, Volume 17, Issue 8, pp 587-592
Date: 09 Aug 2011

Research on the correlation between platelet gelsolin and blood-stasis syndrome of coronary heart disease

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Abstract

Objective

To study the distribution of gelsolin in human platelet and plasma, and the association with blood-stasis syndrome (BSS) of coronary heart disease (CHD).

Methods

Sixty patients with CHD (30 in BSS group and 30 in non-BSS group) and 30 healthy subjects (control group) were included in this study. The classification of the syndrome was based on clinical symptoms and signs. Gelsolin concentration in platelet rich plasma (PRP), platelet poor plasma (PPP), filamentous actin (F-actin) and group-specific component globulin (Gc-globulin) of PPP were determined by enzyme-linked immunosorbent assay (ELISA). The fluorescence intensity of CD62p and cytoplasmic calcium ([Ca2+]i) in human platelets of patients and healthy persons was measured with flow cytometry.

Results

Compared with the control group, gelsolin in PRP of the BSS group increased significantly (P<0.01), while that in PPP of the BSS and non-BSS groups decreased markedly (P<0.05), the CD62p, [Ca2+]i of platelet, F-actin, and Gc-globulin of the BSS and non-BSS groups increased significantly (P<0.01). Compared with the non-BSS group, the gelsolin concentration in PRP of BSS group increased significantly (P<0.01), the [Ca2+]i of platelet of the BSS group increased markedly (P<0.01), while the F-actin and Gc-globulin of the BSS group had no statistical defference (P>0.05).

Conclusions

Gelsolin concentration in PRP was increased and accompanied by the elevated [Ca2+]i of platelet in CHD with BSS, while gelsolin in PPP were lowered markedly. We speculate that plasma gelsolin may clear F-actin from circulation, thus resulting in depletion of plasma gelsolin significantly. This, in addition to the increased calcium influx of platelets, may lead to the gelsolin abnormal expression on platelets during the process of BSS in CHD. Therefore, platelet gelsolin may serve as a new potential biomarker and a therapeutic target of BSS in CHD.

Supported by the National Natural Science Foundation of China (No. 81073086)