Changes in platelet GPIbα and ADAM17 during the acute stage of atherosclerotic ischemic stroke among Chinese

Abstract

Glycoprotein (GP) Ibα ectodomain shedding has important implications for thrombosis and hemostasis. A disintegrin and metalloproteinase 17 (ADAM17) was identified to play an essential role in agonist induced GPIbα shedding. The relationship of GPIbα shedding and ADAM17 in the acute stage of atherosclerotic ischemic stroke (AIS) patients has not been thoroughly studied. A total of 306 patients and 230 controls matched for age, sex, race, history of hypertension and diabetes mellitus were enrolled in the study. GPIbα, ADAM17, glycocalicin were detected by flow cytometry, Western blotting, and enzyme-linked immunosorbent assay (ELISA) respectively. Compared with the control group, the expression of GPIbα in patients with acute ischemic stroke was significantly lower (P=0.000, P<0.01). Plasma glycocalicin and ADAM17 in AIS group were higher than those in control group (P=0.699, P=0.000). Pearson's analysis showed glycocalicin bore no correlation with GPIbα in AIS patients (r=0.095, P>0.05). GPIbα and National Institute of Health Stroke Scale (NIHSS) had negative correlation (r=-0.514, P<0.01). Our findings indicate that ADAM17 may be a risk factor for ischemic stroke in Chinese and the expression of GPIbα can serve as a measure for stroke severity.

Effects of Qing’E Formula on the Expression of Bone Metabolic Markers and VDR mRNA in Postmenopausal Osteoporosis Patients

“…The results of this study show that QEF can reduce bone resorption through the adjustment of VDR mRNA expression. This experiment uses stable and effective active vitamin D 3 reported in literatures as the reference drug for the control study [9]- [11]. Data shows similar drug efficacy between QEF and active vitamin D 3 , as both are able to increase VDR mRNA expression in the body in reducing bone resorption and strengthening the quality and quantity of bones.…”

Case-Control Study of Platelet Glycoprotein Receptor Ib and IIb/IIIa Expression in Patients with Acute and Chronic Cerebrovascular Disease

“…However, a potential explanation for the lack of differentiation between GPIb receptor numbers is the postulated downregulation of GPIb receptors as a result of ectodomain shedding that is induced by platelet agonists during modulation of platelet function [ 22 ]. Indeed, a recent study of Chinese patients with atherosclerotic IS demonstrated lower expression levels of GPIb but higher levels of a disintegrin and metalloproteinase 17 (ADAM17), an enzyme that has been reported to play a major role in GPIb shedding [ 23 ].…”