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
- Mice as model organisms play a vital role in translational research for developmental biology by aiding our understanding of embryonic and placental evolution in health and various disease states. The close similarity between mouse and human placentas is a great asset in reproductive translational research, making the mouse one of the more prominent model organisms in this field. Mice are routinely used to investigate mechanisms of embryonic and placental development, often through experimental manipulations involving engineered or spontaneous genetic mutations and/or xenobiotic treatments. A crucial aspect of fully appreciating the mouse as a model organism for placental research is understanding the anatomy and physiology of the major embryonic (chorion, labyrinth, junctional zone, and yolk sac) and maternal (decidua basalis and metrial gland) placenta components, including knowledge of the specific cell types active during each gestational stage. This paper discusses histochemical and immunohistochemical (IHC) methods that highlight specific tissue layers and cell types present during normal development of the mouse placenta and maternal metrial gland. Altered numbers and/or locations of these common cell types have been demonstrated in embryonic lethal phenotypes, indicating that placental assessments must examine not only the tissue organization but also affected cell populations when determining the cause of early pregnancy loss. - Source: PubMed
Publication date: 2026/05/15
Elmore Susan ACochran Robert ZGanta CharanJensen HeatherLubeck Beth AMahler BethSabio DavidStamper GregBolon Brad - Ex vivo lung perfusion (EVLP) has emerged as a strategy to assess and extend preservation of donor lungs prior to transplantation. However, due to progressive deterioration of the graft, current protocols limit EVLP duration to 10-12 hours. We developed an optimized cellular perfusate, DEVOL solution, designed to support multi-day EVLP and evaluated its performance against standard TransMedics OCS perfusate. - Source: PubMed
Publication date: 2026/05/13
Arnold C JNakata KHassan AAlderete IAykun NAbraham NCarney JXiang YKamaleswaran RJiang HHughes Barbas A SHartwig M G - Cerebral ischemic stroke is caused by impaired blood flow to the brain parenchyma due to acute vessel occlusion. Although current therapies focusing on rapid restoration of blood flow achieve high rates of recanalization, outcomes remain unfavorable in a significant proportion of patients. Part of this discrepancy is due to intravascular inflammation driven by thrombo-inflammatory mechanisms that add to cerebral tissue loss. Despite being an inevitable consequence of vessel occlusion, altered shear stress remains largely overlooked as a contributor to endothelial dysfunction in stroke. To directly assess the impact of disturbed flow on the endothelial phenotype, human brain endothelial cells were cultured under controlled flow conditions using an ibidi pump system and exposed to flow alternating in both magnitude and direction. Subsequently, the expression of key endothelial proteins, including Claudin-5, PECAM-1, CD62e and endoglin, was analyzed. We show here that the sequence of shear-stress modulation, recapitulating the hemodynamic conditions of large-vessel occlusion and subsequent reperfusion in stroke, is sufficient to cause an inflammatory phenotype in human brain endothelial cells. In addition, we demonstrate that platelet activation induces the mechanosensors Piezo1 and syndecan-1, sensitizing brain endothelial cells to shear-stress alterations characteristic of ischemic stroke. Targeting shear-stress-mediated inflammatory activation of the brain endothelium may therefore offer a complementary strategy in stroke therapy, particularly in large-vessel occlusion with abrupt flow changes. - Source: PubMed
Publication date: 2026/04/24
Cordes Yann LDao Huy VietZapantis NikolaosVogt VivianSchuhmann Michael KHaarmann Axel - 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