Pecam1 antibody
- Known as:
- Pecam1 (anti-)
- Catalog number:
- GTX114202
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Pecam1 antibody
Related genes to: Pecam1 antibody
- Gene:
- PECAM1 NIH gene
- Name:
- platelet and endothelial cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- CD31
- Chromosome:
- 17q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-29
- Date modifiied:
- 2016-04-01
Related products to: Pecam1 antibody
Related articles to: Pecam1 antibody
- Skeletal stem/progenitor cells (SSPCs) are pivotal orchestrators of embryonic skeletogenesis, underlying chondrogenesis and osteogenesis, however, the molecular determinants governing SSPC functionality remain elusive. - Source: PubMed
Publication date: 2026/05/16
Li Yang-YangHuang ShaHu OuQin QinYan PulinLin PengWang Ying-BoJin Huai-JianWu JianWu Yu-TongLuo NaMa Qing-HuaCai Rui-LiXie Yang-LiChen LinGan Yi-BoLiu PengHe Jian - The key to constructing suspension cell lines through genetic engineering technology lies in identifying the fundamental components and molecules involved in cell adhesion. In this study, differentially expressed genes between adherent and suspension Vero cells were analyzed using transcriptomics. The biological processes and pathways associated with these differentially expressed genes were examined through GSEA, GO, and KEGG enrichment analyses. The STRING database was employed to construct a protein-protein interaction (PPI) network, and core hub genes were identified using the MCODE and CytoHubba plugins in Cytoscape. Six core hub genes related to cell adhesion in Vero cells were identified: ITGA3, ITGA5, ITGB3, ITGB5, JUP, and PECAM1. - Source: PubMed
Fan YiyangWang YanBi RuixiangZhao YapengGao WanningZhang DerongLi QiongyiBai Jialin - Infectious diseases exacerbate atherosclerosis-associated morbidity and mortality by inducing sustained inflammatory responses characterized by elevated IL-6, TNF-α, IFN-γ, and CXCL10. Persistent CXCL10-driven recruitment of CXCR3⁺ immune cells promotes endothelial dysfunction and atherosclerotic progression. Although mesenchymal stem cells (MSCs) respond to inflammatory cues and secrete CXCL10, the contribution of CXCL10/CXCR3 signaling to intrinsic MSC immunomodulatory programming remains poorly understood. The objective of this study is to investigate whether CXCL10 signaling can modulate MSC-mediated immunoregulation. To address this, Wharton's jelly-derived MSCs (WJ-MSCs) were genetically engineered to express a membrane-anchored CXCL10-Lactadherin C1/C2 fusion protein (CXCL10-LACTC1/C2). This strategy was designed to recapitulate physiological, localized, and sustained CXCL10 signaling, enabling spatially restricted chemokine presentation that more closely mimics cell-associated CXCL10 in inflammatory microenvironments compared with soluble CXCL10. The Lactadherin C1/C2 domain was selected to achieve stable, physiological membrane anchoring without introducing artificial transmembrane domains or compromising CXCL10 bioactivity. CXCL10-LACTC1/C2-expressing MSCs exhibited increased expression of key immunoregulatory mediators, including IDO1, TGF-β1, and IL4I1. Furthermore, conditioned medium derived from these MSCs attenuated TNF-α-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs), as indicated by the modulation of endothelial activation and homeostasis markers (ICAM-1, PECAM-1, KDR, vWF, and NRF2) and improvement of cell viability. Collectively, these findings provide mechanistic insight into CXCL10-mediated MSC immunoregulation and support further investigation of MSC-based and cell-free therapeutic strategies aimed at mitigating CXCL10-driven endothelial inflammation in infection-associated vascular injury and atherosclerotic disease progression. - Source: PubMed
Publication date: 2026/05/22
Molo KayaEge RukenAti̇k KübraÇıtak ElifÇulcuoğlu OrçunDarıcı HakanOrdu Emel - Chronic periodontitis (CP) and postmenopausal osteoporosis (PMOP) are prevalent chronic inflammatory diseases characterized by bone resorption; however, the shared molecular mechanisms between them remain unclear. Hub genes associated with CP and PMOP were identified through bioinformatics analysis. Lipopolysaccharide (LPS)-stimulated MC3T3-E1 osteoblasts were used to establish an in vitro model, followed by lentiviral-mediated matrix metalloproteinase 14 (MMP14) knockdown. Cell viability and apoptosis were assessed using the Cell Counting Kit-8 assay and flow cytometry, respectively. Levels of inflammatory cytokines and oxidative stress markers were measured by enzyme-linked immunosorbent assay. Intracellular ROS were detected using 2',7'-dichlorodihydrofluorescein diacetate fluorescence staining. Western blot analysis was performed to assess the expression of osteoclast-related markers. The involvement of the JAK2/STAT3 pathway was assessed using the JAK2 agonist RO8191 and inhibitor AG490. PDGFRB, MMP14, VWF, PECAM1, FLT1, and CXCR4 were identified as hub genes and were all upregulated in LPS-stimulated MC3T3-E1 osteoblasts. Silencing MMP14 improved cell viability and reduced apoptosis, inflammatory cytokine release (TNF-α, IL-1β, and IL-6), oxidative stress markers (MDA and ROS), and osteoclast-associated markers (CTX-I, TRAP, and Cathepsin K), while restoring SOD activity. Mechanistically, MMP14 silencing decreased the phosphorylation levels of JAK2 and STAT3. The protective phenotype caused by MMP14 silencing was significantly abolished by RO8191 but mimicked by treatment with AG490. MMP14 may represent a potential molecular link between CP-associated bone loss and PMOP. Modulation of the MMP14-JAK2/STAT3 signaling axis may represent a promising research direction for inflammation-related bone loss. - Source: PubMed
Jiang XiliangJia WeiqiMa QinciFan WanpengLuo Shigao - Programmed cell death (PCD) governs tissue homeostasis and shapes tumor-immune interactions. In acute myeloid leukemia (AML), apoptosis evasion drives resistance and poor outcomes, yet the PCD landscape and the role of Coronin 1A (CORO1A) remain insufficiently defined. - Source: PubMed
Publication date: 2026/05/14
Yang ShuoWang JianyiWang MeiqiHan RongWang ShuqingLi JunxuanXu Hui