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Клетки эндотелия капилляров кожи человека: CADMEC/HMVEC. Первичные клеточные линии Cell Applications. Human Dermal Microvascular Endothelial Cells: CADMEC/HMVEC

Клетки Эндотелия Капилляров Кожи (CADMEC/HMVEC) от Cell Applications, Inc. обеспечивают прекрасную модельную систему для изучения многих аспектов эндотелиальных функций и заболеваний, особенно связанных с микрососудистой и капиллярной системами. Эти клетки были торговой маркой Cell Applications, Inc. более 20 лет назад, когда они были впервые предложены, и CADMEC™ означало “Cell Applications’ Dermal Microvascular Endothelial Cells”. Было показано, что HMVEC/CADMEC экспрессируют vWF, CD36 и CD31, способны поглощать DiI-Ac-LDL и являются положительными на функциональную активность при цитокин-стимулированной адгезии лейкоцитов.

Избранные лоты HMVEC были дополнительно тестированы для демонстрации стимуляционно-зависимого ангиогенеза и ключевых для эндотелиальных клеток сигнальных путей (фосфорилирование VEGFR, Akt, MAPK, и экспрессию Tie2, eNOS, Axl и Etk/Bmx). Более подробную информацию смотрите в разделе Тестированные Эндотелиальные Клетки.

CADMEC/HMVEC от Cell Applications, Inc. были использованы во многих исследованиях, например:

• 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 от 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 от 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

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Эндотелий: клетки