Ask about this productRelated genes to: Wnt4 Blocking Peptide
- Gene:
- WNT4 NIH gene
- Name:
- Wnt family member 4
- Previous symbol:
- -
- Synonyms:
- WNT-4
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2016-10-05
Related products to: Wnt4 Blocking Peptide
Related articles to: Wnt4 Blocking Peptide
- Resveratrol is a polyphenolic natural product. It has been demonstrated that resveratrol has protective effects on various neurological diseases. However, the mechanism by which resveratrol protects the neurological function in stroke remains unclear. In this study, we established a stroke rat via middle cerebral artery occlusion (MCAO). The MCAO rats were intraperitoneally administered with resveratrol (30 mg/kg) for 7 consecutive days. Neurological function scoring, cerebral infarct area assessment, tissue collection for subsequent assays, and pathological, neuroinflammatory, and oxidative stress analyses were performed at 24 h post-stroke, while the Morris water maze test for poststroke cognitive impairment (PSCI) was conducted from day 8 to day 14 post-stroke. The differentially expressed proteins (DEPs) were identified through proteomic analysis. The key regulatory pathways were verified through western blotting. Resveratrol significantly reduced the neurological function score, decreased the infarct area, and alleviated PSCI. Resveratrol significantly reduced the levels of inflammatory factors, lowered the malondialdehyde (MDA) level, and increased the levels of glutathione (GSH) and total antioxidant capacity (T-AOC). Proteomic analysis identified 263 DEPs. Protein‒protein interaction analysis suggested that secreted frizzled-related protein 4 (sFRP4)/Wnt pathway might be a potential target of resveratrol. Western blotting confirmed that resveratrol effectively reversed the stroke-induced upregulation of sFRP4, and also abrogated the stroke-induced downregulation of Wnt3a, Wnt4, Wnt5, Wnt11, and β-catenin levels. Additionally, resveratrol reversed the stroke-induced reduction in the levels of ZO-1, Occludin, and Claudin 5. It is concluded that resveratrol maintains the integrity of the blood-brain barrier and modulates the sFRP4/Wnt signaling pathway. - Source: PubMed
Publication date: 2026/05/09
Zhang HuiXu ZezhouWang YifanZhou XianzhiYun QimeiDeng LingHe Binsheng - Sulfate is a vital nutrient for healthy brain development. More than 90 sulfate-related genes are highly conserved across mammalian species, with 16 of these genes being clinically reportable for adverse brain conditions. To determine the potential involvement of additional sulfate-related genes in human neuropathology, this study curated the spatial and temporal expression patterns of all known sulfate biology genes in the human fetal brain from 8 to 37 post conception weeks (pcw) using data from the BrainSpan database and performed network analysis to cluster sulfate-related genes with genes involved in neurodevelopmental processes. A total of 64 sulfate-related genes were abundantly or moderately expressed in 11 brain regions throughout gestation. Steady state expression was observed for some of these genes from 8 to 37 pcw, including genes that encode sulfotransferases (, ), sulfatases (, , , ), sulfatase modifying enzyme (), key enzymes in amino acid metabolism (, ), sulfate transporter (), as well as genes involved in neurodevelopmental processes (, , , , , ). Between 21-24 weeks, there were numerous clusters of sulfate biology genes with neurodevelopmental genes involved in neuronal migration ( and synaptogenesis (, , , ). At 8-13 and 17-21 pcw, fifteen sulfate genes (, , , , , , , , , , , , , , ) were expressed in the hippocampus and clustered with genes involved in neurogenesis, differentiation and synaptogenesis (, , ). Overall, this study identified 48 sulfate-related genes with moderate/abundant expression in the fetal brain that are coexpressed with genes for neurodevelopmental processes but are not considered in clinical settings. These findings provide information for future studies into the physiological roles of sulfate-related genes that are expressed in the fetal brain. - Source: PubMed
Publication date: 2026/05/08
Vijayakumar PrasidheeSummers Kim MDawson Paul A - The early-life intestinal microenvironment plays a pivotal role in shaping immune cell development. Here, we identify a colonic Wnt4-expressing stromal cell, enriched during early-life, that promotes iNKT cell proliferation via BMP-MAPK signaling. These stromal cells are spatially associated with iNKT cells and macrophages and exhibit high Bmp2 expression during the neonatal period. Depletion of BMP2 in Wnt4 stromal cells during, but not after, this time window leads to long-lasting reductions in iNKT cells. These stromal cells are shaped by microbial signals, as germ-free and early-life antibiotic-treated mice exhibit increased Wnt4 stromal cell abundance and elevated Bmp2 expression, with excessive iNKT cell accumulation that lasts into adulthood. These persistent changes in iNKT cells due to early-life perturbations are associated with altered susceptibility to later-life mucosal disorders. Importantly, similar stromal cells are present in fetal and neonatal human colon, and human rBMP2 promotes iNKT cell growth. Together, our findings reveal a neonatal colonic stromal niche, orchestrated by microbial cues, that regulates colonic immune homeostasis in later-life. - Source: PubMed
Publication date: 2026/05/06
Lin XiLee Chloe Hyun-JungZhang TingAntanaviciute AgneHanley ThomasGlickman Jonathan NBharadwaj Nikhila SRosen VickiGumperz Jenny EWaldor Matthew KSimmons AlisonGensollen ThomasBlumberg Richard S - The link between neurodevelopment in infants exposed to maternal gestational diabetes mellitus (GDM) and fetal DNA methylation remains unexplored. We conducted this hypothesis-generating study to investigate the association between fetal DNA methylation and neurodevelopmental outcomes in children of mothers with GDM. We carried out a prospective, observational pilot cohort study comparing infants exposed to maternal GDM with an unexposed control group. Umbilical cord blood DNA methylation was assessed using targeted methylome sequencing covering 3.34 million CpG sites. Infant neurodevelopment was evaluated at age two years using the Bayley-III Scales. Bioinformatics processing identified differentially methylated regions (DMRs), followed by multiple enrichment analyses of DMR-associated genes and partial correlation analyses. Multi-dimensional enrichment analysis of the 1053 identified DMR-associated genes revealed a significant convergence of pathways related to neurogenesis, synaptic components, and axonal guidance. Infants born to mothers with GDM exhibited lower scores in cognitive, language, and motor domains, which were associated with identifiable DNA methylation signatures at birth. Significant correlations were observed in genes essential for brain scaffolding and synaptic circuitry, most notably , the alpha/beta clusters, and . Additionally, methylation patterns in and suggest a potential impact on blood-brain barrier integrity, while associations with and highlight a systemic metabolic 'cross-talk' influencing neurodevelopment. Although these pilot findings are hypothesis-generating and require further functional validation, this study provides pioneering evidence that neurodevelopmental alterations in the offspring of mothers with GDM are potentially associated with intrauterine epigenetic modifications detectable at birth. - Source: PubMed
Publication date: 2026/04/16
González-González Nieves LuisaArmas-González MarinaGonzález-Dávila EnriqueCastro-Conde José RamónGonzález-Campo CandelariaFlores CarlosLorenzo-Salazar José MiguelGonzález-Montelongo RafaelaMuñoz-Barrera AdriánPadrón-Pérez ErikaTascón-Padrón LauraOrribo-Morales Olivia - Preeclampsia (PE), a life-threatening hypertensive disorder of pregnancy, remains a leading cause of maternal-fetal morbidity with unclear pathogenesis. While traditional studies focus on placental dysfunction, the critical role of decidualization-a prerequisite for placental implantation-has been underemphasized. Here, we demonstrate that a high-fat diet (HFD) predisposes mice to PE-like phenotypes, including hypertension, proteinuria, glomerular injury, and placental-fetal growth restriction, which are accompanied by impaired decidualization. HFD triggers robust inflammatory responses in decidual tissue, evidenced by upregulated IL-1β/IL-6/TNF-α and hyperactivated NF-κB signaling, which correlate with reduced expression of decidualization regulators (Bmp2, Wnt4) and marker genes (Dtprp, Prl8a2). These changes lead to compromised decidual vascularization, reduced polyploid cell differentiation, and impaired placental morphogenesis. Our findings reveal a novel association whereby HFD-induced inflammation is linked to disrupted decidual-placental crosstalk via NF-κB activation, providing mechanistic insights into PE pathogenesis and highlighting decidualization as a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/22
Zhao MiaomiaoXu YanxinYan XingyuZhang Cong