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ABSTRACT: It has been suggested that renin-angiotensin system (RAS) gene polymorphism is involved in the pathogenesis of Henoch-Schönlein purpura (HSP) with conflicting reports. We therefore investigate the effect of RAS gene polymorphism on HSP susceptibility and severity in a Chinese cohort. The study included 142 children with HSP and 218 healthy controls that were genotyped for RAS gene polymorphisms. Significantly, differences of T174M-T and ACE-D frequency were found between HSP patients and controls (p(alleo) = .002, OR(alleo) = 2.001; p(alleo) = .007, OR(alleo) = 1.533, respectively). We also found correlations between ACE-I/D and Agt T174M with multiple organ involvements, with significant differences in ACE-D in renal groups (p < 0.05) and Agt T174M in non-renal (p(joint) = .002, p(GI) = .042). Furthermore, decreasing M235T-T and increasing ACE-D were found associated with serious renal complications (p = .019, p = .016). Additionally, ACE-I/D and T174M were significantly associated with high clinical score patients, as opposed to low clinical score patients, when patients were scored depending on the severity of overall complications (p = .045, p = .026). We suggest that RAS gene polymorphisms (ACE-I/D, M235T or T174M) are significantly associated with susceptibility to HSP, organ involvement, and disease severity, which largely account for individual prognosis.
Journal of Renin-Angiotensin-Aldosterone System 12/2010; 11(4):248-55. · 2.44 Impact Factor
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ABSTRACT: Low-molecular-weight heparin (LMWH) is a negatively charged glycoprotein and has a very similar structure to that of cell surface heparin sulfate (HS). Thus, LMWH, an analog of HS, may inhibit positively charged respiratory syncytial virus (RSV) infection through cooperative electrostatic association.
In this study, rats were respectively treated with 400 IU/kg LMWH before, during or after being inoculated with 6 x 10(6) plaque-forming unit (PFU) RSV. RSV and normal control groups were respectively inoculated by RSV and virus-free Dulbecco's modified Eagle's medium (DMEM). HeLa cells in vitro were pretreated with LMWH, elastase (ELA), heparinase (HpaIII) and protamine before being inoculated with 6 x 10(1) PFU RSV. RSV infectivity was determined by in situ hybridization and plaque assay.
After inoculation, the urinary protein excretion and serum parameters in LMWH-treated rats were significantly lower than those in the RSV group. No abnormalities of glomerular structure were observed in LMWH-treated groups whereas swelling and slight hypercellularity in minority glomeruli and foot process effacement were observed in the RSV group. RSV RNA of LMWH-treated rats had weaker expression than that of the RSV group. In vitro, RSV infection in RSV + LMWH, HpaIII + ELAI, protamine + ELAI, ELAI, HpaIII and protamine treatment cells were significantly lower than that of the RSV control, and that in RSV + LMWH was the least. There were no significant differences in RSV infection between ELAI + LMWH and RSV control.
Our study confirmed that there is a correlation between RSV and proteinuria in rats. LMWH can alleviate proteinuria in rats through inhibiting RSV from binding with HS which plays an important role in the onset of RSV infection.
Nephrology 11/2008; 13(7):545-53. · 1.31 Impact Factor
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ABSTRACT: To investigate the changes of angiotensin II receptors expression in cardiomyocytes of both ventricles in pigs with experimental ventricular septal defect (VSD).
Nineteen young pigs were divided into 3 groups: the pigs that received operation to produce experimental VSD, the pigs that underwent sham-operation, and the pigs as normal control. One month after the operation, the pigs were catheterized and then put to death; the cardiomyocytes were taken from their ventricles and were isolated. Radioligand binding assay was done to measure the Bmax and KD of angiotensin II receptor per 10(6) cells.
For both Bmax and KD of angiotensin II receptors, there were no significant differences between the sham-operation group and the control. The Bmax of left ventricle AT1R (188.42 +/- 133.97 fmol/10(6)) and Bmax of right ventricle AT1R (272.14 +/- 232.74 fmol/10(6)) and AT2R (40.42 +/- 34.76 fmol/10(6)) in the operation group were significantly elevated in comparison with the control (Bmax of left ventricle AT1R 29.20 +/- 19.50 fmol/L, and Bmax of right ventricle AT1R 76.72 +/- 51.21 fmol/L and AT2R 9.63 +/- 1.27 fmol/L) respectively, P < 0.05.
Intracardiac left-to-right shunt related volume overload leads to the elevation of AT1R expression in cardiomyocytes, which serves as an important mechanism of ventriclular hypertrophy and remodling in congenital heart disease. The increased expression of AT2R in right ventricle is a possible explanation of the phenomenon that moderately sized VSDs usually show left other than right ventriclular hypertrophy, taking into account that AT2R has been suggested to mediate antitrophic reaction.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 07/2003; 34(3):417-20.
