Inhibition of platelet-derived growth factor-induced mesangial cell proliferation by cyclooxygenase-2 overexpression is abolished through reactive oxygen species.
Standard
Inhibition of platelet-derived growth factor-induced mesangial cell proliferation by cyclooxygenase-2 overexpression is abolished through reactive oxygen species. / Zahner, Gunther; Wolf, Gunter; Schroeder, Saskia; Stahl, Rolf A.K.
In: FEBS LETT, Vol. 580, No. 10, 10, 2006, p. 2523-2528.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Inhibition of platelet-derived growth factor-induced mesangial cell proliferation by cyclooxygenase-2 overexpression is abolished through reactive oxygen species.
AU - Zahner, Gunther
AU - Wolf, Gunter
AU - Schroeder, Saskia
AU - Stahl, Rolf A.K.
PY - 2006
Y1 - 2006
N2 - Proliferation of mesangial cells (MC) is an early event in many forms of glomerulonephritis. We have previously shown that platelet-derived growth factor (PDGF)-induced proliferation of MC was inhibited by the overexpression of cyclooxygenase-2 (COX-2). Since reactive oxygen species (ROS) are important mediators of mitogenic signaling, we evaluated the role of ROS in the COX-2 induced growth arrest in MC. We demonstrate that ROS are reduced in COX-2 overexpressing MC. Intracellular elevation of ROS restored PDGF-induced proliferation, while the expression of the cyclin-dependent kinase inhibitors p21(cip1) and p27(kip1) were decreased in these cells. The data suggest that COX-2 decreases ROS formation which consequently leads to the PDGF-induced inhibition of MC proliferation.
AB - Proliferation of mesangial cells (MC) is an early event in many forms of glomerulonephritis. We have previously shown that platelet-derived growth factor (PDGF)-induced proliferation of MC was inhibited by the overexpression of cyclooxygenase-2 (COX-2). Since reactive oxygen species (ROS) are important mediators of mitogenic signaling, we evaluated the role of ROS in the COX-2 induced growth arrest in MC. We demonstrate that ROS are reduced in COX-2 overexpressing MC. Intracellular elevation of ROS restored PDGF-induced proliferation, while the expression of the cyclin-dependent kinase inhibitors p21(cip1) and p27(kip1) were decreased in these cells. The data suggest that COX-2 decreases ROS formation which consequently leads to the PDGF-induced inhibition of MC proliferation.
M3 - SCORING: Zeitschriftenaufsatz
VL - 580
SP - 2523
EP - 2528
JO - FEBS LETT
JF - FEBS LETT
SN - 0014-5793
IS - 10
M1 - 10
ER -