Anti-Mouse VEGFR-2 Monoclonal antibody (CABT-L4382) Functional Grade

Rat Anti-Mouse VEGFR-2 Monoclonal antibody for BL, WB


Host Species
Antibody Isotype
IgG1, κ
Species Reactivity
Mouse VEGFR-2||||SEAPs soluble receptor
Functional Grade


Alternative Names
KDR; kinase insert domain receptor (a type III receptor tyrosine kinase); FLK1; CD309; VEGFR; VEGFR2


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The mesenchymoangioblast, mesodermal precursor for mesenchymal and endothelial cells


Authors: Slukvin, Igor I.; Kumar, Akhilesh

Mesenchymoangioblast (MB) is the earliest precursor for endothelial and mesenchymal cells originating from APLNR(+)PDGFR alpha+KDR+ mesoderm in human pluripotent stem cell cultures. MBs are identified based on their capacity to form FGF2-dependent compact spheroid colonies in a serum-free semisolid medium. MBs colonies are composed of PDGFR beta(+)CD271(+)EMCN(+)DLK1(+)CD73(-) primitive mesenchymal cells which are generated through endothelial/angioblastic intermediates (cores) formed during first 3-4 days of clonogenic cultures. MB-derived primitive mesenchymal cells have potential to differentiate into mesenchymal stromal/stem cells (MSCs), pericytes, and smooth muscle cells. In this review, we summarize the specification and developmental potential of MBs, emphasize features that distinguish MBs from other mesenchymal progenitors described in the literature and discuss the value of these findings for identifying molecular pathways leading to MSC and vasculogenic cell specification, and developing cellular therapies using MB-derived progeny.

Improvement in circulating endothelial progenitor cells pool after cardiac resynchronization therapy: increasing the list of benefits


Authors: Cristovao, Goncalo; Milner, James; Sousa, Pedro; Ventura, Miguel; Cristovao, Joao; Elvas, Luis; Paiva, Artur; Goncalves, Lino; Ribeiro, Carlos Fontes; Antonio, Natalia

Background Recent studies suggest that circulating endothelial progenitor cells (EPCs) may influence the response to cardiac resynchronization therapy (CRT). The aim of this study was to evaluate the effect of CRT on EPC levels and to assess the impact of EPCs on long-term clinical outcomes. Population and methods Prospective study of 50 patients submitted to CRT. Two populations of circulating EPCs were quantified previously to CRT implantation: CD34(+)KDR(+) and CD133(+)KDR(+) cells. EPC levels were reassessed 6 months after CRT. Endpoints during the long-term follow-up were all-cause mortality, heart transplantation, and hospitalization for heart failure (HF) management. Results The proportion of non-responders to CRT was 42% and tended to be higher in patients with an ischemic vs non-ischemic etiology (64% vs 35%, p = 0.098). Patients with ischemic cardiomyopathy (ICM) showed significantly lower CD34(+)KDR(+) EPC levels when compared to non-ischemic dilated cardiomyopathy patients (DCM) (0.0010 +/- 0.0007 vs 0.0030 +/- 0.0024 cells/100 leukocytes, p = 0.032). There were no significant differences in baseline EPC levels between survivors and non-survivors nor between patients who were rehospitalized for HF management during follow-up or not. At 6-month follow-up, circulating EPC levels were significantly higher than baseline levels (0.0024 +/- 0.0023 vs 0.0047 +/- 0.0041 CD34(+)KDR(+) cells/100 leukocytes, p = 0.010 and 0.0007 +/- 0.0004 vs 0.0016 vs 0.0013 CD133(+)/KDR+ cells/100 leukocytes, p = 0.007). Conclusions Patients with ICM showed significantly lower levels of circulating EPCs when compared to their counterparts. CRT seems to improve the pool of endogenously circulating EPCs and reduced baseline EPC levels seem not to influence long-term outcomes after CRT.

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