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Decreased expression of the p21ras stimulatory factor hSOS in PBMC from inactive SLE patients

Department ‘B’ of Internal Medicine, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel; Diabetes Unit, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel; The Diabetes Unit, Assaf Harofeh Medical Center, Zenifin 70300, Israel

A Mor

Diabetes Unit, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel

M Amit

Department ‘B’ of Internal Medicine, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel; Rheumatology Service, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel

R Rosenberg

Y Ramot

A Mizrachi

Department ‘B’ of Internal Medicine, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel

A J Wysenbeek

Department ‘B’ of Internal Medicine, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel; Rheumatology Service, Assaf Harofeh Medical Center affiliated to Tel-Aviv University, Zerifin, Israel

Expression of the p21ras protooncogene is reported to be increased in animal models and in patients with SLE. However, the expression of p21ras regulatory elements has not been determined. We determined the expression of p21ras, and its regulatory elements p120-ras-GAP and hSOS, in PBMC of 10 patients with inactive SLE (mean SLEDAI score 1.8 0.53) and 10 age-and sexmatched healthy controls. No difference was found between the two groups in the levels of p21ras (3760–513 and 3367–335, P = 0.25) and ras-GAP (1048–261 and 1534–247, P = 0.11) in patients and controls, respectively. In contrast, levels of hSOS were significantly decreased in patients as compared to controls: 955 218 and 2306 327, P = 0.002, respectively. The mitogeninduced proliferative response was comparable in the two groups: SI 20.8 4.2 and 15.03 4.9, P = 0.135, in patients and controls, respectively. Taken together, our data demonstrate that nonactive SLE patients are characterized by reduced hSOS expression and underscore the need for a comprehensive evaluation of p21ras pathway in these patients.

Key Words: SLE • PBMC • p21ras • ras-GAP • hSOS • human

Lupus, Vol. 8, No. 1, 24-28 (1999)
DOI: 10.1191/096120399678847362


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