Hong Jiang

Renmin University of China, Peping, Beijing, China

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Publications (220)593.22 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Atrial fibrillation (AF) is a frequent cause of stroke. More than 90% of thrombi were found in the left atrial appendage (LAA) in non-valvular AF. Transcatheter LAA closure has been developed as a novel approach to reduce the risk of stroke in patients with AF over the last decade. In this article, we review the recent advances and propose the possible challenges regarding the LAA closure for thromboembolism prevention in patients with AF.
    Journal of thoracic disease. 02/2015; 7(2):199-203.
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    ABSTRACT: Autonomic nervous systems play an important role in the initiation and maintenance of atrial fibrillation (AF), and modulation of autonomic nervous system function may contribute to AF control.
    The Canadian journal of cardiology 01/2015; · 3.12 Impact Factor
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    ABSTRACT: Ventricular arrhythmias (VAs) remain the major cause of mortality and sudden cardiac death (SCD) in almost all forms of heart disease. Despite so many therapeutic advances, such as pharmacological therapies, catheter ablation, and arrhythmia surgery, management of VAs remains a great challenge for cardiologists. Evidence from histological studies and from direct nerve activity recordings have suggested that increased sympathetic nerve density and activity contribute to the generation of VAs and SCD. It is well known that renal sympathetic nerve (RSN), either afferent component or efferent component, plays an important role in modulation of central sympathetic activity. We have recently shown that RSN activation by electrical stimulation significantly increases cardiac and systemic sympathetic activity and promotes the incidence of acute ischemia-induced VAs, suggesting RSN has a role in the development of VAs. Initial experience of RSN denervation (RDN) in patients with resistant hypertension showed that this novel and minimally invasive device-based approach significantly reduced not only kidney but also whole-body norepinephrine spillover. In addition, experimental studies find that left stellate ganglion nerve activity is significantly decreased after RDN. Based on these observations, it is reasonable to conclude that RDN may be an effective therapy for the management of VAs. Indeed, RDN has provided a protection against VAs in both animal models and patients. In this article, we review the role of the RSN in the generation of VAs and SCD and the role of RDN as a potential treatment strategy for VAs and SCD.
    Clinical research in cardiology : official journal of the German Cardiac Society. 01/2015;
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    ABSTRACT: Cardiac hypertrophy is the response of the heart to a variety of hypertrophic stimuli; this condition progresses to heart failure and sudden death. MicroRNAs (miRs) are a family of small, non-coding RNAs that mediate posttranscriptional gene silencing. Recent studies have identified miRs as important regulators in cardiac hypertrophy. One specific miR, miR-150 has been reported to be downregulated in hypertrophic murine hearts. However, the role of miR-150 as a regulator of cardiac hypertrophy remains unclear. In the present study, we used gain-of-function and loss-of-function approaches to investigate the functional roles of miR-150 in cardiac hypertrophy induced by aortic banding. The extent of the cardiac hypertrophy was evaluated by echocardiography and by pathological and molecular analyses of heart samples. Our results revealed that transgenic mice that overexpress miR-150 in the heart were resistant to cardiac hypertrophy and fibrosis through down-regulation of serum response factor (SRF). Conversely, the loss of function of miR-150 by genetic knockdown or antagomiR approaches produced the opposite effects. These studies suggest that miR-150 plays an important role in the regulation of cardiac hypertrophy and SRF is involved in miR-150 mediated anti-hypertrophic effect. Thus, miR-150 may be a new therapeutic target for cardiac hypertrophy. This article is protected by copyright. All rights reserved
    Journal of Cellular Biochemistry 01/2015; · 3.37 Impact Factor
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    International journal of cardiology. 01/2015; 182C:189-190.
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    ABSTRACT: Backgroud/Aims: The aim of the study was to evaluate the effects of beta1-adrenergic receptors (β1-ARs) -mediated nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase-1 (HO-1)-high mobility group box 1 protein (HMGB1) axis regulation in hypoxia/reoxygenation (H/R)-induced neonatal rat cardiomyocytes. The neonatal cultured cardiomyocytes were concentration-dependently pretreated by dobutamine (DOB), a selective β1-adrenergic receptor agonist, in the absence and/or presence of LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), SB203580 (a p38mitogen-activated-protein kinase (p38MAPK) inhibitor), Nrf2siRNA and HO-1siRNA, respectively, and then treated by H/R. The effects and mechanisms by which H/R-induced cardiomyocytes injury were evaluated. Significant increase of HO-1 was found in neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Significant change for Nrf2 translocation was also revealed in neonatal cultured cardiomyocytes treated with DOB. Insignificant decreases of NF-kappaB p65 activation and HMGB1 release were observed in H/R-induced neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Importantly, DOB treatment significantly increased the cell viability and decreased the levels of LDH and MDA in H/R-induced cardiomyocytes injury. However, DOB failed to increase HO-1, inhibit NF-kappaB p65 activation, prevent HMGB1 release and attenuate H/R-induced cardiomyocytes injury when the cultured cardiomyocytes were pretreated by Nrf2siRNA, HO-1siRNA, PI3K inhibitor (LY294002) and p38MAPK inhibitor (SB203580), respectively. β1-ARs-mediated Nrf2-HO-1-HMGB1 axis regulation plays a critical protective role in H/R-induced neonatal rat cardiomyocytes injury in vitro via PI3K/p38MAPK signaling pathway. © 2015 S. Karger AG, Basel.
    01/2015; 35(2):767-77.
  • Bo He, Zhibing Lu, Hong Jiang
    International Journal of Cardiology 12/2014; 181C:355-356. · 6.18 Impact Factor
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    International Journal of Cardiology 12/2014; 177(2):676-7. · 6.18 Impact Factor
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    ABSTRACT: Vagus nerve stimulation (VNS) improves left ventricular remodeling by down-regulation of matrix metalloproteinase 9 (MMP-9) and transforming growth factor β1 (TGF-β1). Our previous study found low-level transcutaneous electrical stimulation of the auricular branch of the vagus nerve (LL-TS) could be substituted for VNS to reverse cardiac remodeling. So we hypothesize that LL-TS could ameliorate left ventricular remodeling by regulation of MMP-9 and TGF-β1 after myocardial infarction (MI). Twenty-two beagle dogs were randomly divided into a control group (MI was induced by permanent ligation of the left coronary artery, n=8), a LL-TS group (MI with long-term intermittent LL-TS, n=8) and a normal group (sham ligation without stimulation, n=6). At the end of 6 weeks follow-up, LL-TS significantly reduced LV end-systolic and end-diastolic dimensions, improved ejection fraction and ratio of early (E) to late (A) peak mitral inflow velocity. LL-TS attenuated interstitial fibrosis and collagen degradation in the noninfarcted myocardium compared to the control group. Elevated level of MMP-9 and TGF-β1 in LV tissue and peripheral plasma were diminished in the LL-TS treated dogs. LL-TS improves cardiac function and prevents cardiac remodeling in the late stages after MI by down-regulation of MMP-9 and TGF-β1 expression.
    Journal of Cardiovascular Pharmacology 12/2014; · 2.11 Impact Factor
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    ABSTRACT: Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone resorption. Osteoclasts are multinucleated cells derived from hematopoietic stem cells (HSCs) or monocyte/macrophage progenitor cells and formed by osteoclasts precursors (OCPs) fusion. Cyanidin is an anthocyanin widely distributed in food diet with novel antioxidant activity. However, the effect of cyanidin on osteoclasts is still unknown. We investigated the effect of cyanidin on RANKL-induced osteoclasts differentiation and cell fusion. The results showed that cyanidin had a dual effect on RANKL-induced osteoclastogenesis. Lower dosage of cyanidin (< 1μg/ml) has a promoting effect on osteoclastogenesis while higher dosage of cyanidin (> 10μg/ml) has an inhibitory effect. Fusogenic genes like CD9, ATP6v0d2, DC-STAMP, OC-STAMP and osteoclasts related genes like NFATc1, mitf and c-fos were all regulated by cyanidin consistent to its dual effect. Further exploration showed that low concentration of cyanidin could increase osteoclasts fusion whereas higher dosage of cyanidin lead to the increase of LXR-β expression and activation which is suppressive to osteoclasts differentiaton. All these results showed that cyanidin exhibits therapeutic potential in prevention of osteoclasts related bone disorders. This article is protected by copyright. All rights reserved
    Journal of Cellular Physiology 12/2014; · 3.87 Impact Factor
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    ABSTRACT: Colorectal cancer (CRC) is one of the most common types of cancer worldwide. The majority of mortalities caused by colorectal cancer are due to metastatic disease. As numerous CRC patients experience metastasis to the liver or lung and fail to respond to curative therapies, intensive research efforts have sought to identify the molecular changes or regulatory mechanisms underlying CRC metastasis. In the present study, a stable CRC cell line, HCT16, overexpressing firefly luciferase was constructed and an in vivo metastasis model was established via intravenous injection of this cell line. Using an imaging system, tumor tissue located in the lung and colon was separated and cells were prepared. The microRNA (miRNA) expression profiles of these lung homing or colon homing cells were assessed and compared. A total of 38 differentially expressed miRNAs were selected and confirmed our previous results; several of these have been reported to be involved in the regulation of cancer progression. However, the remaining miRNAs require further investigation. The present profiling may be the first step toward delineating the differential expression of miRNAs in the CRC cells located in the colon and the lung, enabling the elucidation of the regulation associated with miRNAs in colorectal lung metastases. These miRNAs require further validation and functional analysis to evaluate whether they are important in the pathogenesis of colorectal lung metastases or are adopted as markers to predict colorectal metastasis.
    Molecular Medicine Reports 11/2014; · 1.48 Impact Factor
  • Jichun Wang, Xiaorong Hu, Hong Jiang
    International Journal of Cardiology 11/2014; 180C:38-39. · 6.18 Impact Factor
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    ABSTRACT: Activation of efferent vagus fibers exerts an anti-inflammatory role, a mechanism known as the cholinergic anti-inflammatory pathway. We hypothesised that stimulation of atrial ganglionated plexi (GP) may also be anti-inflammatory. Six-hour low-intensity GP stimulation was performed in eight dogs and the serum levels of acetylcholine (Ach), C reactive protein (CRP), interleukin-6 (IL-6), high-mobility group box 1 (HMGB1) were determined with enzyme-linked immunosorbent assay kits. The serum level of acetylcholine was significantly increased (P<0.05) while the serum levels of inflammatory factors of C reactive protein, interleukin-6 and high-mobility group box 1 were markedly decreased after six-hour GP stimulation (all P<0.05). These results suggest that GP stimulation exerts an anti-inflammatory role and might be a therapeutic option for inflammatory heart diseases. Copyright © 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.
    Heart, Lung and Circulation 11/2014; · 1.17 Impact Factor
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    ABSTRACT: To explore the effects of Kindlin-2 RNA interference on vascular smooth muscle cells (VSMCs) migration, adhesion and β1-integrin as well as the relationship between Kindlin-2 and β1-integrin. Primary VSMCs were cultured, infected with Kindlin-2 siRNA lentiviral vectors.VSMCs were divided into three groups:the blank control group, the negative control group and the Kindlin-2 siRNA group. The ability of VSMCs migration was measured by Transwell experiment and wound healing assay. The ability of VSMCs adhesion to extracelluar matrix was determined by cell-extracelluar matrix adhesion assay. The Kindlin-2 and β1-integrin mRNA and protein expression levels were detected by real-time quantitative PCR and Western blot. Total β1-integrin and active β1-integrin expression on the surface of VSMCs was evaluated by flow cytometry. The efficiency of Kindlin-2 siRNA lentivirus infected VSMCs was more than 90%. The number of VSMCs migration in the Kindlin-2 siRNA group was significantly lower than that of the blank control group and the negative group (all P < 0.05). Moreover, the distance of VSMCs migration was shorter than that of the blank control group and the negative group (all P < 0.05). The number of VSMCs adhesion to collagen I was less than that of the blank control group and the negative group (all P < 0.05). A590 nm of the Kindlin-2 siRNA group was also lower than that of the blank control group and the negative group (all P < 0.05). Compared with the blank control group, the expression level of Kindlin-2 mRNA in the Kindlin-2 siRNA group decreased 47% (P < 0.05), but the expression level of β1-integrin mRNA remained unchanged. The Kindlin-2 protein level in the Kindlin-2 siRNA group was lower than that of the blank control group and the negative group (all P < 0.05). β1-integrin protein level was similar among the three groups. Activated β1-integrin on the surface of VSMCs in the Kindlin-2 siRNA group was lower than that of the blank control group and the negative group (all P < 0.05).However, the expression level of total β1-integrin on the VSMCs surface was similar among the three groups. Kindin-2 can regulate VSMCs migration and adhesion and activate β1-integrin on the surface of VSMCs.
    Zhonghua xin xue guan bing za zhi. 11/2014; 42(11):938-943.
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    ABSTRACT: DC-STAMP is a key regulating molecule of osteoclastogenesis and osteoclast precursor (OCP) fusion. Emerging lines of evidence showed that microRNAs play crucial roles in bone metabolism and osteoclast differentiation, but no microRNA has yet been reported to be directly related to OCPs fusion. Through a microarray, we found that the expression of miR-7b in RAW264.7 cells was significantly decreased after induction with M-CSF and RANKL. The overexpression of miR-7b in RAW264.7 cells attenuated the number of TRAP-positive cells number and the formation of multinucleated cells, whereas the inhibition of miR-7b enhanced osteoclastogenesis. Through a dual luciferase reporter assay, we confirmed that miR-7b directly targets DC-STAMP. Other fusogenic molecules, such as CD47, ATP6v0d2, and OC-STAMP, were detected to be downregulated in accordance with the inhibition of DC-STAMP. Because DC-STAMP also participates in osteoclast differentiation through the ITAM-ITIM network, multiple osteoclast-specific genes in the ITAM-ITIM network were detected to identify how DC-STAMP is involved in this process. The results showed that molecules associated with the ITAM-ITIM network, such as NFATc1 and OSCAR, which are crucial in osteoclastogenesis, were consistently altered due to DC-STAMP inhibition. These findings suggest that miR-7b inhibits osteoclastogenesis and cell-cell fusion by directly targeting DC-STAMP. In addition, the inhibition of DC-STAMP and its downstream signals changed the expression of other fusogenic genes and key regulating genes, such as Nfatc1, c-fos, Akt, Irf8, Mapk1, and Traf6. In conclusion, our findings indicate that miR-7b may be a potential therapeutic target for the treatment of osteoclast-related bone disorders.
    Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 11/2014; · 5.44 Impact Factor
  • International Journal of Cardiology 10/2014; 178C:210-211. · 6.18 Impact Factor
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    International Journal of Cardiology 10/2014; 179C:144-145. · 6.18 Impact Factor
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    Bing Huang, Lilei Yu, Hong Jiang
    International Journal of Cardiology 10/2014; 179C:123-124. · 6.18 Impact Factor
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    Bing Huang, Zhibing Lu, Hong Jiang
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    ABSTRACT: Sirs:Recently, Scholz et al. [1] presented an interesting case of ventricular electrical storm in a patient with dilated cardiomyopathy. After high-dose amiodarone therapy (200 mg QD), endocardial ventricular tachycardia (VT)-ablation, epicardial VT-ablation, and followed maximal antiarrhythmic drug therapy, the patient still showed recurrent VT episodes. Subsequently, renal sympathetic denervation (RDN) was successfully performed without affecting blood pressure and renal function. Only one more VT episode that required implantable cardioverter defibrillator therapy recurred during a 5-month follow-up. Before that, similar attempts were made by Ukena et al. [2], Hoffmann et al. [3], and Remo et al. [4], who showed that RDN was an effective and safe approach to the treatment of ischemic or nonischemic electrical storm. However, the underlying mechanisms and the potential role of kidney in the generation of ventricular arrhythmias (VAs) and sudden cardiac death (SCD) remain unclear. ...
    Clinical Research in Cardiology 10/2014; 104(2). · 4.17 Impact Factor
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    ABSTRACT: The autonomic imbalance during acute ischemia is involved in the occurrence of life-threatening arrhythmias.
    PLoS ONE 10/2014; 9(10):e109313. · 3.53 Impact Factor

Publication Stats

1k Citations
593.22 Total Impact Points


  • 2005–2015
    • Renmin University of China
      Peping, Beijing, China
  • 2014
    • Hangzhou First People's Hospital
      Hang-hsien, Zhejiang Sheng, China
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China
  • 2013–2014
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
    • Hubei Polytechnic University
      Hu-pei-ts’un, Shanxi Sheng, China
  • 2010–2014
    • Shandong University
      • • Key Laboratory for Cardiovascular Remodelling and Function Research
      • • Institute of Psychology
      Chi-nan-shih, Shandong Sheng, China
  • 2002–2014
    • Wuhan University
      • Department of Cardiology
      Wu-han-shih, Hubei, China
  • 2009–2010
    • Sichuan University
      • • Analytical Center
      • • College of Chemistry
      Hua-yang, Sichuan, China
  • 2006
    • Nanjing University
      • International Institute for Earth System Science
      Nan-ching, Jiangsu Sheng, China