CDH5 Antibody (Phospho-Tyr731) (OAAF00512)
- Known as:
- CDH5 Antibody (Phospho-Tyr731) (OAAF00512)
- Catalog number:
- oaaf00512
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CDH5 Antibody (Phospho-Tyr731) (OAAF00512)
Related genes to: CDH5 Antibody (Phospho-Tyr731) (OAAF00512)
- Gene:
- CDH5 NIH gene
- Name:
- cadherin 5
- Previous symbol:
- -
- Synonyms:
- 7B4, CD144
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-20
- Date modifiied:
- 2016-10-05
Related products to: CDH5 Antibody (Phospho-Tyr731) (OAAF00512)
Related articles to: CDH5 Antibody (Phospho-Tyr731) (OAAF00512)
- Alcohol influences cardiovascular disease, but whether it does so by affecting endothelial plasticity is unknown. We tested whether alcohol regulates endothelial-to-mesenchymal transition (EndMT) to influence arterial pathology. HCAEC and HUVEC were exposed to inflammatory cytokines or hypoxia in the absence or presence of ethanol (5 to 100 mM). In vivo, carotid ligation was performed in mice gavaged with/without either daily moderate ethanol (2 drink equivalent/d) or episodic binge exposure (7 drink equivalent, 2 days/week) and myoendothelial cells assessed. Cytokines and hypoxia induced EndMT in vitro characterized by loss of endothelial markers, increased mesenchymal markers, and enhanced migratory capacity. Low-to-moderate dose ethanol (5-25 mM) attenuated marker changes, preserving endothelial phenotype, whereas high dose ethanol (50-100 mM) either had no effect or exacerbated EndMT. The inhibitory effect of moderate ethanol on cytokine- and hypoxia-induced changes in αSMA and Cdh5 expression was abrogated by γ-secretase inhibition, consistent with involvement of Notch signaling. Carotid ligation induced neointimal formation and accumulation of myoendothelial cells indicative of EndMT. Daily moderate ethanol significantly attenuated neointimal hyperplasia and diminished the myoendothelial cell population, whereas in contrast, episodic binge ethanol exposure increased pathologic remodeling and myoendothelial cell abundance. Alcohol modulates endothelial trans-differentiation in a biphasic manner. Low-to-moderate alcohol exposure suppresses EndMT and limits pathological remodeling, whereas higher level binge exposure promotes these processes. These findings identify regulation of endothelial plasticity as a potential novel mechanism linking alcohol consumption patterns to vascular disease risk. - Source: PubMed
Publication date: 2026/09/15
Liu WeiminGusti YusofAthar FathimaRajendran Naresh KCahill Paul ARedmond Eileen M - Protein C receptor (PROCR) marks a rare population of mammary epithelial cells with stem-like properties, but their low abundance has hindered characterization of their functional diversity and regulatory programs. Here, we integrate targeted enrichment with single-cell transcriptomic and chromatin accessibility profiling to construct a multimodal atlas of PROCR cells across development. We identify heterogeneous PROCR subpopulations, including a , , population with features consistent with a mammary stem cell (MaSC) state, such as high developmental potency, an EMT-associated program, and an early differentiation position. Integrative analyses reveal dynamic transcriptional regulatory circuits underlying stemness and lineage commitment. Cross-species comparisons uncover analogous PROCR populations in human mammary epithelium, and this stem cell-like signature is enriched in triple-negative and claudin-low tumors. Together, these findings refine the mammary epithelial hierarchy, define regulatory programs underlying stemness and lineage bifurcation, and establish a molecular link between a distinct MaSC state and tumor aggressiveness. - Source: PubMed
Publication date: 2026/09/01
Yan Koon-KiuNekritz ErinXie ZhenJu BenshengDong XinranWerner RachelAlsina-Beauchamp DayaniraRosencrance CelesteMukhopadhyay ParthaPan QingfeiGorbatenko AndrejZhou HongleiYan LeiDing LiangQian ChenxiNatarajan SivaramanChi HongboEaston JohnSilva JoseYu Jiyang - A high triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) ratio is strongly associated with insulin resistance and atherosclerotic cardiovascular risk, but the cellular mechanisms linking this lipid imbalance to vascular injury remain incompletely defined. This study established a combined hyperglycemic/high TG/low HDL-C ratio-mimetic in vitro model using human coronary artery endothelial cells and THP-1-derived macrophages to investigate endothelial inflammation, glycocalyx disruption, monocyte recruitment, foam-cell formation, oxidative stress, and cholesterol efflux. High TG/low HDL-C ratio-mimetic stress significantly reduced endothelial viability, increased cytotoxicity, impaired transendothelial resistance, increased fluorescein isothiocyanate (FITC)-dextran permeability, and promoted syndecan-1 shedding. The lipid-stress condition induced endothelial inflammatory activation, with increased vascular cell adhesion molecule 1 (VCAM1), intercellular adhesion molecule 1 (ICAM1), E-selectin (SELE), C-C motif chemokine ligand 2 (CCL2), interleukin 6 (IL6), and C-X-C motif chemokine ligand 8 (CXCL8) expression, accompanied by enhanced THP-1 adhesion and transmigration. Glycocalyx and junctional injury were supported by increased heparanase (HPSE) expression and reduced syndecan-1 (SDC1), tight junction protein 1 (TJP1), cadherin 5 (CDH5), wheat germ agglutinin (WGA) staining, zonula occludens-1 (ZO-1) continuity, and vascular endothelial cadherin (VE-cadherin) integrity. Endothelial-conditioned lipid stress promoted macrophage foam-cell formation, increased CD36 scavenger receptor (CD36), oxidized low-density lipoprotein receptor 1 (OLR1), and peroxisome proliferator-activated receptor gamma (PPARG) expression, enhanced cholesterol accumulation, and suppressed ATP-binding cassette transporter A1 (ABCA1)-, ATP-binding cassette transporter G1 (ABCG1)-, scavenger receptor class B member 1 (SCARB1)-, and apolipoprotein E (APOE)-associated cholesterol efflux pathways. HDL rescue broadly attenuated endothelial inflammation, oxidative stress, barrier disruption, and macrophage foam-cell formation, whereas ApoA-I exerted protective effects across the selected endothelial and macrophage endpoints in which it was evaluated. CD36 inhibition reduced macrophage lipid accumulation, whereas heparanase inhibition preserved glycocalyx integrity. These findings identify the endothelial glycocalyx-nuclear factor kappa B (NF-κB)-CD36/ABCA1 axis as a mechanistic link between the high TG/low HDL-C ratio and diabetic atherosclerotic vascular dysfunction. - Source: PubMed
Publication date: 2026/09/10
Bi LechangZhao WenLu MingjingJiang NanWang GaofengHuang FeilaiLuo PengchaoWang Guofu - Atopic dermatitis (AD) is increasingly recognized as a systemic inflammatory disease associated with increased cardiovascular risk, yet the mechanisms linking AD to atherosclerosis and clinically relevant biomarkers of early vascular involvement remain poorly defined. We characterized the circulating proteomic profile of moderate-to-severe AD and identified biomarkers associated with subclinical atherosclerosis. In this cross-sectional study, serum samples from patients with AD (n=34), psoriasis (n=34), and healthy controls (n=20) were analyzed using proteomic panels targeting inflammatory and cardiovascular pathways. Participants underwent carotid and femoral ultrasound to detect atheromatous plaques. Compared with controls, AD showed increased circulating Th2 (CCL13, ST2, IL-13), innate (IL-6, IL-18), Th1 (IFN-γ), and Th17 (IL-17RA) markers, together with cardiovascular-related proteins including CCL19, FGF21, HGF, and P-selectin, with enrichment of atherosclerosis-related pathways. In AD, plaques were associated with higher LDL receptor, CDH5, transferrin receptor, CCL19, and CCL25, and lower IGFBP-2 levels, which also correlated with atherosclerosis burden. A composite proteomic score showed good discrimination of plaques (AUC 0.94) and outperformed traditional cardiovascular risk factors. Proteomic profiles and plaque-associated proteins differed markedly from psoriasis. These findings identify a disease-specific systemic proteomic signature in AD linked to early atherosclerosis and highlight circulating biomarkers with potential relevance for cardiovascular risk stratification. - Source: PubMed
Publication date: 2026/09/09
Berna-Rico EmilioNeria FernandoGómez-de la Fuente EnriquePérez-García BibianaAranda Carlos JAbbad-Jaime de Aragón CarlotaPerez-Bootello JavierDomínguez-López RaquelMonge DianaDavo-Mogica MariaBlauvelt AndrewGonzález-Cantero Álvaro - Fibroblasts are mesenchymal cells in the healthy vascular adventitia. In atherosclerosis, single-cell sequencing datasets suggest fibroblasts are abundant in plaques. However, their identity, origin, and fate during plaque progression remain unclear, which we aim to unravel here. - Source: PubMed
Publication date: 2026/09/09
Li GuanliangAsselberghs Sebastiaan E JYu BaixueFeng CongMendez Paul-LennardKasakovski DimitriGoossens PieterAckermans Tia MTillie Renée J H AGijbels Marion JTemmerman LieveXu HeDonners Marjo M P CKheder Dlzar AMaryam SidrahJin HanXue ChenyiHayat SikanderConklin Austin CRomanoski Casey EGiacca MauroMiller Clint LReilly Muredach PChen MingKramann RafaelMees BarendBaker Andrew HSluimer Judith C