Ask about this productRelated 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
- Etamsylate is a classical hemostatic agent, used to control bleeding in various clinical settings. Yet, the precise mechanism of its action is unknown. Hereby, we evaluated the complex effect of etamsylate on platelet-dependent hemostasis, with the aim of supplementing the model of its mechanism of action. Fluorescence microscopy was used to study thrombus formation under flow, exposure of phosphatidylserine (PS), P-selectin, and PECAM-1 in adhered platelets. Flow cytometry was utilized to assess activation markers in non-adhered platelets. Kinetics of clot formation was evaluated by thromboelastometry. Platelet aggregation and ATP secretion was measured by lumiaggregometry. Changes in cytosolic calcium level was measured fluorimetrically. We found that etamsylate (30-300 μM) dose-dependently enhanced platelet adhesion to collagen, as well as agonist-evoked platelet aggregation. Etamsylate per se induced platelet secretion and PS exposure and produced a rapid and sustained rise in cytosolic calcium level. These effects were substantially reduced by ADP receptors antagonists, or ADP/ATP scavenger - apyrase. Etamsylate enhanced platelet responses evoked by collagen and induced a loss of platelet PECAM-1 (negative regulator of collagen GPVI receptor), which was attenuated by calcium signaling blockers, and by calpain inhibitor. Etamsylate significantly augmented coagulation in whole blood, but not in plasma. Etamsylate amplifies a broad range of platelet responses, with particular ability to augment the action of collagen. This study provides insight into the mechanisms through which etamsylate exerts its hemostatic effect. This suggests new potential clinical perspectives for etamsylate usage in novel hemostatic therapies. - Source: PubMed
Publication date: 2026/04/18
Bołtromiuk ElżbietaGołaszewska AgataBielicka NataliaGromotowicz-Popławska AnnaRusak TomaszMisztal Tomasz - Atrophic nonunion is a challenging complication of fracture healing with few noninvasive therapeutic options. Given that sphingosine-1-phosphate (S1P) regulates bone remodeling and angiogenesis, systemic S1P modulation may offer a regenerative strategy; however, its efficacy in nonunion has not been established. - Source: PubMed
Publication date: 2026/04/08
Reinkemeier FelixKorte RalfBakri AliWallner ChristophDrysch MariusSchmidt Sonja VerenaFueth MariaPuscz FlemmingSteubing YoncaLevkau BodoLehnhardt MarcusBehr BjörnWagner Johannes Maximilian - Multiple myeloma (MM) cells interact with different components of the bone marrow (BM) microenvironment, which plays a critical role in MM progression and confers resistance to therapy. Here, we report that monocytes actively control MM cell metabolism by transferring mitochondria to MM cells, thereby increasing their mitochondrial content. Transfer of mitochondria required the expression of CD38 on the surface of MM cells and its ligand CD31 (PECAM-1) on monocytes. The mitochondrial increase in MM cells induced a boost in oxidative phosphorylation (OXPHOS). This monocyte-mediated metabolic adjustment promoted growth, motility, and drug-resistance in both MM cell lines and primary MM cells. Notably, the CD38-targeting monoclonal antibody daratumumab prevented mitochondrial transfer via blocking CD38 on MM cells. Furthermore, in the presence of daratumumab, monocytes acquired a divergent role and obtained mitochondria from MM cells through the process of trogocytosis. Daratumumab-mediated disruption of mitochondrial transfer reduced the mitochondrial content in MM cells, prevented the boost in OXPHOS, significantly impaired MM cell growth and migration, and mitigated drug-resistance. In conclusion, we reveal a crucial metabolic interplay between monocytes and MM cells within the BM microenvironment that promotes tumor growth and induces therapy resistance, providing the rationale for treatment strategies that combine targeting tumor metabolism with existing anti-MM agents. - Source: PubMed
Publication date: 2026/04/16
Raoof RaminDal Collo GiadaSimon-Molas HelgaTzortzi PanagiotaKulaj KonxheDemirez Elif NMassaro CrescenzoPoels RenéeKorst Charlotte L B MO'Neill Chloe ABruins Wassilis S CBroekmans Marloes E CBehradkia PayamKrevvata MariaZweegman SonjaKater Arnon PBaglio Serena RMutis Tunavan de Donk Niels W C J - Hyperglycemia and hypertension are primary contributors to chronic kidney disease (CKD), typically managed by dialysis or kidney transplantation. However, these treatments often have limited efficacy and can contribute to the progression of the disease. Tissue-engineered in vitro kidney models have emerged as promising tools for enhancing the understanding of disease mechanisms and supporting the development of targeted therapies. Yet, many existing models fail to replicate the complex structural and biochemical microenvironment of the native kidney. To address this, a biomimetic diabetic in vitro glomerular filtration barrier (GFB) using kidney-derived decellularized extracellular matrix hydrogel coating on a nanofibrous bacterial cellulose (BC) membrane. This scaffold provides both architectural support and essential cues that promote the attachment and growth of endothelial and podocyte cells. The model, when exposed to hyperglycemic conditions, exhibited altered expression of renal markers, including PECAM-1, nephrin, and podocin. Additionally, the developed model was treated with metformin, a widely used prescription medication, primarily for type 2 diabetes, to mitigate hyperglycemia-induced cellular damage. Functional validation of the hyperglycemic GFB model was performed by assessing the permeability of albumin, glucose, and creatinine, which revealed increased concentrations of these molecules in the filtrate region, indicating impaired filtration function. These results highlight the model's ability to recapitulate key pathological features of diabetic nephropathy but also demonstrate its partial reversal upon therapeutic intervention, thus offering a physiologically relevant platform for studying renal disease progression and screening nephrotoxic drugs, potentially reducing the need for animal models. - Source: PubMed
Publication date: 2026/04/15
Kiranmai GaddamKaki SamuelChameettachal ShibuGhosh AmitTs MeenuKhandelwal MudrikaPati Falguni - Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is definitive, potential curative therapy for various hematological diseases. Poor graft function (PGF) remains a significant complication, characterized by persistent cytopenia despite complete donor chimerism. The bone marrow microenvironment, particularly endothelial cells expressing CD31 (PECAM-1), plays a crucial role in the maintenance and proliferation of hematopoietic stem cells. This study examines the expression of CD31 in the bone marrow endothelial microenvironment of patients with Poor Graft Function (PGF) are compared with those exhibiting Good Graft Function (GGF) following allogeneic hematopoietic stem cell transplantation (allo-HSCT). - Source: PubMed
Publication date: 2026/04/10
Naguib Mary GamalAbdel-Ghafar Nermin Adel NabihMikhaeil Soha Raouf YoussefELKourashy Shaza Abdel-Wahab AhmedBakry Radwa Mohamed MahmoudMohamed Inas Abdelmoaty