## Abstract Porous polystyrene (PS) membranes with pore sizes ranged from nanometer scale to several decades' micrometers were fabricated by the thermally induced phase‐separation technique, and were characterized by scanning electron microscopy (SEM). Oxidation of PS membranes by concentrated sulf
Reduced viability of human vascular endothelial cells cultured on Matrigel™
✍ Scribed by Varpu Ranta; Tomi Mikkola; Olavi Ylikorkala; Lasse Viinikka; Arto Orpana
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 235 KB
- Volume
- 176
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Optimal vascular homeostasis requires efficient control of both proliferation and elimination of vascular endothelial cells. Programmed cell death, or apoptosis, is the main mechanism controlling cell elimination, and it is an essential component of vascular formation. Human vascular endothelial cells die in vitro, if prevented from obligatory survival factors like growth factors or attachment and cell spreading, but very little is known about the mechanisms controlling endothelial cell elimination. Signaling from the extracellular matrix affects the behavior and functions of human umbilical vein endothelial cells (HUVECs), and we have recently demonstrated the beneficial effects of plating on the reconstituted extracellular matrix Matrigel TM , on the inducible nitric oxide production of freshly isolated HUVECs. In this work we observed that cultured HUVECs formed typical capillary-like structures on Matrigel, but unexpectedly, after 24-48 hours their viability was gradually lost. Viability was measured with an assay based on mitochondrial reduction of reagent XTT. No decrease in viability was seen in freshly isolated HUVECs or in cultured fibroblasts during this time. It is known that cells often turn into apoptosis if they receive conflicting information from their surroundings, and apparently signaling from Matrigel to HUVECs, while at their in vitro proliferating phenotype, resulted in launching of the apoptotic machinery. Thus, proliferating and differentiated phenotypes of endothelial cells seemed to have different sensitivity to signals that induce apoptosis.
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