Ask about this productRelated genes to: PROCR antibody
- Gene:
- PROCR NIH gene
- Name:
- protein C receptor
- Previous symbol:
- -
- Synonyms:
- EPCR, CCD41, CD201
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-26
- Date modifiied:
- 2019-04-23
Related products to: PROCR antibody
Related articles to: PROCR antibody
- The selection of appropriate in vitro inflammatory models is critical for mechanistic studies of neuroinflammation and the screening of anti-inflammatory therapeutics. Lipopolysaccharide (LPS) combined with interferon-γ (IFN-γ) and LPS combined with adenosine triphosphate (ATP) are widely used to induce microglial inflammation; however, their distinct phenotypic characteristics and optimal applications have not been systematically compared. In this study, we combined transcriptomic profiling with functional assays to compare these two inflammatory paradigms in BV2 microglia. Our results showed that both models activated the chemokine-cytokine inflammatory network and induced the production of inflammatory mediators and chemokines, but exhibited distinct molecular and functional biases. LPS/IFN-γ stimulation preferentially upregulated genes such as Lcn2, Ccl2, Upp1, and Pim2, which are associated with innate immune activation, chemokine-mediated inflammatory responses, and cell survival signaling, and was accompanied by marked increases in NO and TNF-α production. In contrast, the LPS/ATP model preferentially upregulated genes associated with ECM/cell adhesion, inflammatory and cellular homeostatic regulation, oxidative stress, and calcium-dependent secretion, including Thbs1, Thbd, Srxn1, Syt7, and Procr. Functionally, this model exhibited more pronounced IL-1β maturation and release, relatively lower NO production, and greater mitochondrial dysfunction and cell injury. Pharmacological inhibition of NLRP3 with MCC950 significantly attenuated ATP-induced IL-1β maturation, supporting the involvement of the NLRP3 inflammasome in the LPS/ATP model. Overall, the LPS/IFN-γ model is more suitable for investigating the NO/iNOS-TNF-α axis, IFN-γ-mediated synergistic pro-inflammatory responses, and classical pro-inflammatory activation, as well as for screening anti-inflammatory agents. In contrast, the LPS/ATP model is more appropriate for studying IL-1β maturation and release, NLRP3 inflammasome activation, mitochondrial damage, and inflammation-related cell death, as well as for screening inflammasome inhibitors. Our findings provide an empirical framework for rational model selection in microglial inflammation research. - Source: PubMed
Publication date: 2026/08/07
Zhang XinfengLian ZhuoLei SijieYi TanhuiZhao ShuyinLiu MingxiangGui YilingZhu ChengyiXie QianMa Rong - The functional and molecular definition of progenitors giving rise to blood vessel endothelium in vivo remains disputed. Upon investigating the overlap of seemingly divergent reports currently defining putative endothelial progenitor cells (EPCs) using single-cell RNA-sequencing and flow cytometry, Protein C Receptor (PROCR) and Platelet-Derived Growth Factor Receptor Alpha (PDGFRA) largely overlapped with previously characterized murine aorta's CD34CD31 endovascular progenitors (EVPs). Functional assays and lineage tracing in homeostatic aorta and excisional wounds demonstrated increased clonogenic capacity, engraftment potential, and ability to form differentiated endothelial (D) cells of PROCR PDGFRA EPCs, termed as refined endothelial progenitor cell (rEPC), as compared to PROCRPDGFRA EVPs. Similar PROCR and PDGFRA expression in normal human aorta, and increased clonogenic capacity of CD34CD31PROCR endothelial cells from freshly isolated human term placenta were observed as compared to controls. Functional validation of human rEPCs is supported by PROCR enrichment, while PDGFRA co‑expression in human endothelial progenitor-like cells is supported at the transcriptomic level only. Thus, overlapping PROCR and PDGFRA expression in EVPs narrows the population with true functional progenitor capacity. - Source: PubMed
Publication date: 2026/08/01
Styke CassandraKaur SimranpreetSim Seen-LingZhao JilaiZhou ChenhaoWong Ho YiPatel JatinRoy EdwigeYoder Mervyn CHarvey Richard PShafiee AbbasKhosrotehrani Kiarash - Venous thromboembolism (VTE) is multifactorial, and established hereditary risk factors explain only part of heritable risk. The protein C (PC) pathway is central to anticoagulant control, and common variants in thrombomodulin and endothelial protein C receptor genes (THBD, PROCR) have been proposed as modulators. In 73 participants, we used standardized in vivo coagulation activation with recombinant activated factor VII (15 µg/kg) and measured thrombin markers and activated protein C (APC) over 8 hours. Endothelial colony-forming cell-based ex vivo experiments were performed in 43 participants. In vivo, the APC area-under-the-curve (AUC)/thrombin-antithrombin complex (TAT) AUC ratio, reflecting the endogenous anticoagulant response relative to thrombin generation, provided the best model fit (adjusted R2=0.345). The APC response was lower in individuals with previous VTE (median 0.13 vs. 0.26; P=.009) and PROCR 655A>G carriers (0.11 vs. 0.26; P=.014), but higher in factor V Leiden (FVL) carriers (0.32 vs. 0.14; P=4.3×10-4) and THBD 1418C>T carriers (0.38 vs. 0.13; P=.032). The THBD 1418C>T effect was driven by reduced TAT AUC (30.6 vs. 82.7 pmol×h/L; P=.032), while the PROCR 655A>G effect reflected a lower APC AUC (8.6 vs. 10.7 pmol×h/L; P=0.04998). Ex vivo, the APC AUC/thrombin AUC ratio was lower with previous VTE and PROCR 655A>G, higher with FVL, and not associated with THBD 1418C>T. No in vivo or ex vivo association was observed for PROCR 4678C>G. This study provides in vivo evidence that common THBD and PROCR variants modulate PC pathway function, establishing the APC response as a sensitive endpoint for subtle genetic effects beyond FVL. - Source: PubMed
Publication date: 2026/07/21
Reda SaraSchwarz NadineEckert SebastianMüller JensOldenburg JohannesPötzsch BerndPezeshkpoor BehnazRühl Heiko - Malignant melanoma has a strong propensity for early metastatic dissemination, yet conventional clinicopathological predictors such as Breslow thickness do not fully capture individual metastatic risk. The endothelial protein C receptor (EPCR) exerts context-dependent functions across malignancies, but its clinical significance in melanoma remains unclear. We retrospectively analyzed primary tumor specimens from 62 patients with invasive melanoma; 61 with complete outcome data formed the analytic cohort for metastasis analyses. EPCR expression in melanoma cells was evaluated by immunohistochemistry using semi-quantitative intensity and extent scores (0-3). Tumor-infiltrating lymphocytes were graded according to the Melanoma Institute Australia scoring system. Higher EPCR expression was associated with lower odds of documented lymph-node and distant metastatic involvement. In prespecified parsimonious multivariable logistic regression models adjusted for tumor thickness and ulceration, higher EPCR extent remained independently associated with reduced lymph-node involvement (adjusted odds ratio: 0.36, 95% confidence interval:, 0.17-0.70). EPCR expression showed a positive association with CD8+ tumor-infiltrating lymphocyte scores. Higher EPCR expression in primary melanoma was independently associated with reduced lymph-node involvement and with a CD8+-inflamed tumor microenvironment, suggesting EPCR may complement conventional pathological predictors of metastatic risk. - Source: PubMed
Publication date: 2026/07/14
Fusumae TakayukiFunakoshi TakeruHirai IkukoNakamura YoshioFukuda KeitaroIwata TakashiAmagai MasayukiTanese Keiji - - Source: PubMed
Publication date: 2026/06/30
Smadja David M