Expression of cyclin B1 and cyclin dependent kinase inhibitor p21 in lymphocytes in patients with systemic lupus erythematosus

OBJECTIVE: The roles of cyclins and cyclin dependent kinase (CDK) inhibitors of lymphocytes in the pathogenesis of systemic lupus erythematosus (SLE) are unclear. We measured the expression of cyclin B1 and CDK inhibitor p21 in peripheral blood lymphocytes (PBL) from patients with SLE and controls....

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Published in:Journal of rheumatology 2002-12, Vol.29 (12), p.2537-2544
Main Authors: Ho, Cheong-Yip, Wong, Chun-Kwok, Li, Edmund Kwok-Ming, Tam, Lai-Shan, Lam, Christopher Wai-Kei
Format: Article
Language:English
Subjects:
Adult
Aged
Cell Count
Cyclin B - biosynthesis
Cyclin B1
Cyclin-Dependent Kinase Inhibitor p21
Cyclins - biosynthesis
DNA - analysis
Female
Flow Cytometry
Humans
Lupus Erythematosus, Systemic - blood
Lymphocytes - drug effects
Lymphocytes - metabolism
Male
Middle Aged
Phytohemagglutinins - pharmacology
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Summary:OBJECTIVE: The roles of cyclins and cyclin dependent kinase (CDK) inhibitors of lymphocytes in the pathogenesis of systemic lupus erythematosus (SLE) are unclear. We measured the expression of cyclin B1 and CDK inhibitor p21 in peripheral blood lymphocytes (PBL) from patients with SLE and controls. METHODS: PBL from 40 SLE patients with renal disease (RSLE), 40 SLE patients without renal disease (SLE), and 28 healthy control subjects were cultured with phytohemagglutinin (PHA). Bivariate distribution of cyclin B1 or p21 expression versus cellular DNA content was assessed by flow cytometry. RESULTS: Expression of p21 in lymphocytes was significantly lower in patients with RSLE and with SLE than controls (RSLE vs controls and SLE vs controls, both p < 0.001). Expression of cyclin B1 was similar in all groups. The percentages of RSLE lymphocytes in G0/G1 and S phase were significantly reduced and elevated, respectively, compared with controls. CONCLUSION: Downregulated p21 in PHA stimulated PBL from patients with SLE may be closely related to aberration of cell division in SLE lymphocytes.
ISSN:0315-162X
1499-2752