina Hassibe Thomé, Thomé CH, Patrícia A. Tozetti, Tozetti PA, Paier CRK, Carlos Roberto Koscky Paier, Fabiana O. Buono, Buono FO, Kamila Chagas Peronni, Orellana MD, Maristela Delgado Orellana, Covas DT, Dimas Tadeu Covas, Maria Elisabete Amaral de Moraes, Moraes MEA, Wilson A. Silva, Júlio César Rosa e Silva, Rosa-e-Silva JC, Rui Alberto Ferriani, Ferriani RA, Faça VM, Vítor M. Faça, Omero Benedicto Poli‐Neto, Poli-Neto OB, Tiezzi DG, Daniel Guimarães Tiezzi, Juliana Meola, Meola J
2022 · doi:10.20944/preprints202209.0180.v1 · W4295804368
preprint OA: green CC0 ⤵ 9 in-corpus citations
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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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Condition tags

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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