PECAM1 Antibody
- Known as:
- PECAM1 Antibody
- Catalog number:
- CJC-005175-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- 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
- Gestational diabetes mellitus (GDM) is linked to altered fetal development and an increased risk of offspring developing cardiometabolic diseases in adulthood. The mechanisms responsible are unclear; however, GDM is associated with altered fetoplacental vascularisation, fibrosis and endothelial dysfunction. In non-pregnant individuals with diabetes, similar vascular changes are attributed to disruptions in endothelial-to-mesenchymal transition (EndMT), a key process where endothelial cells adopt a mesenchymal phenotype. Here, we assess whether alterations in the fetoplacental macro- and microvasculature are attributed to EndMT, using human umbilical vein endothelial cells (HUVECs) and human term placental tissue, respectively. Transforming growth factor (TGF)-β2 and interleukin (IL)-1β induced morphological and molecular changes consistent with EndMT in both GDM and non-GDM HUVECs. The ability of TGF-β2 and IL-1β to alter expression of known EndMT regulators, VWF, TGFBR1, IL1B and IL1R1, was diminished in GDM HUVECs; however, all other hallmarks of EndMT were similar. In placental villous tissue, Slug and Snail, two key transcriptional regulators of EndMT, were detected in the villous stroma, suggesting that EndMT probably occurs in the placental microvasculature. We observed a reduction in endothelial marker genes PECAM1, VWF and CDH5 in GDM placentas, suggesting reduced placental vascularisation. This was accompanied by a reduction in EndMT regulators SNAI2, TGB2, TGFB3 and TGFBR2; however, there was no change in mesenchymal markers or other EndMT regulators. This suggests that there may be some alterations in EndMT in GDM but this probably does not fully explain the endothelial dysfunction and altered vascularisation that occurs in the fetoplacental vasculature in pregnancies complicated by GDM. KEY POINTS: Gestational diabetes mellitus (GDM) has been linked to altered placental vascularisation, fibrosis and endothelial dysfunction. Disruptions in endothelial-to-mesenchymal transition (EndMT), a process where endothelial cells adopt a mesenchymal phenotype, has been linked to vascular complications in diabetes, but EndMT in GDM has not been investigated. Transforming growth factor (TGF)-β2 and interleukin (IL)-1β induced morphological and molecular changes consistent with EndMT in GDM and non-GDM human umbilical vein endothelial cells (HUVECs). Although the expression of EndMT mediators, VWF, TGFBR1, IL1B, and IL1R1, was diminished in GDM HUVECs, other EndMT hallmarks were similar. Transcriptional regulators of EndMT, Slug and Snail, were detected in the human term placenta. Despite a reduction in endothelial markers, PECAM1, VWF and CDH5, as well as SNAI2, TGFB2/3 and TGFBR2 in GDM placenta, there was no change in mesenchymal or other EndMT markers. This suggests that, although there may be some changes to EndMT in GDM, the vascular dysfunction is probably not explained fully by alterations in EndMT. - Source: PubMed
Publication date: 2025/05/11
Byford Abigail RFakonti GeorgiaShao ZiyuSoni SharanamEarle Sophie LBajarwan MuathMorley Lara CHolder BethScott Eleanor MForbes Karen - Necrosis at the ischemic distal end of flap transplants increases patients' pain and economic burden. Reactive oxygen species (ROS) and mitochondrial damage are crucial in regulating parthanatos, but the mechanisms linking disrupted macroautophagic/autophagic flux to parthanatos in ischemic flaps remain unclear. The results of western blotting, immunofluorescence staining, and a proteomic analysis revealed that the autophagic protein SNAP29 was deficient in ischemic flaps, resulting in disrupted autophagic flux, increased ROS-induced parthanatos, and aggravated ischemic flap necrosis. The use of AAV vector to restore SNAP29 mitigated the disruption of autophagic flux and parthanatos. Additionally, quantification of the total mA level and RIP-qPCR, MeRIP-qPCR, and RNA stability assessments were performed to determine differential mRNA mA methylation levels and mRNA stability in ischemic flaps. Various and tests were conducted to verify the ability of METTL3-mediated mA methylation to promote SNAP29 depletion and disrupt autophagic flux. Finally, we concluded that restoring SNAP29 by inhibiting METTL3 and YTHDF2 reversed the "autophagy-mitochondrial crisis", defined for the first time as disrupted autophagic flux, mitochondrial damage, mitochondrial protein leakage, and the occurrence of parthanatos. The reversal of this crisis ultimately promoted the survival of ischemic flaps.: AAV = adeno-associated virus; ACTA2/α-SMA = actin alpha 2, smooth muscle, aorta; AIFM/AIF = apoptosis-inducing factor, mitochondrion-associated; ALKBH5 = alkB homolog, RNA demythelase; Baf A1 = bafilomycin A; CQ = chloroquine; DHE = dihydroethidium; ECs = endothelial cells; F-CHP = 5-FAM-conjugated collagen-hybridizing peptide; GO = gene ontology; HUVECs = human umbilical vein endothelial cells; KEGG = Kyoto Encyclopedia of Genes and Genomes; LC-MS/MS = liquid chromatography-tandem mass spectrometry; LDBF = laser doppler blood flow; mA = N6-methyladenosine; MAP1LC3/LC3 = microtubule-associated protein 1 light chain 3; MeRIP = methylated RNA immunoprecipitation; METTL3 = methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit; NAC = N-acetylcysteine; OGD = oxygen glucose deprivation; PAR = poly (ADP-ribose); PARP1 = poly (ADP-ribose) polymerase family, member 1; PECAM1/CD31 = platelet/endothelial cell adhesion molecule 1; ROS = reactive oxygen species; RT-qPCR = reverse transcription quantitative polymerase chain reaction; RIP = RNA immunoprecipitation; SNAP29 = synaptosomal-associated protein 29; SNARE = soluble N-ethylmaleimide-sensitive factor attachment protein receptor; SQSTM1 = sequestosome 1; SRAMP = sequence-based RNA adenosine methylation site predicting; STX17 = syntaxin 17; TMT = tandem mass tag; TUNEL = terminal deoxynucleotidyl transferase dUTP nick end labeling; VAMP8 = vesicle-associated membrane protein 8; WTAP = WT1 associating protein; YTHDF2 = YTH N6-methyladenosine RNA binding protein 2; 3' UTR = 3'-untranslated region. - Source: PubMed
Publication date: 2025/05/08
Yang NingningLai YingyingYu GaoxiangZhang XuziShi JingweiXiang LinyiZhang JiachengWu YuzheJiang XiaoqiongZhang XuanlongYang LiangliangGao WeiyangDing JianWang XiangyangXiao JianZhou Kailiang - Endothelial-to-mesenchymal transition (EndMT) is a biological process that converts endothelial cells to mesenchymal cells with increased proliferative and migrative abilities. EndMT has been implicated in the development of pulmonary vascular remodeling in pulmonary arterial hypertension (PAH), a fatal and progressive lung vascular disease. Transforming growth factor β1 (TGF-β1), an inflammatory cytokine, is known to induce EndMT in many types of endothelial cells including lung vascular endothelial cells (LVEC). An increase in cytosolic free Ca concentration ([Ca]) is a major stimulus for cellular proliferation and phenotypic transition, but it is unknown whether Ca signaling is involved in EndMT. In this study we tested the hypothesis that TGF-β1-induced EndMT in human LVEC is Ca-dependent. Treatment of LVEC with TGF-β1 for 5-7 days resulted in increase in SNAI1/2 expression, induction of EndMT, upregulation of STIM/Orai1 and enhancement of store-operated Ca entry (SOCE). Removal (or chelation) of extracellular or intracellular Ca with EGTA or BAPTA-AM respectively abolished EndMT in response to TGF-β1. Moreover, EGTA diminished TGF-β1-induced increase in SNAI in a dose-dependent manner. Knockdown of either STIM1 or Orai1 was sufficient to prevent TGF-β-mediated increase in SNAI1/2 and EndMT, but did not rescue the continuous adherent junctions. Blockade of Orai1 channels by AnCoA4 inhibited TGF-β-mediated EndMT and restored PECAM1-positive continuous adherent junctions. In conclusion, intracellular Ca signaling plays a critical role in TGF-β-associated EndMT through enhanced SOCE and STIM1-Orai1 interaction. Thus, targeting Ca signaling pathways regulating EndMT may be a novel therapeutic approach to treat PAH and other forms of pre-capillary pulmonary hypertension. - Source: PubMed
Publication date: 2025/05/07
Babicheva AleksandraElmadbouh IbrahimSong ShanshanThompson MichaelPowers RyanJain Pritesh PIzadi AminChen JiyuanYung LaurenParmisano SophiaPaquin ColeWang Wei-TingChen YuqinWang TingAlotaibi MonaShyy John Y-JThistlethwaite Patricia AWang JianMakino AyakoPrakash Y SPabelick Christina MYuan Jason X-J - Our previous findings demonstrated that naïve B cells elicit suppressive CD4 regulatory T (Treg) cells, named as Treg-of-B cells. However, the capability of antigen-specific B cells in that process remains unclear. Using ovalbumin (OVA) as a model antigen, the present study showed that B cells from OVA-immunised mice decreased that ability. Instead, OVA-activated OVA-specific (OB1) B cells induced effector-like T-of-OB1 cells without regulatory function. Phenotypically, Treg-of-B cells reduced the production of interferon (IFN)-γ, interleukin (IL)-17 and IL-2 and expressed CD62L, PD1 and endothelial cell adhesion molecule 1 (PECAM1). Functionally, adoptive transfer of Treg-of-B cells significantly attenuated Th1 cell-mediated delayed-type hypersensitivity (DTH) responses and inhibited IFN-γ-producing Th1 cells, while T-of-OB1 cells did not. Mechanistically, activated antigen-specific B cells increased the expression of costimulatory molecules and promoted higher T cell activation, contributing to effector T cell phenotype. Conversely, Treg-of-B cells exhibited lower T cell activation, possibly mediated through the expression of PECAM1, Dusp2, Dusp5, Ptpn7, Ptpn22 and Ms4a4b. These findings suggest that non-antigen-specific B cells elicit CD4 Treg cells, potentially via attenuating T cell activation, whereas that capacity is absent in antigen-specific B cells. This distinction underscores the critical role of B cell antigen specificity in immune regulation and inflammation. - Source: PubMed
Publication date: 2025/05/04
Chien Chien-HuiYeh Tsai-YingChiang Bor-Luen - Vascular comorbidities complicate stroke pathophysiology, worsen outcomes, and delay recovery. Obesity, in particular, significantly increases stroke-induced brain edema, a fatal complication during infarction, which leads to worsened long-term recovery. Treatment of aflibercept, a VEGF-trap, has been shown to reduce stroke-induced brain edema and attenuate acute neurological deficits in obese mice. However, the effect of aflibercept on long-term stroke recovery is unknown. We found that treating obese stroke mice with aflibercept at 3 hours displayed significantly improved long-term motor and cognitive function. Notably, VEGFR2 expression was upregulated at 3- and 7-days post-stroke, indicating sustained VEGF signaling in obese subjects. Unlike acute treatment of aflibercept at 3 hours post-stroke, delayed treatment (3-day) worsened stroke recovery. While the improved long-term stroke recovery in mice treated aflibercept 3 hours is associated with the upregulated Pecam-1 and Angiopoietin-1 mRNAs and vessel densities in peri-infarct area at 3 months post-stroke, the delayed treatment led to a reduction in both angiogenic marker expression and vessel density. These findings highlight the importance of early intervention with VEGF signaling in obese mice to promote subsequent vascular remodeling during the stroke recovery phase and indicate a critical therapeutic window for VEGF inhibition to treat stroke in subjects with vascular comorbidities. - Source: PubMed
Publication date: 2025/05/02
Ju HyunwooMinker JosephPavlova InaCho SungheeKim Il-Doo