Hong Jiang

Huazhong University of Science and Technology, Wu-han-shih, Hubei, China

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Publications (291)614.31 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: This study was designed to demonstrate that spinal cord stimulation (SCS) could suppress high-frequency stimulation (HFS) induced focal atrial fibrillation (AF) at atrial and pulmonary veins (PVs) sites by inhibiting atrial ganglionated plexus (GP) activity.
    Journal of cardiovascular pharmacology. 08/2014;
  • Jichun Wang, Xiaorong Hu, Hong Jiang
    International journal of cardiology. 08/2014;
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    ABSTRACT: Recently, a beneficial effect of renal sympathetic denervation (RSD) has been seen in patients with ventricular electrical storm. However, the effect of RSD on ventricular electrophysiology remains unclear. Thirty-three mongrel dogs were included in the present study. RSD was performed by radiofrequency ablation of the adventitial surface of the renal artery. In Group 1 (n = 8), programmed stimulation was performed before and after RSD to determinate ventricular effective refractory period (ERP) and action potential duration (APD) restitution properties. The same parameters were measured in 5 other animals that underwent sham RSD to serves as controls. In Group 2 (n = 10), acute myocardial ischemia (AMI) was induced by ligating the proximal left anterior descending coronary artery after the performance of RSD and the ventricular arrhythmia (VA) incidence was calculated during 1-h recording. In another 10 dogs (Group 3), AMI was induced and VA was measured with sham RSD. In Group 1, RSD significantly prolonged ventricular ERP and APD, reduced the maximum slope (Smax) of the restitution curve and suppressed APD alternans at each site. RSD also significantly decreased the spatial dispersions of ERP, APD and Smax. In the 5 control animals, no significant electrophysiological change was detected after sham RSD. The occurrence of spontaneous VA during 1-h of AMI in Group 2 was significantly lower than that in Group 3. These data suggest that RSD stabilizes ventricular electrophysiological properties in normal hearts and reduces the occurrence of VA in AMI hearts.This article is protected by copyright. All rights reserved
    Experimental physiology 08/2014; · 3.17 Impact Factor
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    ABSTRACT: Characteristics of heart failure with preserved ejection fraction (HFPEF) have not yet been fully understood. The objectives of this pilot study are to detect protein expression profile in the sera of HFPEF patients, and to identify potential biomarkers for the disease. Five hundred and seven proteins were detected in the sera of healthy volunteers and patients with either HFPEF or hypertension using antibody microarrays (three in each group). The results showed that the serum concentrations of 17 proteins (e.g. angiogenin, activin A and artemin) differed considerably between HFPEF and non-HFPEF patients (hypertensive patients and healthy controls), while a protein expression pattern distinct from that in non-HFPEF patients was associated with HFPEF patients. The up-regulation of angiogenin in both HFPEF patients with LVEF ≥50% (P = 0.004) and a subset of HFPEF patients with LVEF = 41–49% (P < 0.001) was further validated in 16 HFPEF patients and 16 healthy controls. Meanwhile, angiogenin distinguished HFPEF patients from controls with a mean area under the receiver operating characteristic curve of 0.88 (P < 0.001) and a diagnostic cut-off point of 426 ng/ml. Moreover, the angiogenin levels in HFPEF patients were positively correlated with Lg(N-terminal pro-B-type natriuretic peptide, NT-proBNP) (P < 0.001). In addition, high angiogenin level (≥426 ng/ml) was a predictor of all-cause death within a short-term follow-up duration, but not in the longer term of 36 months. This pilot study indicates that the aforementioned 17 potential biomarkers, such as angiogenin, may hold great promise for both diagnosis and prognosis assessment of HFPEF.
    Journal of Cellular and Molecular Medicine 08/2014; · 4.75 Impact Factor
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    ABSTRACT: Renal sympathetic nerve (RSN) activity plays a key role in systemic sympathetic hyperactivity. Previous studies have shown that cardiac sympathetic hyperactivity, especially the left stellate ganglion (LSG), contributes to the pathogenesis of ventricular arrhythmias (VAs) after acute myocardial infarction (AMI).
    Journal of Cardiovascular Electrophysiology 07/2014; · 3.48 Impact Factor
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    ABSTRACT: Abstract The expansion of a polyglutamine domain in the protein ataxin3 causes spinocerebellar ataxia type-3 (SCA3). However, there is little information to date about the upstream proteins in the ubiquitin-proteasome system of pathogenic ataxin3-80Q. Here, we report that BAG2 (Bcl-2 associated athanogene family protein 2) and BAG5 (Bcl-2-associated athanogene family protein 5) stabilise pathogenic ataxin3-80Q by inhibiting its ubiquitination as determined based on western blotting and co-immunofluorescence experiments. The association of the BAG2 and BAG5 proteins with pathogenic ataxin3-80Q strengthens the important roles of the BAG family in neurodegenerative diseases.
    The International journal of neuroscience. 07/2014;
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    ABSTRACT: High mobility group box 1 protein (HMGB1) has an important role in myocardial ischemia/reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been shown to inhibit HMGB1 expression. In the present study, the effect of sodium butyrate on myocardial I/R injury in rats was investigated. Anesthetized male rats were intraperitoneally administered sodium butyrate (100 or 300 mg/kg) 30 min prior to the induction of ischemia. The rats were then subjected to ischemia for 30 min followed by reperfusion for 4 h. Infarct size, lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were then measured. The expression of HMGB1 was assessed using western blot analysis. The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05). In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05). Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-α, IL-6 and HMGB1 induced by I/R injury (P<0.05). In conclusion, the results from the present study suggest that preconditioning with sodium butyrate may attenuate myocardial I/R injury by inhibition of the expression of inflammatory mediators during myocardial I/R.
    Experimental and therapeutic medicine 07/2014; 8(1):229-232. · 0.34 Impact Factor
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    ABSTRACT: : Electrical carotid baroreceptor stimulation (CBS) has shown therapeutic potential for resistant hypertension and heart failure by resetting autonomic nervous system, but the impacts on arrhythmias remains unclear. The present study evaluated the effects of CBS on ventricular electrophysiological properties in normal dog heart and arrhythmias following acute myocardial infarction (AMI). In the acute protocol anesthetized open chest dogs were exposed to 1 hour left anterior descending coronary occlusion, as AMI model. Dogs were received either sham treatment (Control group, n=8) or CBS (CBS group, n=8), started 1 hour before AMI. CBS resulted in pronounced prolongation of ventricular effective refractory period and reduction of the maximum action potential duration restitution slope (from 0.85±0.15 in the baseline state to 0.67±0.09 at the end of 1 hour, P<0.05) before AMI. Number of premature ventricular contractions (277±168 in the Control group vs 103±84 in the CBS group, P<0.05) and episodes of ventricular tachycardia/ventricular fibrillation (7±3 in the Control group vs 3±2 in the CBS group P<0.05) was decreased compared with the control group during AMI. CBS buffered low frequency/high frequency ratio raise during AMI. Ischemic size was not affected by CBS. CBS may have a beneficial impact on ventricular arrhythmias induced by AMI through modulation of autonomic tone.
    Journal of cardiovascular pharmacology. 06/2014;
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    ABSTRACT: High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia-reperfusion (I/R) injury. B-type natriuretic peptide (BNP) postconditioning has been reported to reduce myocardial I/R injury. The present study investigated whether postconditioning of BNP could reduce myocardial I/R injury by inhibiting HMGB1 expression and the potential mechanisms in rats. The left anterior descending coronary arteries of rats were occluded to induce ischemia for 30 min and reopened to imitate reperfusion for 4 h. The rats were treated with BNP (0.03 μg/kg min, i.v.) 15 min before reperfusion until the end of the procedure, with or without treatment of LY294002 (an inhibitor of phosphoinositide 3-kinase (PI3K), 0.3 mg/kg, i.v.), which was injected 20 min before reperfusion. Lactate dehydrogenase (LDH), creatine kinase (CK), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and infarct size were measured. Phospho-Akt, total Akt, and HMGB1 expression were assessed by immunoblotting. The results showed that treatment of BNP postconditioning could significantly decrease the infarct size and the levels of LDH and CK after 4-h reperfusion (all p < 0.05). BNP postconditioning could also significantly inhibit the increases of TNF-α and IL-6 (both p < 0.05). In addition, BNP postconditioning could significantly inhibit HMGB1 expression induced by I/R (p < 0.05). Administration of LY294002 abolished the effects of BNP postconditioning on myocardial I/R injury and the expressions of phospho-Akt and HMGB1 (all p < 0.05). The present study suggests that postconditioning of BNP could protect against myocardial I/R injury which may be associated with inhibiting HMGB1 expression, while PI3K/Akt signaling pathway may be involved in the expression of HMGB1 and the protective effect of BNP postconditioning.
    Inflammation 04/2014; · 2.46 Impact Factor
  • Xiaorong Hu, Weipan Xu, Hong Jiang
    International journal of cardiology 04/2014; · 6.18 Impact Factor
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    ABSTRACT: Polymorphism of the apolipoprotein E (APOE) gene has been defined as a modifying factor for age at onset (AO) in neurodegenerative disorders. The AO of spinocerebellar ataxia type 3 or Machado-Joseph disease (SCA3 or MJD) is inversely correlated with expanded CAG repeat lengths in the ATXN3 gene; however, AO is only partially explained by the expanded CAG repeats. We performed a case-control study to explore whether APOE genotypes play a role in AO of SCA3 or MJD from the Chinese Han population. The APOE genotypes were analyzed in an independent cohort of 155 patients with SCA3 or MJD and 191 controls both from Mainland China. Our study demonstrated that SCA3 or MJD patients experienced an earlier onset if they were carriers of APOE ε2 allele, which decreased the AO by nearly 4 years. This study may also reconfirm the effect of the APOE gene on SCA3 or MJD patients from different races and indicated that certain APOE alleles might be genetic modifiers for AO in SCA3 or MJD.
    Neurobiology of aging 03/2014; · 5.94 Impact Factor
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    ABSTRACT: Isoproterenol (ISO) has been reported to inhibit high mobility group box 1 (HMGB1) protein release via heme oxygenase‑1 (HO‑1) induction in lipopolysaccharide (LPS)‑activated RAW 264.7 cells and increase the survival rate of cecal ligation and puncture (CLP)‑induced septic mice. Therefore, it was examined whether ISO‑mediated HO‑1 induction inhibits HMGB1 release in cardiac myocytes and attenuates myocardial ischemia/reperfusion (I/R) injury in rats. Anesthetized male rats were pretreated with ISO [intraperitoneal (i.p.) injection of 10 mg/kg] prior to ischemia in the absence and/or presence of zinc protoporphyrin IX (ZnPPIX, i.p., 10 mg/kg), which is an inhibitor of HO‑1, and then subjected to ischemia for 30 min followed by reperfusion for 24 h. The myocardial I/R injury and oxidative stress were assessed. In addition, the HO‑1 protein and HMGB1 expression were measured by western blot analysis. ISO significantly attenuated the myocardial I/R injury, reduced oxidative stress, and induced HO‑1 and reduced HMGB1 release. However, all these effects caused by ISO were significantly reversed in the presence of ZnPPIX. These results suggested that ISO has a pivotal role in the protective effects on myocardial I/R injury. This protection mechanism is possibly due to the inhibition of HMGB1 release via the induction of HO‑1.
    Molecular Medicine Reports 03/2014; · 1.17 Impact Factor
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    ABSTRACT: Phenotypic switching of vascular smooth muscle cells (VSMCs) plays an initial role in neointimal hyperplasia, the main cause of many occlusive vascular diseases. The aim of this study was to measure the effects of resveratrol (RSV) on the phenotypic transformation of VSMCs and to investigate its mechanism of action. Cultured VSMCs isolated from rat thoracic aorta were prepared with serum starvation for 72 hours followed by RSV treatment (50-200 μmol/L) and 10% serum stimulation. Male Sprague-Dawley rats, subjected to carotid arteries injury from a balloon catheter, were exposed to intraperitoneal injection of RSV (1 mg/kg) or saline and were killed after 7 or 28 days. Compared with cells in the serum-induced group, VSMCs in the RSV or N-[N-(3, 5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) treatment group exhibited significant decreases of proliferation and migration. The total and cytoplasmic Notch-1 levels were declined by RSV, accompanied by a significant increase in smooth muscle α-actin and smooth muscle myosin heavy chain protein. The expression of Notch-1, Jagged-1, Hey-1, and Hey-2 mRNA in balloon-injured arteries at 7 days was decreased by RSV treatment. Arteries from RSV-treated rats showed less neointimal hyperplasia, lower collagen content, and a lower rate of cells positive for proliferating cell nuclear antigen 28 days after injury, compared with saline controls. The results indicate that RSV can attenuate phenotypic switching of VSMCs after arterial injury through inhibition of the Notch pathway.
    Journal of cardiovascular pharmacology 03/2014; 63(3):233-9. · 2.83 Impact Factor
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    ABSTRACT: Vascular smooth muscle cells (VSMCs) are known to undergo functional changes that contribute to the pathogenesis of atherosclerosis and restenosis. Wnts are a family of secreted glycoproteins that bind to transmembrane Frizzled receptors and initiate signaling cascades with indispensable roles during cell migration, adhesion, proliferation, and survival. The present study reports that wingless‑type MMTV integration site family, member 3a (Wnt3a) activates the canonical Wnt pathway in rat VSMCs by triggering the phosphorylation of β‑catenin at position Ser675 and GSK‑3β at position Ser9. Phosphorylation of these two proteins increases VSMC migration and adhesion. In a search for the downstream mediators of Wnt3a's effects on VSMC migration and adhesion, Wnt3a treatment was observed to increase integrin‑linked kinase (ILK) protein expression. ILK is a serine/threonine protein kinase that is thought to control cell migration and adhesion by regulating the affinity of β1‑integrin for the extracellular matrix. Wnt3a treatment of VSMCs also activated β1‑integrin without changing the quantity of protein expressed on the cell surface. These results demonstrate that Wnt3a enhances migration and adhesion of VSMCs by activating β1‑integrin.
    Molecular Medicine Reports 02/2014; · 1.17 Impact Factor
  • Hong Jiang, Ying Yu, Junbo Ge
    Chinese medical journal 02/2014; 127(3):580-5. · 0.90 Impact Factor
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    ABSTRACT: Cerebral amyloid angiopathy (CAA) is a common degenerative disease presenting intracerebral hemorrhage (ICH) in older people. Uric acid (UA) is a natural antioxidant, and may have a beneficial role in neurodegenerative diseases. Nevertheless, the role of UA in CAA remains unknown. In the present study, we compared serum UA levels in CAA-associated ICH patients (n = 82) and age/sex-matched controls (n = 82). Serum UA levels in possible CAA were significantly decreased when compared with healthy controls (232.68 ± 77.70 vs. 309.42 ± 59.83 μmol/L; p < 0.001). Furthermore, UA levels in patients clinically diagnosed as probable CAA were significantly lower than those in patients diagnosed as possible CAA (193.06 ± 56.98 vs. 232.68 ± 77.70 μmol/L; p = 0.014). These differences were still significant after adjusting for renal function and dyslipidemia (p < 0.001 and p = 0.002, respectively). However, there were no associations between serum UA levels and the distribution of hemorrhagic lesion, as well as neurological impairment. Our observations indicate that serum UA levels were decreased in CAA patients. UA might play a neuroprotective role in CAA and serve as a potential biomarker for reflecting the severity of Aβ deposition.
    Neurological Sciences 01/2014; · 1.41 Impact Factor
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    ABSTRACT: Each approach for artificial cornea design is toward the same goal: to develop a material that best mimics the important properties of natural cornea. Accordingly, the selection and optimization of corneal substitute should be based on their physicochemical properties. In this study, three types of polyvinyl alcohol (PVA) hydrogels with different polymerization degree (PVA1799, PVA2499 and PVA2699) were prepared by freeze-thawing techniques. After characterization in terms of transparency, water content, water contact angle, mechanical property, root-mean-square roughness and protein adsorption behavior, the optimized PVA2499 hydrogel with similar properties of natural cornea was selected as a matrix material for artificial cornea. Based on this, a biomimetic artificial cornea was fabricated with core-and-skirt structure: a transparent PVA hydrogel core, surrounding by a ringed PVA-matrix composite skirt that composed of graphite, Fe-doped nano hydroxyapatite (n-Fe-HA) and PVA hydrogel. Different ratio of graphite/n-Fe-HA can tune the skirt color from dark brown to light brown, which well simulates the iris color of Oriental eyes. Moreover, morphologic and mechanical examination showed that an integrated core-and-skirt artificial cornea was formed from an interpenetrating polymer network, no phase separation appeared on the interface between the core and the skirt.
    Journal of Materials Science Materials in Medicine 01/2014; · 2.14 Impact Factor
  • Hong Jiang, Changjiu Li, Lin Yu, Wei He
    Journal of Non-Crystalline Solids 01/2014; · 1.72 Impact Factor
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    ABSTRACT: Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial effects on cardiac function and ventricular remodeling. The present study aimed to investigate the expression of ghrelin and the growth hormone (GH) secretagogue receptor 1a (GHSR-1a), and the association with cardiac remodeling in rats with myocardial infarction (MI). Twenty-four hours after ligation of the anterior descending artery (LAD), adult male Sprague-Dawley rats were randomized to 3 d, 7 d and 28 d group. Sham animals underwent thoracotomy and pericardiotomy, but not LAD ligation. Expression of both ghrelin and GHSR-1a was assessed by means of immunohistochemistry and real-time PCR. Plasma ghrelin levels were measured by ELISA kit. In addition, cardiac remodeling was assessed by Echocardiographic and haemodynamic measurements. Plasma and cardiac expression of ghrelin decreased on days 3, 7 and 28 compared with the sham group (P < 0.05). In contrast the GHSR-1a mRNA levels increased during the same days (P < 0.05). Decreased positive immunoreaction for ghrelin and increased positive GHSR-1a was also observed in infarcted heart. Interestingly, plasma ghrelin correlated negatively with left ventricular end-diastolic pressure(r = -0.59, P = 0.002) and left ventricular end-diastloic dimension (r = -0.73, P < 0.01). The ghrelin system may play an important role regulating cardiac remodeling after MI and present as a potential significant target for pharmacological modulation and treating cardiac remodeling.
    Regulatory Peptides. 01/2014;
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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 01/2014; · 5.46 Impact Factor

Publication Stats

2k Citations
614.31 Total Impact Points


  • 2014
    • 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
    • Hainan University
      Heilongjiang Sheng, China
    • Zhejiang Cancer Hospital
      Hang-hsien, Zhejiang Sheng, China
    • Hubei Polytechnic University
      Hu-pei-ts’un, Shanxi Sheng, China
    • First People's Hospital Chenzhou
      Chenchow, Hunan, China
  • 2006–2014
    • Central South University
      • • Department of Neurology
      • • State Key Laboratory of Medical Genetics
      Ch’ang-sha-shih, Hunan, China
    • Nanjing University
      • International Institute for Earth System Science
      Nan-ching, Jiangsu Sheng, China
  • 2005–2014
    • Renmin University of China
      Peping, Beijing, China
  • 2002–2014
    • Wuhan University
      • Department of Cardiology
      Wu-han-shih, Hubei, China
  • 2011–2012
    • Fudan University
      • Institutes of Biomedical Sciences
      Shanghai, Shanghai Shi, China
  • 2004–2012
    • Xiangya Hospital of Central South University
      Ch’ang-sha-shih, Hunan, China
  • 2009–2010
    • Sichuan University
      • Analytical Center
      Chengdu, Sichuan Sheng, China
    • Government of the People's Republic of China
      Peping, Beijing, China