Browsing by Author "Zheng, Xilong"

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    Association between Cardiac Autonomic Neuropathy and Coronary Artery Lesions in Patients with Type 2 Diabetes
    (2020-12-30) Liu, Lei; Wu, Qiansheng; Yan, Hong; Chen, Baoxian; Zheng, Xilong; Zhou, Qiang
    Objective. Cardiac autonomic neuropathy (CAN) is a common and serious complication of diabetes mellitus with various systemic involvements, such as atherosclerotic cardiovascular disease. We aimed to evaluate the association between CAN and coronary artery lesions in patients with type 2 diabetes. Research Design and Methods. We retrospectively reviewed the medical records of 104 patients with type 2 diabetes and coronary artery disease (CAD). We evaluated heart rate variability (HRV) parameters (SDANN, SDNN, and pNN50) to assess cardiac autonomic function. The severity of coronary lesions was assessed by the Gensini scores and the number of affected vessels. Correlation analyses between HRV parameters and the severity of coronary lesions and clinical parameters were performed. Results. Spearman’s correlation analysis showed a significant negative correlation between SDANN and Gensini scores (,). Interestingly, this finding remained significant after adjusting for clinical covariates (,). However, there was no association between HRV parameters and the severity of coronary lesions as assessed by the number of affected vessels. Clinical parameters were not significantly correlated with HRV parameters (all ).Conclusions. Cardiac autonomic neuropathy might be related to the degree of coronary atheromatous burden in patients with type 2 diabetes. Screening for cardiac autonomic neuropathy might potentially be beneficial in the risk stratification of patients with type 2 diabetes.
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    Myeloperoxidase-oxidized high density lipoprotein impairs atherosclerotic plaque stability by inhibiting smooth muscle cell migration
    (2017-01-10) Zhou, Boda; Zu, Lingyun; Chen, Yong; Zheng, Xilong; Wang, Yuhui; Pan, Bing; Dong, Min; Zhou, Enchen; Zhao, Mingming; Zhang, Youyi; Zheng, Lemin; Gao, Wei
    Abstract Background High density lipoprotein (HDL) has been proved to be a protective factor for coronary heart disease. Notably, HDL in atherosclerotic plaques can be nitrated (NO2-oxHDL) and chlorinated (Cl-oxHDL) by myeloperoxidase (MPO), likely compromising its cardiovascular protective effects. Method Here we determined the effects of NO2-oxHDL and Cl-oxHDL on SMC migration using wound healing and transwell assays, proliferation using MTT and BrdU assays, and apoptosis using Annexin-V assay in vitro, as well as on atherosclerotic plaque stability in vivo using a coratid artery collar implantation mice model. Results Our results showed that native HDL promoted SMC proliferation and migration, whereas NO2-oxHDL and Cl-oxHDL inhibited SMC migration and reduced capacity of stimulating SMC proliferation as well as migration, respectively. OxHDL had no significant influence on SMC apoptosis. In addition, we found that ERK1/2-phosphorylation was significantly lower when SMCs were incubated with NO2-oxHDL and Cl-oxHDL. Furthermore, transwell experiments showed that differences between native HDL, NO2-oxHDL and Cl-oxHDL was abolished after PD98059 (MAPK kinase inhibitor) treatment. In aortic SMCs from scavenger receptor BI (SR-BI) deficient mice, differences between migration of native HDL, NO2-oxHDL and Cl-oxHDL treated SMCs vanished, indicating SR-BI’s possible role in HDL-associated SMC migration. Importantly, NO2-oxHDL and Cl-oxHDL induced neointima formation and reduced SMC positive staining cells in atherosclerotic plaque, resulting in elevated vulnerable index of atherosclerotic plaque. Conclusion These findings implicate MPO-catalyzed oxidization of HDL may contribute to atherosclerotic plaque instability by inhibiting SMC proliferation and migration through MAPK-ERK pathway which was dependent on SR-BI.
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    Plasma Homocysteine and Autonomic Nervous Dysfunction: Association and Clinical Relevance in OSAS
    (2020-07-09) Liu, Lei; Wu, Qiansheng; Yan, Hong; Zheng, Xilong; Zhou, Qiang
    Objective. Elevated plasma homocysteine (Hcy) is an independent risk factor for cardiovascular diseases, but the precise mechanism of Hcy in cardiovascular disease remains elusive. This study is aimed at evaluating the association between Hcy levels and autonomic nervous system and at investigating their clinical relevance in obstructive sleep apnea syndrome (OSAS). Methods. A total of 191 subjects with OSAS were enrolled for this cross-sectional study. Heart rate variability (HRV) represents the status of the autonomic nervous system and is a well-known index that allows studying the autonomic modulation. HRV and polysomnography parameters were collected based on Holter monitors and polysomnography system. The software computed all the basic HRV parameters including SDANN, SDNN and pNN50. Correlation analyses between Hcy and HRV parameters and echocardiographic parameters were performed. Results. Compared with the mild-moderate OSAS group, the prevalence of male and smoking and Hcy levels were considerably higher in the severe OSAS group (,, and , respectively). Also, there were significant linear relationships between Hcy quartiles with the proportion of severe OSAS ( for the trend). Interesting, there is a negative linear correlation between SDANN and Hcy quartiles ( for the trend). Spearman’s correlation analysis showed a significant negative correlation between SDANN and Hcy levels (,). Interestingly, the relationship of it remains significant after adjustment for clinical covariates (,). However, echocardiographic parameters were not significantly correlated with Hcy or HRV parameters (all ).Conclusions. Elevated plasma Hcy level is linearly correlated with cardiac autonomic nervous function disorders in patients with OSAS.
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    Porcine Circovirus Cap-Induced Apoptosis of Non-Infected PK15 Cells
    (2019-07-16) Rowell, Jared S.; Czub, Markus; Zheng, Xilong; Jirik, Frank Robert; Knight, Cameron G.; Corcoran, Jennifer A.
    Porcine Circovirus 2 (PCV2) is a pathogen of major importance for swine production around the world. Despite development of several vaccines and robust vaccination programs, PCV2 continues to persistently transmit within and between swine herds causing infections marked by immunosuppression via lymphocyte depletion. This study aims to improve understanding of porcine circovirus diseases (PCVD) pathogenesis caused by PCV capsid cytotoxicity which activates apoptosis in non-infected bystander cells. Putatively non-pathogenic Porcine Circovirus 1 (PCV1) was also included to help understand why there is a difference in pathogenicity between PCV1 and PCV2. Porcine Circovirus 3 (PCV3) has recently emerged worldwide as a possible etiological agent of clinical syndromes observed in swine that are similar to PCVD caused by PCV2. The capsid protein of PCV3 (PCV 3 Cap) was also included in this study to provide initial information regarding the cytotoxicity of this protein. Results were obtained through flow cytometric analysis of apoptosis using Annexin V-FITC and 7-AAD to measure apoptosis markers and cell death respectively. Flow cytometry results were reinforced by also utilizing a TUNEL assay in conjunction with confocal imaging to detect cells undergoing DNA fragmentation leading to apoptosis. Results show that monomeric PCV2 Cap, 1% formaldehyde inactivated and dialyzed PCV2, PCV1 virus-like particles (VLPs), PCV2 VLPs, and PCV3 VLPs are all able to activate apoptosis in porcine kidney (PK15) cells at a rate of ~%30 after a 24-hour exposure; this apoptotic similar to apoptosis caused by 50 µM etoposide, which is a strong chemical inducer of apoptosis. These results coupled with preliminary data obtained by pre-treating PK15 cells with caspase-8 or caspase-9 inhibitors suggest the involvement of caspase-8 and caspase-9 in PCV2 Cap induced apoptosis and lend weight to the idea of PCV2 Cap as a primary virulence factor during infections. In contrast, PCV1 Cap induced apoptosis does not appear to involve caspase-8 or caspase-9 indicating an alternate pathway to PK15 cell apoptosis, while PCV3 Cap appears to induce PK15 cell apoptosis with some involvement of caspase-9.
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    Tyrosine kinase pathways, smooth muscle function and iNOS induction
    (1997) Zheng, Xilong; Hollenberg, Morley Donald