H.sapiens - Heart, Fetal, SC (Kim,nature,2014)
Ontology highlight
ABSTRACT:
ORGANISM(S): 9606
SUBMITTER: 
Christian von Mering
PROVIDER: 992070419 | PAXDB | 2014
REPOSITORIES: PAXDB
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| bioprojects-abundance-files-v4.0.zip | Other |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description: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.
2026-01-05 | PXD067401 | Pride
Project description:Expression profiles in Adult Heart and Fetal Heart normal tissues.
2008-06-12 | E-GEOD-2035 | biostudies-arrayexpress
Project description:TBX5 ChIP from the Fetal Heart
| PRJNA587057 | ENA
Project description:10x Multiome from Human Fetal Heart
| PRJNA1162163 | ENA
Project description:10x Multiome from Human Fetal Heart
| PRJNA1162162 | ENA
Project description:Fetal cartilage fully regenerates following injury while in adult mammals cartilage injury leads to osteoarthritis (OA). OA is characterized by cartilage breakdown and joint inflammation and associated with significant pain and socioeconomic costs. As no clinically satisfactory treatment is available to date, disease-modifying therapies aimed to achieve cartilage regeneration are urgently required. The inherent regeneration potential of fetal individuals may hold answers to this unmet need. Therefore, to characterize the differences in fetal and adult response to cartilage injury, we carried out histology and comprehensive proteome analyses on fetal (day 80/150-day gestation) and adult cartilage samples one (fetal samples) and three (adult and fetal samples) days after surgical induction of a full-thickness cartilage lesion. In addition, proteins secreted by inflamed fetal MSCs in vitro were compared with the in vivo response to injury to evaluate their therapeutic potential. Histology of synovial samples revealed the presence of neutrophils one day post injury (p.i.) and an influx of macrophages into the subsynovial tissue on day 3 p.i. in fetal samples. In contrast, adult synovial samples showed invasion of neutrophils on day 3 p.i. Activation and migration of Iba1+- macrophages of the synovial lining was observed both in fetal and adult animals. Comparative mass spectrometry revealed 57 proteins significantly up-regulated (> 2FC, FDR<0.05), and 67 proteins significantly down-regulated (<-2 FC) upon injury in adults. Neutrophil-related proteins and acute phase proteins were the two major upregulated protein groups in adult cartilage following injury compared to fetal sheep. In contrast, several immunomodulating proteins and growth factors were significantly higher expressed in the fetus than the adult. Comparison of the in vitro MSCs with the in vivo fetal proteome revealed shared upregulation of 17 proteins, which were considered to be of potential therapeutic interest. The results of this study support our molecular understanding of successful fetal cartilage healing and new therapeutic strategies to induce regeneration in adult articular cartilage by modulating the inflammatory environment. The shared protein upregulation in fetal cartilage in vivo and in fetal MSCS during in vitro inflammation supports the possible therapeutic potential of these factors in specific and fetal MSCs in general.
2022-02-17 | PXD027486 | Pride
Project description:Fetal growth restriction (FGR) is a heterogeneous disorder of pregnancy associated with pathologically low fetal and neonatal weights. We hypothesized that FGR consists of multiple placental subtypes, similar to what we have observed in preeclampsia. To address this hypothesis, we assembled a fetal growth-focused human placental microarray data set (N=97) consisting of 20 new normotensive suspected FGR samples (below), in addition to term controls (N=26) and hypertensive suspected FGR samples (N=51) from GSE75010.
2018-10-13 | GSE100415 | GEO
Project description:The placenta is a dynamic reproductive organ for cattle reproduction and is indispensable for embryonic blood supply, nutrition transportation, and fetal calf development, and it directly affects the development of fetal calf in utero. However, the detailed molecular mechanism of placenta act on fetal calf still remains unclear.In the present study,we used the proteome of placenta to identify the key gene and protein in Low weight(LW) fetal calves and High weight(HW) fetal calves, and reveal the fetal calf growth-related candidate biomarkers by integrative analysis.Placenta proteomics provide new insight into the physiological mechanisms and potential biomarkers for fetal calf development in utero,which can be employed to enhance breeding efficiency and genetic improvement in cattle.
2025-05-06 | PXD043483 | Pride
Project description:Fetal lung development is a complex biological process, which involves temporal and spatial regulations of many genes. To understand molecular mechanisms of this process, we investigated gene expression profiling of lungs at gestational day 18, 19, 20, 21, new born, and adult rats using in-house rat DNA microarray containing 6,000 known genes and 4,000 ESTs. 1,512 genes passed SAM test and 583 genes (402 known genes and 181 ESTs) had a 2-fold change at least at one time point. K-means cluster analysis revealed 7 major expression patterns. Furthermore, using GeneMapp, we identified 3 regulatory pathways: TGF beta signaling pathway, cell cycle, and G-protein signaling; and 2 metabolism pathways: proteasome degradation and glycolysis. Our results suggest a complex regulatory pathway for fetal lung development. Loop Design as following: D18-D19-D20-D21-NB-AD-D18
2010-07-01 | E-GEOD-3302 | biostudies-arrayexpress
Project description:We sequenced 2 heart samples from human fetal donors and detected the differential expressed mRNAs and lncRNAs. The network of significant differential expressed transcripts could be associated to developmental program.
2016-02-10 | GSE68279 | GEO