The Key Laboratory of Cardiovascular Remodeling and Function Research
The Key Laboratory of Cardiovascular Remodeling and Function Research
PubMed | Henan Province Peoples Hospital, The Key Laboratory of Cardiovascular Remodeling and Function Research and Luoyang Orthopedic Traumatological Hospital
Type: Journal Article | Journal: International journal of environmental research and public health | Year: 2015
In this study, a multiple linear regression model to evaluate the risk of morbidity and mortality of ischemic cardiovascular disease is demonstrated. In this model, predictor variables are selected from physiological chemicals in a blood test of the subjects. Meanwhile, the calculated risk score is selected as a response variable. Four major latent variables including hepatic, nephric, metabolic, and BMI (Body Mass Index) are revealed by performing statistical and principal component analysis for the collected survey data. The analyzed result also shows that the cardiac disorder is correlated with symptoms of abnormal BMI, hepatic disorder, nephric disorder, and metabolic disorder. Thus, the risk of morbidity and mortality of ischemic cardiovascular disease can be assessed from the proposed multiple regression model.
Liu M.-H.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Li Y.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Han L.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Zhang Y.-Y.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
And 8 more authors.
Molecular Immunology | Year: 2017
Background Atherosclerosis (AS) is the most common and serious complication of type 2 diabetes mellitus (T2DM) and is accelerated via chronic systemic inflammation rather than hyperglycemia. Adipose tissue is the major source of systemic inflammation in abnormal metabolic state. Pro-inflammatory CD4+T cells play pivotal role in promoting adipose inflammation. Adipose-derived stem cells (ADSCs) for fat regeneration have potent ability of immunosuppression and restricting CD4+T cells as well. Whether T2DM ADSCs are impaired in antagonizing CD4+T cell proliferation and polarization remains unclear. Methods We constructed type 2 diabetic ApoE−/− mouse models and tested infiltration and subgroups of CD4+T cell in stromal-vascular fraction (SVF) in vivo. Normal/T2DM ADSCs and normal splenocytes with or without CD4 sorting were separated and co-cultured at different scales ex vivo. Immune phenotypes of pro- and anti-inflammation of ADSCs were also investigated. Flow cytometry (FCM) and ELISA were applied in the experiments above. Results CD4+T cells performed a more pro-inflammatory phenotype in adipose tissue in T2DM ApoE−/− mice in vivo. Restriction to CD4+T cell proliferation and polarization was manifested obviously weakened after co-cultured with T2DM ADSCs ex vivo. No obvious distinctions were found in morphology and growth type of both ADSCs. However, T2DM ADSCs acquired a pro-inflammatory immune phenotype, with secreting less PGE2 and expressing higher MHC-II and co-stimulatory molecules (CD40, CD80). Normal ADSCs could also obtain the phenotypic change after cultured with T2DM SVF supernatant. Conclusion CD4+T cell infiltration and pro-inflammatory polarization exist in adipose tissue in type 2 diabetic ApoE−/− mice. T2DM ADSCs had impaired function in restricting CD4+T lymphocyte proliferation and pro-inflammatory polarization due to immune phenotypic changes. © 2017 Elsevier Ltd
Li Z.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Wang L.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Hu X.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Zhang P.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
And 5 more authors.
International Journal of Cardiovascular Imaging | Year: 2017
To assess the elastic mechanical properties of atherosclerotic plaque with different morphological properties by intravascular ultrasound elastography (IVUSE). 30 purebred New Zealand rabbits were fed a high-cholesterol diet; the abdominal aorta endothelium was balloon-injured after 2 weeks; at week 12, 2 plaques with moderate echo from each rabbit were chosen for in situ imaging, and 2 consecutive frames near the end-diastole images in situ were used to construct an IVUS elastogram. Shear strain (SS) and area strain (AS) were greater for eccentric than centripetal plaque (SS: 2.65(2.45)% vs. 1.79 ± 0.97%, p < 0.05; AS: 4.81(4.99)% vs. 3.23 ± 1.75%, p < 0.05) but were lower with low than high plaque burden (SS: 2.14 ± 0.37% vs. 3.40 ± 0.34%, p < 0.05; AS: 3.88 ± 0.60% vs. 5.81 ± 0.54%, p < 0.05). SS and AS were significantly greater for plaque with negative than no remodeling (SS: 3.98 ± 1.53% vs. 1.82(1.40)%, p < 0.017; AS: 6.94 ± 2.24% vs. 2.59(2.87)%, p < 0.017) and were found correlated with eccentric index and plaque burden (R2 = 0.365 and R2 = 0.359, both p < 0.05). Plaques associated with eccentricity, high plaque burden and negative remodeling showed greater strain than those with centripetalism, low plaque burden and positive remodeling. Eccentric index and plaque burden may be useful to predict the elastic stability of plaque. © 2017 Springer Science+Business Media Dordrecht
Xing Y.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Yan F.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Liu Y.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Liu Y.,Shandong University |
Zhao Y.,The Key Laboratory of Cardiovascular Remodeling and Function Research
Biochemical and Biophysical Research Communications | Year: 2010
In this study, we examined whether matrine could inhibit the differentiation of 3T3-L1 preadipocytes and further explored the possible inhibitory mechanisms. Evidenced by Oil Red O staining and AdipoRed assay, matrine dose-dependently inhibited lipid accumulation at concentrations of 125, 250 and 500 μg/ml. At molecular level, the expression of transcription factors, PPARγ and C/EBPα, was reduced by matrine during adipogenesis. After treatment for 6 days, the mRNA levels of adipocyte-specific genes, such as aP2, LPL, adiponectin and leptin, were also down-regulated by matrine in a dose-dependent manner. Moreover, 500 μg/ml matrine inhibited the phosphorylation of ERK1/2 at the early stage of differentiation. Our results indicate that inhibition of 3T3-L1 preadipocyte differentiation by matrine is associated with the suppression of ERK1/2 phosphorylation. Thus, matrine has the potential to be an alternative natural product for the treatment of obesity. © 2010 Elsevier Inc. All rights reserved.
Xu F.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Xu F.,Shandong University |
Chen Y.G.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Chen Y.G.,Shandong University |
And 16 more authors.
Journal of Cellular and Molecular Medicine | Year: 2011
This study aimed to investigate the association of the aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphism, which exists in 30-50% of East Asians, and risk of acute coronary syndrome (ACS). We enrolled 1092 unrelated Han Chinese, including 546 with ACS and 546 age- and sex-matched controls. Subjects with ALDH2 mutant genotypes showed significantly higher ACS than did controls (46.7%versus31.9%,P< 0.001). Logistic regression analysis revealed the ALDH2 mutant independently associated with ACS (odds ratio [OR] 1.95, 95% confidence interval [CI]: 1.31-2.92,P= 0.001), but the association was weaker on adjusting for alcohol consumption (OR 1.82, 95% CI: 1.23-2.70,P= 0.003). Similar results were found in a subgroup analysis of patients with primary ST-segment elevation myocardial infarction (STEMI). The ALDH2 mutant was significantly associated with level of high-sensitivity C-reactive protein (hs-CRP) in patients with ACS (P= 0.002) and in controls (P= 0.009) and number of circulating endothelial progenitor cells (EPCs) (P= 0.032); furthermore, inclusion of hs-CRP level and EPCs number as independent variables in regression analysis reduced the importance of ALDH2 polymorphism in ACS or primary STEMI. However, ALDH2 polymorphism was not associated with number of coronary arteries with significant stenosis, Gensini score or flow-mediated dilation of the brachial artery. Our results suggest that ALDH2 mutation is a genetic risk marker for ACS, which is explained in part by alcohol consumption, inflammation and number of circulating EPCs. © 2011 The Authors Journal compilation © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Yang J.,Shandong University |
Yang J.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Yu Y.,Shandong University |
Yu H.,Shandong University |
And 5 more authors.
European Journal of Pain | Year: 2010
Previous studies suggested that brain-derived neurotrophic factor (BDNF) might act as an important modulator in chronic pain states. However, no systematic study has used knock-out mice to clarify its effect on visceral sensitivity. In the present study, 2,4,6-trinitrobenzene sulfonic acid (TNBS) was administered to heterozygous (BDNF+/-) knock-out and wild-type (BDNF+/+) mice to induce colitis. Visceral response to colorectal distension (CRD) and bladder reactivity were recorded. Results demonstrated that in normal state, BDNF+/- and BDNF+/+ mice did not differ in the visceral response to CRD at <60 mm Hg pressure and the bladder reactivity; however, with ≥60 mm Hg pressure, BDNF+/- mice showed a weaker visceral response to CRD. In inflammatory state of colitis, TNBS induced upregulation of BDNF in dorsal root ganglia of both genotypes while BDNF+/- mice showing significantly lower sensitivity in the colon at ≥30 mm Hg and lower sensitivity in bladder than BDNF+/+ mice. The two genotypes showed no significant difference in inflammatory severity. Thus, BDNF deficiency results in developmental changes in colonic nociception in both control and inflammatory states, which are more significant in inflammatory state. For bladder reactivity, BDNF deficiency leads to lower sensitization in inflammatory state but has no effect in control state. Perspective: This article highlights the role of BDNF in colonic and referred bladder hyperalgesia in mice. The findings might help in determining novel pharmaceutical interventions targeted at BDNF to relieve abdominal pain. © 2009 European Federation of International Association for the Study of Pain Chapters.
Li T.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Chen W.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
An F.,The Key Laboratory of Cardiovascular Remodeling and Function Research |
Tian H.,Shandong University |
And 4 more authors.
Tohoku Journal of Experimental Medicine | Year: 2011
Probucol, a lipid-lowering agent with anti-oxidant properties, has been implicated in protection against atherogenesis, whereas its effect on plaques stability remains to be fully elucidated. The present study was aimed to test the hypothesis that probucol may attenuate inflammation and increase stability of vulnerable atherosclerotic plaques using a rabbit model. After abdominal aortic balloon injury, 45 rabbits were fed a 1% cholesterol diet for 24 weeks. From week 12 to week 24, the animals were treated with probucol (1% by weight in the diet), simvastatin (5 mg·kg -1, positive control) or no drugs (control), respectively. At the end of week 22, recombinant-p53 adenovirus was injected into the abdominal aortic plaques. Two weeks later, plaque disruption was induced by injection of Chinese Russell's viper venom and histamine. The results showed that the incidence of plaque disruption in probucol or simvastatin groups was significantly lower than that in the control group (7.15% or 14.29% vs. 71.43% respectively, both P < 0.01). Probucol significantly increased the thickness of fibrous caps and decreased plaque vulnerability index. Serum concentrations of inflammatory cytokines and matrix metalloproteinases, and expression levels of Toll-like receptor (TLR)-2, TLR-4, monocyte chemoattractant protein-1, intercellular adhesion molecule 1, scavenger receptor A, CD36 and oxidized low-density lipoprotein receptor 1 within the lesions were markedly lower in both treatment groups than in the control group. We conclude that probucol increases the stability of vulnerable plaques, possibly through its lipid lowering, anti-inflammation and scavenger receptors suppression effects, suggesting probucol as a promising pharmacologic approach to stabilize vulnerable plaques. © 2011 Tohoku University Medical Press.
PubMed | Shandong University and The Key Laboratory of Cardiovascular Remodeling and Function Research
Type: Journal Article | Journal: Journal of translational medicine | Year: 2016
Trimetazidine, as an anti-ischemic and antioxidant agent, has been demonstrated to have many cardioprotective effects. However, whether early administration of trimetazidine has an effect on diabetic cardiomyopathy and the mechanisms underlying the effect have not yet been elucidated.We established a type 2 DCM rat model by high-fat diet and low-dose streptozotocin. Rats were separated into different groups: control, diabetes, and diabetes+trimetazidine (n=6, each). Cardiac autophagy, cardiac functions, and cardiomyocyte apoptosis were monitored.Rats with type 2 DCM showed severe insulin resistance, left ventricular dysfunction, increased cardiomyocyte apoptosis, and reduced cardiac autophagy. Collagen volume fraction (CVF) and perivascular collagen area/luminal area (PVCA/LA) ratio were significantly higher in the diabetic group than the control group. We found that trimetazidine treatment ameliorated metabolic disturbance and insulin resistance, reduced cardiomyocyte apoptosis, and restored cardiac autophagy. CVF and PVCA/LA ratio were also lower in the diabetes+trimetazidine group than the diabetic group (CVF, 4.750.52% vs. 11.041.67%, p<0.05; PVCA/LA, 8.370.51 vs. 17.972.66, p<0.05). Furthermore, trimetazidine inhibited phosphorylation of ERK and P38 MAPK to reduce myocardial fibrosis. Inhibited phosphorylation of AMPK was restored and the interaction between Bcl-2 and Beclin1 was enhanced in diabetes+trimetazidine group, resulting in the initiation of autophagy and alleviation of apoptosis.Early administration of trimetazidine could ameliorate diabetic cardiomyopathy by inhibiting myocardial fibrosis and cardiomyocyte apoptosis and enhancing autophagy. Therefore, trimetazidine may be a good choice in the prevention of diabetic cardiomyopathy if applied at the early stage of diabetes.