Dataset Information

Proteomic Comparisoadsfasn of Intact and Fetoscopy-Induced Fetal Membrane Sites

ABSTRACT: Iatrogenic preterm premature rupture of fetal membranes (iPPROM) following fetoscopic interventions remains a major barrier to the advancement of fetal therapies. The mechanisms underlying iPPROM are poorly understood, but the inability of fetal membrane (FM) defects to heal spontaneously likely plays a key role, contrasting with the regenerative potential of amniotic membranes in other contexts. To assess the impact of fetoscopic procedures on FMs, tissue samples from patients who underwent laser surgery for twin-to-twin transfusion syndrome (16–27 weeks gestation, n=8) were collected after cesarean delivery at 29–35 weeks. Samples were categorized by proximity to the trocar site and analyzed using proteomic and histological methods. While differential expression analysis in the amnion revealed no significant changes, pathway enrichment indicated increased collagen deposition at defect sites. In the chorion, sevendifferentially expressed proteins were identified, largely linked to enhanced intercellular contact stability. These findings suggest the amnion may respond to mechanical stress by reinforcing structural integrity through collagen deposition, while the chorion may attempt to stabilize cell junctions. However, no other signs of tissue regeneration were observed. This study provides molecular and cellular evidence that FMs lacks a substantial healing response post-surgery, underscoring the need for biologically informed repair strategies.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Fetal Membrane

SUBMITTER: Lukas Moser

LAB HEAD: Martin Ehrbar

PROVIDER: PXD067401 | Pride | 2026-01-05

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	20231205_001_autoQC01.raw	Raw
	20231205_004_S602571_6_C3C_Chorion.raw	Raw
	20231205_005_S602559_5_C2A_Amnion.raw	Raw
	20231205_006_S602555_5_HA_Amnion.raw	Raw
	20231205_006_S602555_5_HA_Amnion_DDA.raw	Raw

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Project description:Cellular differentiation and lineage commitment are considered to be robust and irreversible processes during development. Recent work has shown that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. This raised the question of whether transcription factors could directly specify somatic cell fates in cells such as pancreatic ? cells, contractile cardiomyocytes and neurons. We hypothesized that combinatorial expression of chondrocyte-specific transcription factors could directly convert human amnion cells into chondrosarcoma. Starting from a pool of candidate genes, we identified a combination of only five genes (5F pool), BCL6, T (also called BRACHYURY), c-MYC, MITF and BAF60C (also called SMARCD3) that rapidly and efficiently convert postnatal human amnion into chondrosarcoma. The cells generated expressed multiple cartilage-specific genes such as collagen type II ?1, link protein-1 and aggrecan, and exhibited characteristics of cartilage both in vivo and in vitro. Expression of the endogenous genes for T and MITF was initiated, implying that the cell conversion is due to not only the forced expression of the transgenes, but also the cellular reprogramming by the transgenes. The same set of genes converted human placental artery-derived endothelial (hPAE) cells and menstrual blood-derived cells into chondrosarcoma cells, implying that this conversion is independent of cell types. Direct conversion system from non-cartilage tissue to cartilaginous tissue contributes substantially to a major advance toward cartilage development, oncogenesis of chondrocytes, and cell-based therapy. We hypothesized that combinatorial expression of chondrocyte-specific transcription factors could directly convert human amnion cells into chondrosarcoma. Starting from a pool of candidate genes, we identified a combination of only five genes that rapidly efficiently convert postnatal human amnion into chondrosarcoma.

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Proteomic Comparisoadsfasn of Intact and Fetoscopy-Induced Fetal Membrane Sites

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