ABSTRACT
ABSTRACT Introduction: There are few circulating biomarkers for valvular heart disease. Angiopoietin (Ang) 1, Ang2, and vascular endothelial growth factor are important inflammation-associated cytokines. The aim of this study was to investigate the clinical significance and association of Ang1, Ang2, and vascular endothelial growth factor in valvular heart disease. Methods: This is a retrospective study; a total of 62 individuals (valvular heart disease patients [n=42] and healthy controls [n=20]) were included. Plasma levels of Ang1, Ang2, and vascular endothelial growth factor were detected by enzyme-linked immunosorbent assays. We retrospectively collected the baseline characteristics and short-term outcomes; logistic regression was performed to identify predictor for short-term mortality. Results: Ang2 was significantly decreased in the valvular heart disease group compared with the healthy control group (P=0.023), while no significant difference was observed in the Ang1 and vascular endothelial growth factor levels. The Ang2 level of New York Heart Association (NYHA) I/II patients — but not NYHA III/IV patients — was significantly decreased compared with that of healthy control individuals (NYHA I/II: P=0.017; NYHA III/IV: P=0.485). Univariable logistic regression analysis indicated that Ang2 was a significant independent predictor for short-term mortality (odds ratio 18.75, P=0.033, 95% confidence interval 8.08-102.33). Ang1 was negatively correlated with Ang2 (P=0.032, Pearson's correlation coefficient =-0.317) and was positively correlated with vascular endothelial growth factor (P=0.019, Pearson's correlation coefficient = 0.359). Conclusion: Ang2 might serve as a therapeutic and prognostic target for valvular heart disease.
ABSTRACT
The effect of high-frequency repetitive transcranial magnetic stimulation (rTMS) on potassium-chloride cotransporter-2 (KCC2) protein expression following spinal cord injury (SCI) and the action mechanism were investigated.SCI models were established in SD rats.Five groups were set up randomly:normal control group,SCI 7-day (7D) model group,SCI 14-day (14D) model group,SCI-7D rTMS group and SCI-14D rTMS group (n=5 each).The rats in SCI rTMS groups were treated with 10 Hz rTMS from 8th day and 15th day after SCI respectively,once every day,5 days every week,a total of 4 weeks.After the model establishment,motor recovery and spasticity alleviation were evaluated with BBB scale once a week till the end of treatment.Finally,different parts of tissues were dissected out for detection of variations of KCC2 protein using Western blotting and polymerase chain reaction (PCR) technique.The results showed that the BBS scores after treatment were significantly higher in SCI-7D rTMS group than in SCI-14D rTMS group (P＜0.05).As compared with normal control groups,The KCC2 protein in SCI model groups was down-regulated after SCI,and the decrease was much more significant in SCI-14D model group than in SCI-7D group (P＜0.05).As compared with SCI model groups,KCC2 protein in rTMS groups was up-regulated after the treatment (P＜0.05).The up-regulation of KCC2 protein content and expression was more obvious in SCI-7D rTMS group than in SCI-14D rTMS group (P＜0.05).It was concluded that 10 Hz rTMS can alleviate spasticity in rats with SCI,which might be attributed to the up-regulation of KCC2 protein.It was also suggested that the high-frequency rTMS treatment after SCI at early stage might achieve more satisfactory curative effectiveness.
ABSTRACT
Our previous studies demonstrated that CD151 gene promoted neovascularization in ischemic heart model.To improve the delivery efficacy and target specificity of CD1 51 gene to ischemic heart,we generated an adeno-associated virus (AAV) vector in which CD151 expression was controlled by the myosin light chain (MLC-2v) promoter to achieve the cardiac-specific expression of CD 151 gene in ischemic myocardium and to limit unwanted CD151 expression in extracardiac organs.The function of this vector was examined in rat ischemic myocardium model.The protein expression of CD151 in the ischemic myocardium areas,liver and kidney was confirmed by using Western blot,while the microvessels within ischemic myocardium areas were detected by using immunohistochemistry.The results showed that MLC-2v significantly enhanced the expression of CD151 in ischemic myocardium,but attenuated its expression in other organs.The forced CD151 expression could increase the number of microvessels in the ischemic myocardium.This study demonstrates the AAV-mediated and MLC-2v regulated CD151 gene is highly expressed in the ischemic myocardium and cardiac-specific delivery that is more efficiently targets CD151 to the ischemia myocardium after myocardial infarction.
ABSTRACT
The effects of magnetic stimulation on spinal cord injury-induced migration of white matter astrocytes were studied using an established animal model. Ethidium bromide was injected into the dorsal spinal cord funiculus of adult Sprague-Dawley rats on the left side at T10-11. Animals then received 1.52 Tesla-pulsed magnetic stimulation for 5 min at different frequencies (0-20 Hz) for 14 consecutive days. Selected animals received the non-competitive MEK1/2 inhibitor U0126 (10 μM), prior to stimulation at 10 Hz. Lesion volumes were measured in hematoxylin/eosin-stained sections. Expression of glial fibrillary acidic protein (GFAP), microtubule associated protein-2 (MAP-2) and extra-cellular signal-regulated kinase1/2 (ERK1/2) near the epicenter of injury was examined by Western blotting with quantification using an image analysis system. Lesion volumes decreased and GFAP and p-ERK1/2 expression increased with increasing magnetic stimulation frequency (0-10 Hz). MAP-2 expression was not affected at any frequency. Pretreatment with U0126 reduced GFAP and ERK1/2 expression and increased lesion volumes in response to stimulation at 10 Hz. It is concluded that magnetic stimulation increases the migration of astrocytes to spinal cord lesions. Activation of the ERK1/2 signaling pathway is proposed to mediate astrocyte migration and glial scar formation in response to spinal cord injury.