Jiandong Luo

Guangzhou Medical University, Shengcheng, Guangdong, China

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Publications (5)17.63 Total impact

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    ABSTRACT: Maternal high fat diet (HFD) is associated with cardiovascular disease later in life. This study tested the hypothesis that maternal HFD causes programming of increased cardiac angiotensin II receptor type 2 (AGTR2) expression, resulting in heightened cardiac susceptibility to ischemic injury in male offspring in a sex-dependent manner. Pregnant rats were divided between control and HFD (high fat diet-fed during gestation) groups. Maternal HFD resulted in cardiac hypertrophy in only male offspring, but had no effect on cardiac systolic and diastolic function in both male and female offspring. In addition, maternal HFD increased heart susceptibility to ischemia-reperfusion injury in adult male offspring, but not female offspring. There was an increase in Agtr2 mRNA and protein abundance in male, but not female offspring. However, maternal HFD had no effect on angiotensin II receptor type 1 (AGTR1) expression in both male and female offspring. HFD resulted in decreased glucocorticoid receptors (GRs) binding to the glucocorticoid response elements (GREs) at the Agtr2 promoter, which was due to decreased GRs in the heart of adult male offspring. Inhibition of AGTR2 with PD123319 abrogated maternal HFD-induced increase in cardiac ischemic vulnerability in male adult rats. The results demonstrate that maternal HFD causes programming of increased Agtr2 gene expression in the heart by downregulation of GR, contributing to the heightened cardiac vulnerability to ischemic injury in adult male offspring in a sex-dependent manner. Copyright 2015 by The Society for the Study of Reproduction.
    Biology of Reproduction 07/2015; 93(2). DOI:10.1095/biolreprod.115.129916 · 3.32 Impact Factor
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    ABSTRACT: Transforming growth factor beta (TGF-β) is suggestive of a molecular target for cancer therapy due to its involvement in cell cycle, differentiation, and morphogenesis. Meanwhile, survivin is identified as an apoptosis inhibitor and involved in tumorgenesis. Here, we aimed to investigate the potential associations between TGF-β and survivin in glioblastoma U87 cell line. Survivin small interfering RNA (siRNA), Western blotting, and cell cycle analysis were introduced to detect relevant proteins in TGF-β pathways. In this study, we observed a concentration- and time-dependent increase of survivin expression after treatment with TGF-β1. However, the kinase inhibitors U0126 and LY294002 inhibited the upregulation of survivin in comparison with DMSO. In addition, survivin siRNA effectively abrogated survivin expression in U87 cells, therefore affected cells' entry into the S phase of cell cycle, and then repressed the expression of epidermal growth factor receptor (EGFR) and matrix metalloproteinase 9 (MMP9) in comparison with non-transfection. In conclusion, the present study shows that TGF-β upregulates survivin expression via ERK and PI3K/AKT pathway, leading to glioblastoma cell cycle progression. Thus, the blockade of survivin will allow for the treatment of glioblastoma, partially attributing to the inhibition of EGFR and MMP9 expression.
    Molecular Neurobiology 02/2015; DOI:10.1007/s12035-015-9121-6 · 5.14 Impact Factor
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    ABSTRACT: Autophagy is activated in ischemic heart diseases, but its dynamics and functional roles remain unclear and controversial. In this study, we investigated the dynamics and role of autophagy and the mechanism(s), if any, during postinfarction cardiac remodeling. Acute myocardial infarction (AMI) was induced by ligating left anterior descending (LAD) coronary artery. Autophagy was found to be induced sharply 12-24 hours after surgery by testing LC3 modification and Electron microscopy. P62 degradation in the infarct border zone was increased from day 0.5 to day 3, and however, decreased from day 5 until day 21 after LAD ligation. These results indicated that autophagy was induced in the acute phase of AMI, and however, impaired in the latter phase of AMI. To investigate the significance of the impaired autophagy in the latter phase of AMI, we treated the mice with Rapamycin (an autophagy enhancer, 2.0 mg/kg/day) or 3-methyladenine (3MA, an autophagy inhibitor, 15 mg/kg/day) one day after LAD ligation until the end of experiment. The results showed that Rapamycin attenuated, while 3MA exacerbated, postinfarction cardiac remodeling and dysfunction respectively. In addition, Rapamycin protected the H9C2 cells against oxygen glucose deprivation in vitro. Specifically, we found that Rapamycin attenuated NFκB activation after LAD ligation. And the inflammatory response in the acute stage of AMI was significantly restrained with Rapamycin treatment. In vitro, inhibition of NFκB restored autophagy in a negative reflex. Sustained myocardial ischemia impairs cardiomyocyte autophagy, which is an essential mechanism that protects against adverse cardiac remodeling. Augmenting autophagy could be a therapeutic strategy for acute myocardial infarction.
    PLoS ONE 11/2014; 9(11):e112891. DOI:10.1371/journal.pone.0112891 · 3.23 Impact Factor
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    ABSTRACT: The mechanisms underlying the myocardial protection of valsartan against ischemia/reperfusion (I/R) injury are complicated and remain unclear. The aim of this study was to investigate whether autophagy machinery was involved in the protection against I/R injury that is induced by valsartan. In vivo rat hearts were subjected to ischemia by 30 min ligation of the left anterior descending coronary artery, followed by a 120 min reperfusion. 3‑methyladenine (3‑MA), a specific inhibitor on autophagic sequestration, was used to inhibit autophagy. The hemodynamics, infarct size of the ventricle and LC3B protein were measured. Western blot analysis was performed to investigate the mechanism by which autophagy was induced by valsartan. Valsartan preconditioning resulted in a significant decrease in infarct size and induced autophagy in the rat heart subjected to I/R injury. The hemodynamics assay showed that the valsartan‑induced cardiac functional recovery was attenuated by 3‑MA. By contrast, 3‑MA decreased the improvement induced by valsartan on the histology and infarction of the rat heart subjected to I/R injury. Valsartan preconditioning induced autophagy via the AKT/mTOR/S6K pathway, independent of Beclin1. In conclusion, valsartan preconditioning induced autophagy via the AKT/mTOR/S6K pathway, which contributed to the myocardial protection against I/R injury.
    Molecular Medicine Reports 09/2013; 8(6). DOI:10.3892/mmr.2013.1708 · 1.55 Impact Factor
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    ABSTRACT: Safe and effective gene delivery is essential to the success of gene therapy. We synthesized and characterized a novel nonviral gene delivery system in which folate (FA) molecules were functioned as blockers on cationic polyrotaxanes (PR) composed of poly(ethylenimine) (PEI)(600)-grafted α-cyclodextrin rings linearized on polyethylene glycol to form FA-terminated PR-PEI(600) (FPP). The FA terminal caps of FPP target cell surfaces abundant in FA receptor (FR), a common feature of tumor cells. The structure of FPP was characterized by using (1)H nuclear magnetic resonance ((1)H NMR). The delivery particle was composed of chemically bonded PEG (4000), α-cyclodextrins (CD), and PEI (600 Da) at a molar ratio of 1:17:86.7, and the particle size and zeta potential of FPP/pDNA polyplexes were measured using dynamic light scattering. FPP/pDNA exhibited a lower cytotoxicity, strong specificity to FR, and high efficiency of delivering DNA to target cells in vitro and in vivo with the reporter genes. Furthermore, the FPP/DNA complex showed an enhanced antitumor effect in the nude mice compared with other delivery systems, such as PEI-25K. Together, these results suggest that FPP may be useful for gene therapy.
    Molecular Pharmaceutics 04/2012; 9(5):1067-76. DOI:10.1021/mp200315c · 4.38 Impact Factor

Publication Stats

26 Citations
17.63 Total Impact Points


  • 2012-2014
    • Guangzhou Medical University
      Shengcheng, Guangdong, China