Showing posts with label VEGF. Show all posts
Showing posts with label VEGF. Show all posts

Tuesday, November 12, 2019

Human Brain Microvascular Endothelial Cells and BBB

Fc-saxatilin used to Modulate Blood-Brain Barrier (BBB)
Highlights
•Fc-saxatilin prevents VEGF-induced permeability in Neuromics' human brain microvascular cells (HBMECs).
 •Fc-saxatilin inhibits VEGF-induced Src and Fak phosphorylation in HBMECs.
 •Fc-saxatilin blocks the downregulation of claudin-5 expression by VEGF in HBMECS.

Hyun-Jung Choi, Na-Eun Kim, Il Kwon, Dukhwan Choi, Jayoung Kim, Ji Hoe Heo. (2019). Fc-saxatilin inhibits VEGF-induced permeability by regulating claudin-5 expression in human brain microvascular endothelial cells. Microvascular Research. DOI: https://doi.org/10.1016/j.mvr.2019.103953

Figure: Fc–saxatilin attenuates the phosphorylation of Fak induced by VEGF. A) HBMECs were treated with pretreated with vehicle (PBS, 0) or Fc-saxatilin (50, 100, or 300 ng/ml) in the basal medium (0.5% FBS) for 10 min and treated with VEGF (100 ng/ml) for 1 h. Control cells were incubated in the control medium without Fc-saxatilin and VEGF. Cell lysates were subjected to an immunoblot analysis with antibodies against either phospho-Fak, Fak, or actin, as indicated. Representative data from three separate experiments are shown. B) Bands in the immunoblots were quantified using ImageJ and normalized to actin (n = 3); *P < 0.05 compared to the vehicle only-treated control or VEGF-treated control.

These cells are also used to formulate our 3-D Blood-Brain Barrier Model.

Saturday, September 26, 2015

Retinal Microvascular Endothelial Cells & Diabetic Retinopathy

HRMECS in Action

Our Human Retinal Microvascular Endothelial Cells in this publication on Diabetic Retinopathy. In this study, the authors show that human retinal microvascular endothelial cells exposed to high levels of glucose regulate miR-200b repression through histone methylation and that inhibition of PRC2 increases miR-200b while reducing VEGF: Michael Anthony Ruiz, Biao Feng, and Subrata Chakrabarti. Polycomb Repressive Complex 2 Regulates MiR-200b in Retinal Endothelial Cells: Potential Relevance in Diabetic Retinopathy. PLoS One. 2015; 10(4): e0123987. Published online 2015 Apr 17. doi: 10.1371/journal.pone.0123987...To investigate PRC2 and miR-200b regulation in the context of diabetic retinopathy, the major cell type used for investigation was the human retinal microvascular endothelial cell (HRMECs,Neuromics/ Olaf Pharmaceuticals, Worchester, MA, Cat# HEC09)...

Figure: High levels of glucose alter VEGF and miR-200b expression in HRMECs. A: HRMECs exposed to various concentrations of D-glucose for 24 hours exhibited differential mRNA levels of VEGF. Compared to 5mM D-glucose, VEGF expression was significantly increased at 15mM and 25mM D-glucose concentrations, with no change at 20mM L-glucose. B: Measured by WST-1 assay, HRMECs exposed to increasing concentrations of D-glucose for 24 hours exhibited decreased cell viability at 25mM, 50mM and 100mM compared to 5mM. C: HRMECs exposed to 25mM (high glucose; HG) glucose for 24 and 48 hours demonstrated significantly increased VEGF mRNA compared to 5mM (normal glucose; NG). These differences were not observed at time points earlier than 24 hours. D,E: HRMECs exposed to 5mM D-glucose (NG) 25mM D-glucose (HG) and 20mM L-glucose+5mM D-glucose (osmotic control; OSM). HRMECs cultured for 24 hours and 48 hours in HG showed significantly decreased levels of miR-200b with parallel increased levels of VEGF expression compared to NG and OSM. F,G: VEGF is also increased at the protein level in HG compared to NG as measured by Western Blotting. [* p < 0.05 compared to NG; n = 6; data expressed as mean ± SEM, normalized to β-actin or U6 and expressed as a fold change of NG]. doi:10.1371/journal.pone.0123987.

Check out our growing catalog of Human Endothelial Cells-Artery, Microvascular, Vein, Umbilical Cord Derived + Culture Media.

Tuesday, January 27, 2015

Human Growth Factor+Neurotrophin+Cytokine Array-Test 40 Markers in on Assay

Sensitive, Specific and Cost Effective

Neuro-immuno and degenerative diseases and disorders commonly show dysregulation of Growth Factors and Cytokines. Using our Quantibody Neuroscience Arrays, we have measured the blood serum of clients with Neuro-inflammatory/immune response diseases/disorders including Autism Spectrum Disorder (ASD). Most showed lowered levels of Growth Factors/Neurotrophins and elevated levels of Inflammatory Response Cytokines.

In order to expand the number of biomarkers measured, we are pleased to announce the addition of our New Growth Factor+Neurotrophin+Cytokine Array. This will enable us to further determine the "finger prints" of these diseases/disorders at the protein level. This array includes: Immunogen: Amphiregulin, BDNF, bFGF, BMP-4, BMP-5, BMP-7, beta-NGF, EGF, EGFR, EG-VEGF (PK1), FGF-4,FGF-7 (KGF), GDF-15, GDNF, Growth Hormone, HB-EGF, HGF, IGFBP-1, IGFBP-2, IGFBP-3, IGFBP-4, IGFBP-6, IGF-1, Insulin, M-CSF R, NGFR (TNFRSF16), NT-3, NT-4, Osteoprotegerin (TNFRSF11B), PDGF-AA, PLGF, SCF, SCF R (CD117/c-kit), TGF alpha, TGF beta 1, TGF beta 3, VEGF-A, VEGFR2, VEGFR3 and VEGF-D.

I will continue to post testing results here.