Jianning Zhang

Shandong University, Chi-nan-shih, Shandong Sheng, China

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Publications (3)6.18 Total impact

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    ABSTRACT: The aim of this study was to investigate whether C1q/TNF-related protein 9 (CTRP9) could stabilize the mature plaques by targeting macrophages in the apolipoprotein E knockout (ApoE KO) mice model. In vivo, the mice were subjected to high fat diet and constrictive collars on the right carotid artery for eight weeks, a lentiviral vectors expressing CTRP9 (LV-CTRP9) or green fluorescence protein (LV-eGFP) as a control was intravenously injected into ApoE KO mice. Delivery of LV-CTRP9 resulted in low contents of macrophages and lipids, and high contents of collagen and vascular smooth muscle cells in the carotid mature plaques. In addition, CTRP9 also decreased pro-inflammatory cytokines in mature plaques. In vitro, RAW264.7 macrophages were pretreated with or without LV-CTRP9 transfection, and then stimulated with oxLDL (50μg/mL). We found that the expression levels of tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) in the LV-CTRP9 group were significantly lower than those in the LV-eGFP group after exposure to oxLDL. The present data indicate that CTRP9 overexpression enhances the plaque stability in ApoE KO mice by reducing pro-inflammatory cytokines in macrophages. Our study suggests that the therapeutic approaches to enhance CTRP9 production could be valuable for plaque stabilization. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Feb 2015 · Biochemical and Biophysical Research Communications
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    ABSTRACT: Although heme oxygenase-1 (HO-1) has been implicated in protection against atherogenesis, its role in vulnerable plaques remains to be fully elucidated. This study was aimed to explore the effect of HO-1 on the progression and stabilization of vulnerable plaques and the possible mechanism. We established a vulnerable plaque model by local transfection with recombinant p53 adenovirus to plaques in rabbits fed a high-cholesterol diet. HO-1 activity was modulated by intraperitoneal injection of hemin or Sn-protoporphyrin IX (SnPP). HO-1 induction by hemin inhibited the progression of atherosclerotic lesions and changed the plaque morphology and composition into a more stable phenotype. In addition, hemin treatment is associated with a reduction in matrix metalloproteinase-9, interleukin-6 and tumor necrosis factor-α production, an increase in interleukin-10 level, as well as a decrease of TUNEL labeled apoptosis of smooth muscle cells in lesions. Compared with the control group, aortic nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity decreased markedly, whereas endothelial nitric oxide synthase (eNOS) activity increased significantly in the Hemin group. In contrast, inhibition of HO-1 by SnPP induced reversed effects and augmented plaque progression and vulnerability. After pharmacological triggering, the incidence of plaque disruption in SnPP group was significantly higher than that in control group (79% vs. 33%, P<0.05), while no plaque in Hemin group developed disruption (0% vs. 33%, P<0.05). These findings suggest that HO-1 induction could delay progression and enhance stability of atherosclerotic plaques, possibly through the attenuation of plaque inflammation and apoptosis, and the suppression of iNOS/NO production.
    No preview · Article · Dec 2011 · European journal of pharmacology
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    ABSTRACT: 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.
    No preview · Article · Sep 2011 · The Tohoku Journal of Experimental Medicine