@article {Albrightson404, author = {C R Albrightson and P Nambi and B Zabko-Potapovich and G Dytko and T Groom}, title = {Effect of thrombin on proliferation, contraction and prostaglandin production of rat glomerular mesangial cells in culture.}, volume = {263}, number = {1}, pages = {404--412}, year = {1992}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {The effect of thrombin on mesangial cell function was investigated. Thrombin caused a dose-dependent increase in [3H] thymidine incorporation (EC50 = 0.36 +/- 0.09 U/ml), intracellular calcium [(Ca++)i] mobilization (EC50 = 1.9 +/- 0.5 U/ml) and prostaglandin E2 (PGE2) production (EC50 = 0.25 +/- 0.02 U/ml) in rat glomerular mesangial cells. These effects were blocked by the thrombin inhibitor, hirudin (KB = 10.4 +/- 0.2 nM). The role of (Ca++)i mobilization and arachidonate metabolism in thrombin-stimulated proliferation was tested by the addition of the calcium channel blocker, nifedipine, and the cyclooxygenase inhibitor, indomethacin, to mesangial cell cultures. Indomethacin, at doses that completely inhibited the thrombin-mediated production of PGE2, had no significant effect on proliferation. The Ca++ channel blocker, nifedipine, inhibited both PGE2 production and [3H] thymidine incorporation in a dose-dependent fashion, but only at concentrations considered nonspecific. In addition to its effects on PGE2, thymidine incorporation and Ca++ mobilization, thrombin caused mesangial cell contraction as determined by a substrate distortion technique. This effect was not inhibited by indomethacin. These results indicate that thrombin can alter mesangial cell function in vitro.}, issn = {0022-3565}, URL = {https://jpet.aspetjournals.org/content/263/1/404}, eprint = {https://jpet.aspetjournals.org/content/263/1/404.full.pdf}, journal = {Journal of Pharmacology and Experimental Therapeutics} }