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Search Results: 1 - 10 of 41693 matches for " Jing X. Kang "
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Reduction of heart rate by omega-3 fatty acids and the potential underlying mechanisms
Jing X. Kang
Frontiers in Physiology , 2012, DOI: 10.3389/fphys.2012.00416
Abstract: An elevated resting heart rate is one of the strongest predictors of cardiovascular mortality and is independently associated with sudden cardiac death (SCD). Agents capable of reducing heart rate without significant side effects are therefore of particular interest for the prevention of SCD. Recent human and animal studies have shown that omega-3 fatty acids can reduce heart rate. Our work has shown that omega-3 fatty acids significantly reduce membrane electrical excitability of the cardiac myocyte by lowering its resting membrane potential and the duration of the refractory period through inhibition of ion channels. We propose that these actions may be the underlying mechanisms for the omega-3 fatty acid-induced reduction of heart rate observed in both humans and animals. The heart rate-lowering capability of omega-3 fatty acids may contribute to their preventive effect against SCD.
A simplified method for analysis of polyunsaturated fatty acids
Jing X Kang, Jingdong Wang
BMC Biochemistry , 2005, DOI: 10.1186/1471-2091-6-5
Abstract: We simplified the conventional method by combining the extraction and methylation into a single step (omitting the procedure of prior extraction). Various biological samples including cultured cells, animal tissues and human specimens have been tested using the new method. Statistical analysis indicates that the recovery of long chain fatty acids from tissue samples by the simplified method is significantly higher than that by the traditional method, but there is no difference in relative fatty acid composition between the two methods. This simplified method can significantly save time and materials, and reduce the potentials of sample loss and contamination.The lipid extraction procedure prior to methylation employed conventionally in lipid analysis can be omitted without affecting the recovery of long chain (≥ 18 C) fatty acids and their composition. The simplified method is rapid, easy-to-use, suitable for analysis of total long chain polyunsaturated fatty acid contents (e.g. n-6 and n-3 fatty acids) in various biological samples, especially when the number of samples to be analyzed is large and/or the specimen size is small.Fatty acid composition of cell membrane is an important determinant of cell function [1]. Manipulation of cellular fatty acid composition has been a widely used approach to modulating the biological responsiveness of different cell types. Recently, fatty acid profile, particularly the ratio of omega-6 (n-6) to omega-3 (n-3) polyunsaturated fatty acids, of cells or tissues has become a biomarker for monitoring the outcome of dietary interventions (i.e., fatty acid supplementation) and for identifying the risk factors for lipid related diseases (e.g. cardiovascular disease) [2]. Measurement of the n-6/n-3 fatty acid ratio can be also used to identify animal phenotypes, such as the fat-1 transgenic mice that we created recently [3]. Thus, analysis of fatty acid composition is a commonly used technique in lipid research.Analysis of fatty acid com
Down-regulation of the M6P/IGF-II receptor increases cell proliferation and reduces apoptosis in neonatal rat cardiac myocytes
Zhihong Chen, Yinlin Ge, Jing X Kang
BMC Cell Biology , 2004, DOI: 10.1186/1471-2121-5-15
Abstract: We down-regulated the expression of M6P/IGF2R in neonatal rat cardiac myocytes and examined the effect on cell proliferation and apoptosis. Infection of neonatal cardiomyocytes with an adenovirus expressing a ribozyme targeted against the M6P/IGF2R significantly reduced the level of M6P/IGF2R mRNA, as determined by RT-PCR and Ribonuclease Protection Assay (RPA). M6P-containing protein binding and endocytosis as well as the M6P/IGF2R-mediated internalization of 125I-IGF-II were lower in the ribozyme-treated cells than the control myocytes, indicating that the number of functional M6P/IGF2R in the ribozyme treated cells was reduced. Accordingly, a marked increase in cell proliferation and a reduced cell susceptibility to hypoxia- and TNF-induced apoptosis were observed in the ribozyme-treated cells.These findings suggest that M6P/IGF2R may play a role in regulation of cardiac myocyte growth and apoptosis. Down regulation of this gene in cardiac tissues might be a new approach to prevention of cell death or promotion of mitogenesis for certain heart diseases.The mannose 6-phosphate/insulin-like growth factor-II receptor (M6P/IGF2R) is a unique protein that interacts with multiple ligands, some of which are important growth regulatory factors [1]. The M6P/IGF2R participates in internalization and lysosomal degradation of IGF-II, a mitogen normally acting through the IGF-I receptor to stimulate cell proliferation [2]. The M6P/IGF2 receptor is required for the activation of TGF-β [3], a potent growth inhibitor for many cell types. This receptor is also involved in the binding, transport and activation of newly-synthesized lysosomal enzymes, such as cathepsins [4,5], which have been recently implicated in the induction of apoptosis [6]. On the basis of these functions, the M6P/IGF2R has been proposed to play a significant role in regulation of cell growth and apoptosis [7].Apoptosis, or programmed cell death, is a tightly regulated process used to remove excess, hazardous
Decreased expression of the mannose 6- phosphate/insulin-like growth factor-II receptor promotes growth of human breast cancer cells
Zhihong Chen, Yinlin Ge, Natalie Landman, Jing X Kang
BMC Cancer , 2002, DOI: 10.1186/1471-2407-2-18
Abstract: In this study, using viral and ribozyme strategies we reduced the expression of M6P/IGF2R in human breast cancer cells and then examined the effect on growth and apoptosis of these cells.Our results showed that infection of MCF-7 cells with the adenovirus carrying a ribozyme targeted against the M6P/IGF2R mRNA dramatically reduced the level of transcripts and the functional activity of M6P/IGF2R in these cells. Accordingly, cells treated with the ribozyme exhibited a higher growth rate and a lower apoptotic index than control cells (infected with a control vector). Furthermore, decreased expression of M6P/IGF2R enhanced IGF-II-induced proliferation and reduced cell susceptibility to TNF-induced apoptosis.These results suggest that M6P/IGF2R functions as a growth suppressor and its loss or mutation may contribute to development and progression of cancer. This study also demonstrates that adenoviral delivery of the ribozyme provides a useful tool for investigating the role of M6P/IGF2R in regulation of cell growth.With one million new cases each year, breast cancer is the most common cancer among women and is the leading cause of death in women 30 to 70 years of age in the world. Breast cancer results from genetic and environmental factors including diet, radiation and hormones [1-5]. The molecular events involved in breast carcinogenesis, however, remain to be elucidated.Numerous studies have shown that polypeptide growth factors such as insulin-like growth factors (IGFs) are mitogens for breast cancer cells [6-9]. The IGF-I and IGF-II signal through a common tyrosine kinase receptor, the insulin-like growth factor 1 receptor (IGF1R), and have mitogenic and cell survival actions that may promote tumor development. Modulation of this mitogenic pathway occurs in part via the M6P/IGF2R, which functions in the internalization and degradation of IGF-II [10]. M6P/IGF2R is also important in activation of TGF-β, a potent growth inhibitor for most cell types, and in binding,
Variations of multi-parameter observations in atmosphere related to earthquake
F. Jing,X. H. Shen,C. L. Kang,P. Xiong
Natural Hazards and Earth System Sciences (NHESS) & Discussions (NHESSD) , 2013, DOI: 10.5194/nhess-13-27-2013
Abstract: Anomalies of multi-parameters (outgoing longwave radiation, surface latent heat flux, air temperature, relative humidity, and air pressure) before the 12 May 2008 Wenchuan Ms =8.0 earthquake were discussed in order to obtain the seismic precursors. Multi-parameter data were computed based on multi-year background data. The results indicated that these parameters had significant variations prior to this event. The anomaly of outgoing longwave radiation was observed firstly, which gives an early warning. Next were air temperature, relative humidity, and air pressure, which had quasi-simultaneous variations in the basin and the mountain region close to the epicenter. The last was surface latent heat flux, which happened the day before this event. The characteristics of the parameter variations for this event are similar to other earthquakes, which is demonstrated in some other publications. The variations can be attributed to solid earth degassing and chemical reactions in the atmosphere. Additionally, the emission of gases from solid earth into the atmosphere could be ascribed to the tectonic stress of the Wenchuan earthquake.
Effects of Coptis extract combined with chemotherapeutic agents on ROS production, multidrug resistance, and cell growth in A549 human lung cancer cells
Chengwei He, Rong Rong, Jing Liu, Jianbo Wan, Keyuan Zhou, Jing X Kang
Chinese Medicine , 2012, DOI: 10.1186/1749-8546-7-11
Abstract: A549 cells were treated with different doses of COP and BER, combined with 5-FU, CPT, and TAX. Cell viability was measured by an XTT (2,3-bis-(2-methoxy-4- nitro-5-sulfophenyl)-2 H-tetrazolium-5-carboxanilide) assay. Intracellular ROS levels were determined by measuring the oxidative conversion of cell permeable 2′,7′-dichlorofluorescein diacetate to fluorescent dichlorofluorescein. MDR of A549 cells was assessed by rhodamine 123 retention assay.Both COP and BER significantly inhibited A549 cell growth in a dose-dependent manner. Combinations of COP or BER with chemotherapeutic agents (5-FU, CPT, and TAX) exhibited a stronger inhibitory effect on A549 cell growth. In addition, COP and BER increased ROS production and reduced MDR in A549 cells.As potential adjuvants to chemotherapy for non–small cell lung cancer, COP and BER increase ROS production, reduce MDR, and enhance the inhibitory effects of chemotherapeutic agents on A549 cell growth.The herb Coptis (COP) is used to treat “damp heat” syndrome in Chinese medicine [1]. Its major constituent is berberine (BER), an isoquinoline alkaloid [2]. The anticancer effects of COP and BER on both hematological and nonhematological cancers have been well documented [3]. Since 2000, experimental studies have confirmed the cytotoxicity of BER in various cancer cell lines, including YES (esophageal carcinoma) [4], HK1 (nasopharyngeal carcinoma) [5], HeLa (cervical carcinoma) [6], HepG2 (hepatocellular carcinoma) [7]. Our previous studies [9,10] have also shown that COP inhibits the growth of breast cancer cells.Non–small cell lung cancer (NSCLC) accounts for approximately 85% of lung cancers, and only responds to 15%–25% single agents and 25%–40% combined chemotherapy [11]. NSCLC is typically resistant to apoptosis induced by standard chemotherapy, which causes excessive levels of reactive oxygen species (ROS), leading to impaired intracellular ionic homeostasis by damaging cellular macromolecules and inducing apoptosis [12].
Transgenic Mice Convert Carbohydrates to Essential Fatty Acids
Victor J. Pai, Bin Wang, Xiangyong Li, Lin Wu, Jing X. Kang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0097637
Abstract: Transgenic mice (named “Omega mice”) were engineered to carry both optimized fat-1 and fat-2 genes from the roundworm Caenorhabditis elegans and are capable of producing essential omega-6 and omega-3 fatty acids from saturated fats or carbohydrates. When maintained on a high-saturated fat diet lacking essential fatty acids or a high-carbohydrate, no-fat diet, the Omega mice exhibit high tissue levels of both omega-6 and omega-3 fatty acids, with a ratio of ~1:1. This study thus presents an innovative technology for the production of both omega-6 and omega-3 essential fatty acids, as well as a new animal model for understanding the true impact of fat on human health.
Docosahexaenoic acid suppresses arachidonic acid-induced proliferation of LS-174T human colon carcinoma cells
Piet Habbel, Karsten H Weylandt, Katja Lichopoj, Johannes Nowak, Martin Purschke, Jing-Dong Wang, Cheng-Wei He, Daniel C Baumgart, Jing X Kang
World Journal of Gastroenterology , 2009,
Abstract: AIM: To investigate the impact of arachidonic acid (AA) and docosahexaenoic acid (DHA) and their combination on colon cancer cell growth.METHODS: The LS-174T colon cancer cell line was used to study the role of the prostaglandin precursor AA and the omega-3 polyunsaturated fatty acid DHA on cell growth. Cell viability was assessed in XTT assays. For analysis of cell cycle and cell death, flow cytometry and DAPI staining were applied. Expression of cyclooxygenase-2 (COX-2), p21 and bcl-2 in cells incubated with AA or DHA was examined by real-time RT-PCR. Prostaglandin E2 (PGE2) generation in the presence of AA and DHA was measured using a PGE2-ELISA.RESULTS: AA increased cell growth, whereas DHA reduced viability of LS 174T cells in a time- and dose-dependent manner. Furthermore, DHA down- regulated mRNA of bcl-2 and up-regulated p21. Interestingly, DHA was able to suppress AA-induced cell proliferation and significantly lowered AA-derived PGE2 formation. DHA also down-regulated COX-2 expression. In addition to the effect on PGE2 formation, DHA directly reduced PGE2-induced cell proliferation in a dose-dependent manner.CONCLUSION: These results suggest that DHA can inhibit the pro-proliferative effect of abundant AA or PGE2.
Inhibiting Delta-6 Desaturase Activity Suppresses Tumor Growth in Mice
Chengwei He, Xiying Qu, Jianbo Wan, Rong Rong, Lili Huang, Chun Cai, Keyuan Zhou, Yan Gu, Steven Y. Qian, Jing X. Kang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047567
Abstract: Recent studies have shown that a tumor-supportive microenvironment is characterized by high levels of pro-inflammatory and pro-angiogenic eicosanoids derived from omega-6 (n？6) arachidonic acid (AA). Although the metabolic pathways (COX, LOX, and P450) that generate these n？6 AA eicosanoids have been targeted, the role of endogenous AA production in tumorigenesis remains unexplored. Delta-6 desaturase (D6D) is the rate-limiting enzyme responsible for the synthesis of n？6 AA and increased D6D activity can lead to enhanced n？6 AA production. Here, we show that D6D activity is upregulated during melanoma and lung tumor growth and that suppressing D6D activity, either by RNAi knockdown or a specific D6D inhibitor, dramatically reduces tumor growth. Accordingly, the content of AA and AA-derived tumor-promoting metabolites is significantly decreased. Angiogenesis and inflammatory status are also reduced. These results identify D6D as a key factor for tumor growth and as a potential target for cancer therapy and prevention.
A Protective Lipidomic Biosignature Associated with a Balanced Omega-6/Omega-3 Ratio in fat-1 Transgenic Mice
Giuseppe Astarita, Jennifer H. McKenzie, Bin Wang, Katrin Strassburg, Angela Doneanu, Jay Johnson, Andrew Baker, Thomas Hankemeier, James Murphy, Rob J. Vreeken, James Langridge, Jing X. Kang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0096221
Abstract: A balanced omega-6/omega-3 polyunsaturated fatty acid (PUFA) ratio has been linked to health benefits and the prevention of many chronic diseases. Current dietary intervention studies with different sources of omega-3 fatty acids (omega-3) lack appropriate control diets and carry many other confounding factors derived from genetic and environmental variability. In our study, we used the fat-1 transgenic mouse model as a proxy for long-term omega-3 supplementation to determine, in a well-controlled manner, the molecular phenotype associated with a balanced omega-6/omega-3 ratio. The fat-1 mouse can convert omega-6 to omega-3 PUFAs, which protect against a wide variety of diseases including chronic inflammatory diseases and cancer. Both wild-type (WT) and fat-1 mice were subjected to an identical diet containing 10% corn oil, which has a high omega-6 content similar to that of the Western diet, for a six-month duration. We used a multi-platform lipidomic approach to compare the plasma lipidome between fat-1 and WT mice. In fat-1 mice, an unbiased profiling showed a significant increase in the levels of unesterified eicosapentaenoic acid (EPA), EPA-containing cholesteryl ester, and omega-3 lysophosphospholipids. The increase in omega-3 lipids is accompanied by a significant reduction in omega-6 unesterified docosapentaenoic acid (omega-6 DPA) and DPA-containing cholesteryl ester as well as omega-6 phospholipids and triacylglycerides. Targeted lipidomics profiling highlighted a remarkable increase in EPA-derived diols and epoxides formed via the cytochrome P450 (CYP450) pathway in the plasma of fat-1 mice compared with WT mice. Integration of the results of untargeted and targeted analyses has identified a lipidomic biosignature that may underlie the healthful phenotype associated with a balanced omega-6/omega-3 ratio, and can potentially be used as a circulating biomarker for monitoring the health status and the efficacy of omega-3 intervention in humans.
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