Polyclonal Antibody (Concentrated): PECAM1
- Known as:
- Polyclonal Antibody (Concentrated): PECAM1
- Catalog number:
- PA1950
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Bouster Immunoleader
- Gene target:
- Polyclonal Antibody (Concentrated): PECAM1
Related genes to: Polyclonal Antibody (Concentrated): PECAM1
- 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: Polyclonal Antibody (Concentrated): PECAM1
Related articles to: Polyclonal Antibody (Concentrated): PECAM1
- The increasing prevalence of bone-related diseases and the desire to improve patient outcomes are driving research into bone replacement materials that overcome the limits of current bone substitutes. Molybdenum (Mo) is a promising candidate as an implant and degradable bone replacement material because it combines three key properties: mechanical strength, biocompatibility, and resorbability. However, little is known about the cellular mechanisms induced by Mo on bone regeneration. This study exposed a complex in vitro bone model as quadruple culture with primary human osteoblasts, osteocytes, osteoclasts, and endothelial cells, to Mo powder extracts to understand cell-material interactions in a multicellular system. Extracts with a final concentration of 1 mM Mo in quadruple cultures induced osteogenic differentiation by stimulation of gene expression and ALP activity, and gene expression, as well as enhanced calcium deposition of osteoblasts. Furthermore, expression of osteoblasts increased significantly and network formation of HUVEC with stimulated expression occurred. However, CD31 () expression and endothelial network density were reduced, indicating a complex, mixed angiogenic response. In contrast, Mo inhibited osteoclast formation and slowed down osteocyte differentiation, reducing , , and gene expression. Additionally, the RANKL ()/OPG () ratio of osteocytes was shifted toward OPG after Mo treatment. Cellular effects are most likely caused by the presence of molybdate anions. In summary, Mo extracts stimulated early bone healing factors involved in osteogenesis, vascularization, and mineralization, while osteoclastogenesis was inhibited. These dual effects in vitro provide mechanistic evidence supporting the potential of Mo as a growth factor-free bone replacement material and establish a cellular foundation for further preclinical development. - Source: PubMed
Publication date: 2026/05/07
Wirsig KatharinaBernhardt Anne - Mouse mammary epithelial cells possess a remarkable ability to regenerate the entire mammary gland through precisely regulated differentiation, involving complex molecular, morphological, and functional changes. Here, we performed comprehensive transcriptomic profiling of HC11 mouse mammary epithelial cells undergoing lactogenic differentiation using RNA sequencing and integrative bioinformatics. We identified 566 differentially expressed genes, reflecting extensive transcriptional reprogramming and activation of biosynthetic, metabolic, and secretory programs. Strong up-regulation of terminal and lactogenic differentiation markers, including Wap, Csn2, Lpl, Cd36, Lalba, Btn1a1, Xdh, Gata3, and Cebpb, signified maturation into a secretory phenotype. Functional evaluation via gene set enrichment analysis revealed transcriptional enrichment of mTOR, prolactin, insulin, ErbB, and autophagy-associated pathways, consistent with anabolic readiness and terminal differentiation. Conversely, p53, Wnt, and FoxO pathways were down-regulated, marking a transition from proliferation to differentiation. Transcription factors (FoxO1, Zbtb16, and Srebf1) and epigenetic regulators (Gadd45a and Hist1h1e) exhibited dynamic changes, underscoring coordinated transcriptional and chromatin remodeling. Gene set enrichment and protein-protein interaction analyses identified 10 hub genes, Agt, Ccnd1, Igf1, Mki67, Myc, Calm4, Rasgrp1, Cd69, Il6, and Pecam1, as central drivers of differentiation. Clustering of uniquely regulated genes further implicated roles in milk synthesis, protease activity, and lineage stabilization. Together, these findings define a transcriptional framework for lactogenic differentiation in the HC11 cell line model and provide a basis for future mechanistic studies. - Source: PubMed
Publication date: 2026/05/04
Ahmad WaqarPanicker Neena GopinathanRizvi Tahir AMustafa Farah - Collateral perfusion and neurovascular stability critically influence outcomes after ischemic stroke; however, no pharmacological agent is currently approved to enhance these processes. - Source: PubMed
Publication date: 2026/04/20
Lee Han-GyulKwon Tae WooJung MinhoLee Won MyoungLee Chang-DaeKwon SeungwonLee SanghyunCho Ik-HyunMoon Sang-Kwan - The goal of this study was to gain insight into an understudied physiological mechanism that may influence skeletal muscle atrophy following spinal cord injury (SCI). Specifically, we quantified skeletal muscle blood flow (BF) rates in paralyzed hindlimbs throughout the acute to subacute recovery period in a severe contusion SCI model. Secondary objectives were to characterize temporal changes in circulating and tissue-level markers of capillary density and vascular dysfunction, and vascular-related gene expression within hindlimb skeletal muscle. We hypothesized that SCI would reduce skeletal muscle BF and be accompanied by increases in circulating markers of vascular dysfunction, along with reductions in skeletal muscle capillary density and vascular-related gene expression. Four-month-old Sprague-Dawley male rats underwent T9 laminectomy (SHAM surgery) or severe contusion SCI. Hindlimb skeletal muscle mass, absolute BF rates, and mass-corrected BF rates were lower at 1-, 2-, and 4-weeks in SCI vs SHAM, with the most distinct BF differences present in the soleus (~50% lower, p<0.001). Bulk RNA-sequencing revealed that genes related to coagulation, blood vessel maintenance, and endothelial cell health were lower in soleus muscle after SCI, with most differences occurring at 1-2 weeks. Circulating PECAM-1, a marker of vascular dysfunction, was higher 2-3 weeks post-SCI (p<0.05), while no differences in soleus capillary density were detected. Our results reveal reduced limb perfusion and signs of vascular dysfunction in paralyzed hindlimb skeletal muscle during the acute post-SCI period in a rodent severe SCI model. Future studies examining mechanisms of vascular dysfunction after SCI or testing interventions to improve vascular function should consider this timeframe. - Source: PubMed
Publication date: 2026/04/30
Clayton Zachary SNguyen Branden LKok Hui JeanReynolds Michael CConover Christine FWnek Russell DBuckley Kinley HKura Jayachandra ROtzel Dana MLuo Yangyi EBarton Elisabeth RBeck Darren TMcCullough Danielle JYarrow Joshua F - Cardiac fibrosis is a defining pathological feature of diabetic cardiomyopathy (DCM), and excessive activation of cardiac fibroblasts plays a critical role in regulating cardiomyocyte function through paracrine signaling. CCN1 (cellular communication network factor 1), an extracellular matrix protein involved in intercellular communication, has been suggested to influence cardiac remodeling, although its specific impact on cardiomyocytes in DCM has remained unclear. In this study, we found that CCN1 expression was markedly elevated in cardiac tissues from DCM mouse models and in insulin-resistant cell models, with fibroblasts serving as the primary source. Proteomic analysis and co-culture experiments demonstrated that CCN1 suppressed cardiomyocyte macroautophagy/autophagy. To determine its role in vivo, we generated fibroblast-specific knockout mice and established a DCM model, demonstrating that deletion ameliorated cardiac dysfunction and restored autophagic activity. We further identified ITGAV-ITGB1/integrin αvβ1 as the receptor mediating CCN1 signaling in cardiomyocytes. Molecular dynamics simulations and co-immunoprecipitation experiments confirmed that CCN1 engaged ITGAV-ITGB1/integrin αvβ1 through its cysteine-knot-containing (CT) domain. Mechanistically, this interaction activated the downstream PTK2/FAK-MTOR signaling pathway, leading to inhibition of cardiomyocyte autophagy. Together, these findings reveal a previously unrecognized fibroblast-cardiomyocyte signaling axis in which fibroblast-derived CCN1 drives DCM progression by suppressing autophagy through ITGAV-ITGB1/integrin αvβ1-dependent signaling. This work provides mechanistic insight into the pathogenesis of DCM and identifies CCN1 as a potential therapeutic target for mitigating disease onset and progression.: AAV9: adeno-associated virus serotype 9; ADGRE1/EMR1/F4/80: adhesion G protein-coupled receptor E1; BafA1: bafilomycin A; BSA: bovine serum albumin; C8: compound 8; CCN1: cellular communication network factor 1; CF: cardiac fibroblast; CSA: cross-sectional area; DCM: diabetic cardiomyopathy; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; ELISA: enzyme-linked immunosorbent assay; HE: hematoxylin and eosin; HFD: high-fat diet; HG: high glucose; IR: insulin resistance; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MD: molecular dynamics; MTOR: mechanistic target of rapamycin kinase; NRCM: neonatal rat cardiomyocyte; PDGFRA: platelet derived growth factor receptor alpha; PECAM1/CD31: platelet and endothelial cell adhesion molecule 1; PTK2/FAK: protein tyrosine kinase 2; PTPRC/CD45: protein tyrosine phosphatase receptor type C; RPS6KB1: ribosomal protein S6 kinase B1; S100A4/FSP1: S100 calcium binding protein A4; SQSTM1/p62: sequestosome 1; STZ: streptozotocin; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling; WGA: wheat germ agglutinin. - Source: PubMed
Publication date: 2026/05/07
Hu Bo-AngZhang LeiSong MingKong Yan-RuJiao Ya-QiongJia XuZhu PingLi Yu-LinTi YunZhang WeiWang Zhi-HaoZhong Ming