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V Shah

Publications and source records attributed to V Shah.

169 records · Page 10Linked to original sources
PubMedDate not supplied

Metastasis of human colon tumor cells in vivo: correlation with the overexpression of plasminogen activators and 72 kDa gelatinase.

Metastatic spread of tumor cells depends upon intravasation of malignant cells from the primary site and extravasation into the distant organs following remodeling of the basement membrane. We have investigated the metastatic potential of five tumorigenic human colon carcinoma cell lines, LS 174T, SW 620, WiDr, SW 480 and Caco-2 using intrasplenic injection in nude mice. LS 174T is most aggressive causing liver metastasis in all animals within 6 weeks. SW 620 and WiDr produced liver metastasis in 70% and 30% of the animals but after a period of 12 weeks whereas SW 480 and Caco-2 were not metastatic. LS 174T exhibited high cell-associated urokinase-type plasminogen activator (u-PA) and high secreted u-PA and tissue plasminogen activator (t-PA) levels. WiDr, SW 480 and Caco-2 had essentially similar low levels of cell associated u-PA but WiDr had higher secreted u-PA levels as comprated to the SW 480 and Caco-2 cells. The level of secreted MMP-2 (72 kDa gelatinase) was highest in the most metastatic cell line, LS 174T, and lower in other less metastatic ones. These data show that metastatic behavior of human colon tumor cells correlates with the enhanced secretion of plasminogen activators and MMP-2 by these cells.

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PubMedDate not supplied

Pycnogenol protects vascular endothelial cells from t-butyl hydroperoxide induced oxidant injury.

The active oxygen induced and free radical mediated oxidation of biological molecules, membranes, and tissues has been suggested as a major cause of cancer, atherosclerosis, and aging. Damage of endothelial cells may lead to cardiovascular and cerebrovascular diseases. In the present study, the antioxidant effect of pycnogenol (procyanidins extracted from Pinus maritima) was investigated in vitro using vascular endothelial cells. Confluent monolayers of bovine pulmonary artery endothelial cells (PAEC) were preincubated with different concentrations of pycnogenol for 16 h, washed, and then exposed to an organic oxidant t-butyl hydroperoxide (tBHP) for 3 or 4 h. Cellular injury was assessed by measuring cell viability with methylthiazol tetrazolium (MTT) assay and by determining the release of intracellular lactate dehydrogenase (LDH). Lipid peroxidation products of PAEC were monitored as malondialdehyde (MDA) with a thiobarbituric acid fluorometric assay. Incubation of tBHP (75, 100, or 125 microM) with PAEC decreased cell viability, increased LDH release, and elevated MDH production. Preincubation of PAEC with pycnogenol (10-80 micrograms/mL) before tBHP exposure significantly increased cell viability, decreased LDH release, and reduced MDA production. These results demonstrate that pycnogenol can protect vascular endothelial cells from oxidant injury. The data thus suggest that pycnogenol may be useful for the prevention of disorders associated with oxidative damage.

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