(Cllick to Enlarge) Cell Applications Dermal Microvascular Endothelial Cells / Human Microvascular Endothelial Cells (CADMEC / HMVEC) Mono-layer (L), vessel-like structures formed in an angiogenesis assay (M), and immunolabeled for CD31/PECAM (green). Nuclei are visualized with PI (red) (R).
Human Dermal Microvascular Endothelial Cells: CADMEC/HMVEC
Description
Human Dermal Microvascular Endothelial Cells (CADMEC / HMVEC) from Cell Applications, Inc. provide an excellent model system to study many aspects of endothelial function and disease, especially those related to the microvasculature and capillary systems. These cells were trademarked by Cell Applications, Inc. over 20 years ago, when they were first offered, and CADMEC™ stands for “Cell Applications’ Dermal Microvascular Endothelial Cells”. HMVEC/CADMEC have been shown to express vWF, CD36 and CD31, are able to uptake DiI-Ac-LDL and are positive for functional activity by cytokine-stimulated leukocyte adherence.
Select HMVEC lots have been additionally tested to demonstrate stimulation-dependent angiogenesis and key endothelial cell signaling pathways (phosphorylation of VEGFR2). See the Pre-Screened Endothelial Cell Product Page for more information.
CADMEC/HMVEC from Cell Applications, Inc. have been used in numerous research publications, for example to:
- Show that cytokine-activated microvascular endothelial cells upregulate expression of α2-6-linked sialic acids which are the ligands for CD22 on the surface of the B cells, increasing the adhesion between the two cell types
- Show that IL-1, TNF and IFN stimulated ICAM-1 and E-selectin production by microvascular endothelial cells and resulted in a higher leukocyte adhesion that could be prevented by dexamethasone
- Demonstrate that FGF-2, but not FGF-13, induces proliferation of microvascular endothelial cells, and that neither growth factor affected IL-6 production
- Map VEGF signaling pathway by demonstrating that c-Src phosphorylates VEGFR-2 and IQGAP1, leading to activation of b-Raf, causing endotheial cell proliferation and angiogenesis
- Demonstrate that mechanical signals promote endothelial cell proliferation via VEGFR2/Akt signaling cascade leading to inactivation of GSK3β and preventing cyclin D1 degradation
- Show that endothelial permeability caused by advanced glycation end products results from RhoA/ROCK and p38 dependent moesin phosphorylation leading to actin reorganization
- Demonstrate, along with Human Coronary Artery Endothelial Cells, also from Cell Applications, Inc., the role of AMP-activated protein kinase (AMPK) in preservation of the tight junctions, explaining the heightened vascular permeability when AMPK is inhibited due to exposure to lipopolysaccharides during sepsis
- Demonstrate that the endothelial to mesenchymal transition associated with portal venous stenosis is mediated by increased serum levels of TGF-b1 in idiopathic portal hypertension patients, which induced fibroblast-like morphology, reduction of CD34 expression, and induction of α-smooth muscle actin, COL1A1 and phospho-Smad2, and that BMP-7 was able to prevent these changes (Kitao, 2009);
- Reveal a critical role for the α7 nAChR in mediating the effects of nicotine on the endothelium
- Show that abnormal matrix composition characteristic for systemic sclerosis, leads to reduced proliferation, reduced NO-to-O2- ratio, increased apoptosis, and altered protein expression associated with endothelial to mesenchymal transition, all leading to impaired vascular function and angiogenesis
- Develop anti-tumor apoptosis-inducing peptides that selectively target angiogenic cells and a targeted gene delivery system, PEI-g-PEG-RGD, for efficient expression of soluble fragment of VEGF receptor Flt-1 (sFlt-1) gene in order to inhibit tumor-related angiogenesis
- Identify a novel tumor-derived angiogenic factor, gastrin-releasing peptide, and its small molecule inhibitor, 77427
- Evaluate, along with Human Pulmonary Artery Endothelial Cells (HPAEC) and Human Umbilical Cord Vascular Endothelial Cells (HUVEC), all obtained from Cell Applications, Inc., the cytotoxic effects of a novel pore-forming protein, proposed as an anti-tumor agent
- To confirm the antioxidant and anti-inflammatory effects of blueberry and cranberry anthocyanins and hydroxycinnamic acids against H2O2 and TNFα induced damage to microvascular endothelial cells, by demonstrating reduction in oxidative stress and lowered production of IL-8, MCP-1 and ICAM-1 and show that procyanidins isolated from cocoa inhibit the expression of ErbB2 gene, decreasing cell proliferation and angiogenesis (Kenny, 2004);
- Demonstrate secretion of adipogenic factor(s) by microvascular endothelial cells
Details
| Tissue | Normal healthy human neonatal foreskin or adult skin capillaries | |
|---|---|---|
| QC | No bacteria, yeast, fungi, mycoplasma | |
| Character | Factor VIII-related Ag, DiI-Ac-LDL uptake | |
| Bioassay | Attach, spread, proliferate in Growth Med | |
| Cryovial | 500,000 CADMEC frozen in Basal Med w/ 10% FBS, 10% DMSO | |
| Kit | Cryovial frozen CADMEC (100-05), Gr Med (112-500), Subcltr Rgnt Kit, 2 Attchmnt Factor-Coated T-25 Flasks (121-25-02), Attchmnt Fctr Soln (123-100) | |
| Proliferating | Shipped in Tsfr Med, 3rd psg (flasks or plates) | |
| Doublings | At least 16 | |
| Applications | Laboratory research use only (RUO). Not for human, clinical, diagnostic or veterinary use. |
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