Ask about this productRelated genes to: CD144 antibody
- 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: CD144 antibody
Related articles to: CD144 antibody
- Heat acclimation (HA) has emerged as a proven protective intervention to augment thermotolerance and mitigate heat stress (HS)-induced myocardial injury. Despite its clinical significance, the regulatory roles of noncoding RNAs associated with HA-mediated cardioprotection remain largely unexplored. This study conducted comprehensive transcriptomic profiling to delineate the molecular mechanisms underlying HA-induced cardioprotection against HS. Using well-characterized rat models of HS and HA preconditioning, we performed high-throughput sequencing on myocardial tissues to map circRNA/lncRNA expression landscapes. Bioinformatic analyses were integrated with functional validation to identify key regulatory elements. HA preconditioning markedly attenuated HS-induced injury, reducing inflammatory cytokines (IL-1β ↓ 24.36%, IL-4 ↓ 11.3%) while elevating IL-6 (+25.67%), suggesting immunomodulatory rewiring. HS leads to elevated serum HSP70 levels. Analysis identified nine core molecular candidates-miR-196c-5p, miR-212-3p, miR-212-5p, Rffl, Rassf1, Ppp3cc, Zbtb20, Cdh5, and Cxcl2-and delineated two central ceRNA regulatory axes: MSTRG.6276.3-miR-196c-5p-Rffl and MSTRG.4016.1-miR-122-5p-Rassf1. These networks potentially coordinate mitochondrial integrity, hypoxic adaptation, and apoptotic regulation through modulation of inflammatory signaling, metabolic homeostasis, and calcium pathways. The findings establish a noncoding RNA-defined regulatory framework for HA-mediated cardioprotection, revealing novel therapeutic targets for cardiovascular disorders triggered by thermal stress. - Source: PubMed
Publication date: 2026/04/29
Fan LiJunChen JiaJunZhang QingHanSong MingXiaoGuo ZiYiChen XueWeiLu JunYuWang Jing - Producing functional proteins involves multiple steps during mRNA translation on the ribosomes. However, co-translational regulatory mechanisms remain poorly characterized in intact mammalian systems. As a proof-of-concept, we developed a multi-omics approach to investigate endothelial-specific, co-translational regulation by modifying the translating ribosome affinity purification (TRAP) in vivo. We simultaneously co-immunoprecipitated (IP) polysome-associated mRNAs and proteins from the hearts of hemagglutinin-tagged ribosomal protein L22 mice (RiboTag) crossed with inducible endothelial-specific Cdh5CreERT2 mice (RiboTag). To perturb endothelial function, female mice were injected with E. coli lipopolysaccharide (LPS) (6 mg/Kg, i.p., 12 h). Hearts were homogenized, with ~ 10% used for input RNA-Seq and proteomics controls, and the remainder for IP of ribosome-bound polyadenylated mRNA and proteins. Endothelial cell transcripts (pecam1, cdh5) were enriched > 5-fold, while markers characteristic of other cell types were significantly depleted (< 0.05 q-value). We aligned transcriptomic and proteomic datasets (> 1250 overlapping terms) to identify pathways associated with concordant and discordant co-translational regulation. LPS was identified as the upstream regulator of the co-translational dataset that was concordantly regulated. Upregulated mRNAs but not proteins related to glycolysis were discordantly regulated. These findings validate our proof-of-concept multi-omics approach as a predictive platform for identifying disease-relevant pathways regulated at the co-translational level in vivo. - Source: PubMed
Publication date: 2026/04/28
Warren Chad MSwaminathan BhairaviLanga PaulinaVilla Stephanie RThompson Walter CChrzanowska MagdalenaKitajewski Jan KSolaro R JohnWolska Beata MGoldspink Paul H - During mouse development, hematopoietic stem and progenitor cells (HSPCs) originate from hemogenic endothelial cells (ECs) through a process of endothelial-to-hematopoietic transition. These HSPCs are thought to fully sustain adult hematopoiesis. However, it remains unknown whether adult ECs retain hemogenic potential. Here, we used in vivo genetic lineage tracking at population and single-cell (sc) levels, scRNA sequencing, and bone marrow (BM) transplantation to detect hemogenic ECs in adult mice. We identify and characterize BM-resident, adult /VE-Cadherin ECs that produce hematopoietic cell-progeny in vitro and in mice. These adult hemogenic ECs and their hematopoietic cell progeny give rise to hematopoietic cells following adoptive transfer into adult mice. Furthermore, blood cells generated from adult and developmental ECs comparably home to peripheral tissues, where they similarly contribute to inflammatory responses. Thus, our results identify previously unrecognized BM-derived adult hemogenic ECs that generate HSPC and functional mature blood cells. - Source: PubMed
Publication date: 2026/04/27
Feng Jing-XinYang Mei-TingLi LiliLi Caiyi CLivak FerencChen JackZhao YongmeiWang DunruiBhandoola AvinashTaylor NaomiTosato Giovanna - Alcohol consumption 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. - Source: PubMed
Publication date: 2026/04/16
Liu WeiminGusti YusofAthar FathimaRajendran Naresh KCahill Paul ARedmond Eileen M - CD31EMCN (type H) vessels orchestrate the bone metabolic microenvironment, yet the epigenetic control of their endothelial identity remains unclear. N6-methyladenosine (m6A), catalyzed by Mettl3, is essential for mRNA fate and emerging as a regulator of skeletal homeostasis. After isolating and validating type H bone microvascular endothelial cells (H-BMECs) from mouse femora, we used lentiviral shRNA and endothelial-specific Cdh5-Cre;Mettl3 mice to silence Mettl3 in vitro and in vivo. m6A-seq and RNA-seq pinpointed downstream targets; qPCR, Western blot, MeRIP-qPCR, RNA stability, migration, and tube formation assays dissected mechanisms. Local platelet-derived growth factor-BB (PDGF-BB) administration was employed to rescue Mettl3-null phenotypes. Mettl3 expression and global m6A levels were reduced in ovariectomy-induced osteoporosis. Knock-down or genetic deletion of Mettl3 decreased m6A methylation within the 3'UTR of Pdgfrb, accelerated Pdgfrb mRNA decay, blunted PI3K/AKt signaling and impaired H-BMEC proliferation, migration and tube formation. Consequently, type H vessels and trabecular bone mass were markedly diminished. PDGF-BB ligand delivery restored Pdgfrb abundance, reactivated PI3K/AKt, and fully reversed vascular and skeletal defects in Mettl3-null mice. Mettl3-mediated m6A methylation preserves Pdgfrb mRNA stability in bone endothelial cells and is associated with the maintenance of type H vessels, thereby coupling angiogenesis to bone formation. Targeting the Mettl3-m6A-Pdgfrb/PI3K-AKt axis may represent a potential therapeutic strategy for estrogen-deficiency-induced bone loss. - Source: PubMed
Zhou ShijieZhu YihuaYun LiLi MuzheZhang TianchiWumiti TaxiZhou QinfengChen ShuangliuHu YueHan ZhitaoZhang ChunleiTong KaiZhang YafengMa YongGuo YangWang Lining