Endothelial progenitor cells in systemic lupus erythematosus.
OBJECTIVE
Systemic lupus erythematosus (SLE) is an autoimmune-mediated disease, characterized by inflammation of small arteries and arterioles. Patients with SLE suffer from a 17-fold higher risk for developing atherosclerosis than healthy individuals. Endothelial progenitor cells (EPCs) have been shown to be critically involved in microvascular repair under both physiological and pathological conditions. The aim of the present study was to analyze EPC regeneration and mobilization in SLE patients with variable disease activity and undergoing different treatment regimens.


METHODS
Forty-eight patients with SLE were analyzed. Healthy, age- and sex-matched individuals served as controls. Total circulating EPCs were enumerated by FACS analysis, and regenerative activity of the cells was analyzed by a colony-forming assay. Vasomodulatory mediators were quantified by  ELISA.


RESULTS
SLE patients did not show lower or higher percentages of total circulating EPCs, but they displayed significantly lower colony numbers as compared with healthy controls, indicating impaired EPC regeneration and mobilization. Low and high disease activity were associated with decreased EPC regeneration, while moderate disease activity was not. Hypertension and, to some extent, renal involvement were associated with reduced colony formation. Patients not receiving hydroxychloroquine (HCQ) treatment and those undergoing glucocorticoid therapy showed impaired EPC regeneration as well.


CONCLUSIONS
SLE patients suffer from both defective regeneration and mobilization of EPCs. Such an impairment of the EPC system, as one key regulatory element in the process of vasorepair, could potentially promote microvascular damage in SLE. Long-term glucocorticoid therapy may further suppress the EPC system, while HCQ may prevent regeneration of the cells.
Department of Medicine, Nephrology and Rheumatology, University Hospital Göttingen, Göttingen - Germany.
Susann
S
Patschan
Daniel
D
Patschan
Marta
M
Potulski
Elvira
E
Henze
Jürgen
J
Scholze
Gerhard Anton
GA
Müller
D000293:Adolescent; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D002452:Cell Count; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology*; D003114:Colony-Forming Units Assay; D066026:Endothelial Progenitor Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D006886:Hydroxychloroquine / Q000627:therapeutic use; D006973:Hypertension / Q000503:physiopathology; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008180:Lupus Erythematosus, Systemic / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012038:Regeneration / Q000187:drug effects / Q000502:physiology*; D055815:Young Adult
D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D006886:Hydroxychloroquine