Dataset Information

Characterization of stromal cells isolated from endometriotic lesions

ABSTRACT: Endometriosis shows significant lesion heterogeneity, but pathophysiological mechanisms leading to differences in clinical presentation are poorly understood. Here we utilized primary stromal cells from different types of endometriotic lesions to better understand the molecular mechanisms that lead to endometriosis heterogeneity. For this aim, endometrial stromal cells (ESCs) were obtained from eutopic endometrium (EU), endometrioma (OMA), superficial (SF) and deep (DE) endometriosis lesions and analyzed in vitro for their behavior regarding proliferation, migration, and contractility. Proteomics was used to explore the molecular mechanism underlying the observed changes.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Endometrial Stromal Cell, Epithelial Cell

DISEASE(S): Endometriosis

SUBMITTER: Marianne Spalinger

LAB HEAD: Marianne Spalinger

PROVIDER: PXD066685 | Pride | 2025-12-15

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	20250528_002_C38661_S949515_Eu1.raw	Raw
	20250528_003_C38661_S949516_Eu2.raw	Raw
	20250528_004_C38661_S949517_Eu3.raw	Raw
	20250528_005_C38661_S949518_Eu4.raw	Raw
	20250528_006_C38661_S949519_Eu5.raw	Raw

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Publications

Endometrial Stromal Cells from Endometriosis Patients Reflect Lesion-Type-Specific Heterogeneity.

Rodriguez Gutierrez Daniel D Spalinger Marianne R MR Astourian Alina A Evrova Olivera O Berclaz Lucie L Hartmann Monique M Dedes Ioannis I Imesch Patrick P Metzler Julian M JM Witzel Isabelle I Shilaih Mohaned M Vongrad Valentina V Leeners Brigitte B

Cells 20251128 23

Endometriosis, a disease affecting about one out of ten women, is characterized by the growth of endometrial-like tissue outside the uterine cavity. There is significant disease heterogeneity, but the pathophysiological mechanisms underlying differences in clinical presentation are poorly understood. Here, we investigated endometrial stromal cells (ESCs) from different types of endometrial lesions (endometrioma, superficial, and deep endometrial lesions), which revealed distinct differences in p ...[more]

PMID: 41369380

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Project description:Abstract Background Vertebral endplate signal intensity changes visualized by magnetic resonance imaging termed Modic changes (MC) are highly prevalent in low back pain patients. Interconvertibility between the three MC subtypes (MC1, MC2, MC3) suggests different pathological stages. Histologically, granulation tissue, fibrosis, and bone marrow edema are signs of inflammation in MC1 and MC2. However, different inflammatory infiltrates and amount of fatty marrow suggest distinct inflammatory processes in MC2. Aims The aims of this study were to investigate i) the degree of bony (BEP) and cartilage endplate (CEP) degeneration in MC2, ii) to identify inflammatory MC2 pathomechanisms, and iii) to show that these marrow changes correlate with severity of endplate degeneration. Methods Pairs of axial biopsies (n=58) spanning the entire vertebral body including both CEPs were collected from human cadaveric vertebrae with MC2. From one biopsy, the bone marrow directly adjacent to the CEP was analyzed with mass spectrometry. Differentially expressed proteins (DEPs) between MC2 were identified and bioinformatic enrichment analysis was performed. The other biopsy was processed for paraffin histology and BEP/CEP degenerations were scored. Endplate scores were correlated with DEPs. Results Endplates from MC2 were significantly more degenerated. Proteomic analysis revealed an activated complement system, increased expression of extracellular matrix proteins, angiogenic, and neurogenic factors in MC2 marrow. Endplate scores correlated with upregulated complement and neurogenic proteins. Discussion The inflammatory pathomechanisms in MC2 comprises activation of the complement system. Concurrent inflammation, fibrosis, angiogenesis, and neurogenesis indicate that MC2 is a chronic inflammation. Correlation of endplate damage with complement and neurogenic proteins suggest that complement system activation and neoinnervation may be linked to endplate damage. The endplate-near marrow is the pathomechanistic site, because MC2 occur at locations with more endplate degeneration. Conclusion MC2 are fibroinflammatory changes with complement system involvement which occur adjacent to damaged endplates.