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Updated: Jul 16, 2026
A Uniform Shear Assay for Human Platelet and Cell Surface Receptors via Cone-plate Viscometry
Published on: June 5, 2019
[Relations of ulcerative colitis to anti-beta2-glycoprotein antibodies and to platelet activation status]
Yan-hang Gao1, Pu-jun Gao, Chun-guang Wang
1Department of Gastroenterology, First Hospital of Jilin University, Changchun 130021, China.
Objective:
To explore the relations of ulcerative colitis (UC) to anti-beta2-glycoproteinI antibodies (abeta(2)GPI) and platelet activation status.
Methods:
Peripheral blood samples were collected from 56 UC patients, 34 males and 22 females, aged 43.5 (21 - 66), including 36 in active stage and 20 in remission stage, and 25 sex- and age-matched controls. The level of abeta(2)GPI was detected by ELISA. The platelet activation markers, platelet activation complex-1 (PAC-1) and P-selectin (CD62P) were detected by immunofluorescence staining and flow cytometry.
Results:
The A value of IgG abeta(2)GPI of the active UC group was 0.61 +/- 0.13, significantly higher than those of the remittent UC group and the control group (0.50 +/- 0.13 and 0.22 +/- 0.14, both P < 0.01), and there was a significant difference between the remittent UC group and the control group (P < 0.01). The A value of IgM abeta(2)GPI of the active and remittent UC groups were 0.43 +/- 0.13 and 0.38 +/- 0.12, both significantly higher than that of the control group (0.20 +/- 0.12, both P < 0.01), however, there was no significant difference between the active UC and remittent UC groups (P > 0.05). The PAC-I positive rate of the active UC and remittent UC groups were 30.6% +/- 7.6% and 19.6% +/- 7.8%, both significantly higher than that of the control group (6.3% +/- 1.7%, both P < 0.01), and there was a significant difference between the active and remittent groups too (P < 0.01). The CD62P positive rates of the active UC and remittent UC groups were 45.0% +/- 8.8% and 31.9% +/- 7.8% respectively, both significantly higher than that of the control group (9.2% +/- 2.7%, both P < 0.01), and there was a significant difference between the active and remittent groups too (P < 0.01). In the active UC group, more severe the state of illness, the higher the A value of IgG abeta(2)GPI, and the positive rates of PAC-I and CD62P, and these values were all positively correlated with the state of illness (F(abeta2GPI) = 3.679, P < 0.05, F(PAC-I(%)) = 5.346, P < 0.01, and F(CD62P(%)) = 5.418, P < 0.01 respectively).
Conclusion:
The abeta(2)GPI level and the platelet activation state are closely correlated with the pathogenesis and development of UC.
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