蔡冬青
主要从事细胞与分子生物学、再生医学、组织再生与衰老和成体干细胞的研究。
个性化签名
- 姓名:蔡冬青
- 目前身份:
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- 学位:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
生物化学
- 研究兴趣:主要从事细胞与分子生物学、再生医学、组织再生与衰老和成体干细胞的研究。
蔡冬青,教授,博士生导师,2007年入选“新世纪百千万人才工程”国家级人选。1987年获医学学士学位,在香港中文大学医学院获博士学位,在美国康奈尔大学威尔医学院(Weill Medical College of Cornell University)任博士后,2003年3月以引进海外人材应聘任职暨南大学,为再生医学教育部重点实验室学术带头人。蔡冬青博士主要从事细胞与分子生物学、再生医学、组织再生与衰老和成体干细胞的研究。专业技术特长:分子生物学、蛋白组、功能性基因组、功能性蛋白因子的筛选、分离、纯化及表达,蛋白与蛋白的相互作用,细胞生物学,信号分子及信号传递通路,干细胞与组织修复与再生。近年的研究主要集中在:(1)心血管和肌肉系统衰老与再生;(2)组织、器官特异性靶向;(3)成体干细胞治疗。已证明所提出:“衰老使细胞内及细胞外产生不利于组织和器官再生的衰老表型,必须对其进行干预方能有效再生年老受损组织与器官。”假想的正确性,共发表文章40多篇,参与翻译书一本。在海外完成课题10多个。2003年回国后,主持863项目1项,国家自然科学基金项目3项,广东省自然科学基金重点项目1项,广东省、广州市科技攻关项目各1项,作为主要成员获香港资助局(RGC)和香港创新科学基金(ITF)项目各1项,科研经费为1194万。正在申请国际专利1项。蔡冬青博士是“Physiological Genomics”、“Life Science” 、“American Journal of Physiology-Cell Physiology”、 “Archives of Biochemistry and Biophysics” 和 “Cancer Letters ” 的审稿人。
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1747
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成果阅读
360
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成果数
7
【期刊论文】BDNF-mediated enhancement of inflammation and injury in the aging heart
蔡冬青, Dongqing Cai, Jacquelyne M. Holm, Inga J. Duignan, Jingang Zheng, Munira Xaymardan, , Andrew Chin, Victoria L. T. Ballard, Jonathan N. Bella, and Jay M. Edelberg
Physiol Genomics 24: 191-197, 2006.,-0001,():
-1年11月30日
Cai, Dongqing, Jacquelyne M. Holm, Inga J. Duignan, Jingang Zheng, Munira Xaymardan, Andrew Chin, Victoria L. T. Ballard, Jonathan N. Bella, and Jay M. Edelberg. BDNF-mediated enhancement of inflammation and injury in the aging heart. Physiol Genomics 24: 191-197, 2006. First published December 13, 2005; doi: 10.1152/physiolgenomics.00165.2005.-Aging is associated with shifts in autocrine and paracrine pathways in the cardiac vasculature that may contribute to the risk of cardiovascular disease in older persons. To elucidate the molecular basis of these changes in vivo, phage-display biopanning of 3-and 18-mo-old mouse hearts was performed that identified peptide epitopes with homology to brainderived neurotrophic factor (BDNF) in old but not young phage pools. Quantification of cardiac phage binding by titration and immunostaining after injection with BDNF-like phage identified a twofold increased density of the BDNF receptor, truncated Trk B, in the aging hearts. Studies focused on the receptor ligand using a rat model of transient myocardial ischemia revealed increases in cardiac BDNF associated with local mononuclear infiltrates in 24-but not 4-mo-old rats. To investigate these changes, both 4-and 24-mo-old rat hearts were treated with intramyocardial injections of BDNF (or PBS control), demonstrating significant inflammatory increases with activated macrophage (ED1) in BDNF-treated aging hearts compared with aging controls and similarly treated young hearts. Additional studies with permanent coronary occlusion following intramyocardial growth factor pretreatment revealed that BDNF significantly increased the extent of myocardial injury in older rat hearts (BDNF 35
brain-derived neurotrophic factor, functional proteomics, Trk B
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【期刊论文】Ubiquitin expression is up-regulated in human and rat skeletal muscles during aging
蔡冬青, Dongqing Cai, a, * K.K.H. Lee, b M. Li, c M.K. Tang, b and K.M. Chan d
D. Cai et al./Archives of Biochemistry and Biophysics 425(2004)42-50,-0001,():
-1年11月30日
In this study, we have used two-dimensional electrophoresis, protein sequencing, immunoblotting, and immunohistochemistry to identify proteins that were differentially expressed during aging in human and rat skeletal muscles. Ubiquitin was identified. It was expressed at high levels in old fast-twitch muscles but at low levels in young fast-twitch muscles. It was also discovered that exogenous ubiquitin could suppress the growth of C2C12 cells, in vitro. The reduction in C2C12 cell growth was not attributed to an increase in apoptosis but to an inhibition in cell cycle entry. Furthermore, it was possible to induce muscles to degenerate in vivo by injecting a high dose of exogenous ubiquitin into young healthy skeletal muscles. These results suggest that hyperactivity of the ubiquitin-proteasome pathway is involved in the aging process of fast-twitch muscles. In addition, ubiquitin-dependent growth suppression in satellite cells may be associated with the poor healing potential of old skeletal muscles.
Aging, Ubiquitin, Skeletal muscles, Proteomics
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【期刊论文】Age-associated impairment in TNF-α cardioprotection from myocardial infarction
蔡冬青, Dongqing Cai, Munira Xaymardan, Jacquelyne M. Holm, Jingang Zheng, Jorge R. Kizer, and Jay M. Edelberg
Am J Physiol Heart Circ Physiol 285: H463-H469, 2003.,-0001,():
-1年11月30日
Cai, Dongqing, Munira Xaymardan, Jacquelyne M. Holm, Jingang Zheng, Jorge R. Kizer, and Jay M. Edelberg. Age-associated impairment in TNF-α cardioprotection from myocardial infarction. Am J Physiol Heart Circ Physiol 285: H463-H469, 2003. First published May 8, 2003; 10.1152/ajpheart.00144.2003.—Age-associated dysfunction in cardiac microvascular endothelial cells with impaired induction of cardioprotective platelet-derived growth factor (PDGF)-dependent pathways suggests that alterations in critical vascular receptor(s) may contribute to the increased severity of cardiovascular pathology in older persons. In vivo murine phage-display peptide library biopanning revealed a senescent decrease in cardiac microvascular binding of phage epitopes homologous to tumor necrosis factor-α (TNF-α), suggesting that its receptor(s) may be downregulated in older cardiac endothelial cells. Immunostaining demonstrated that TNF-receptor 1 (TNF-R1) density was significantly lower in the subendocardial endothelium of the aging murine heart. Functional studies confirmed the senescent dysregulation of TNF-receptor pathways, demonstrating that TNF-α induced PDGF-B expression in cardiac microvascular endothelial cells of 4-mo-old, but not 24-mo-old, rats. Moreover, TNF-mediated cardioprotective pathways were impaired in the aging heart. In young rat hearts, injection of TNF-significantly reduced the extent of myocardial injury after coronary ligation: TNF-α, 7.9±1.9% left ventricular injury (n=4) versus PBS, 16.2±7.9% (n=10; P<0.05). The addition of PDGF-AB did not augment the cardioprotective action of TNF-α. In myocardial infarctions of older hearts, however, TNF- induced significant postcoronary occlusion mortality (TNF-α 80% vs. PBS 0%; n=10 each, P<0.05) that was reversed by the coadministration of PDGF-AB. Overall, these studies demonstrate that aging-associated alterations in TNF-α receptor cardiac microvascular pathways may contribute to the increased cardiovasular pathology of the aging heart. Strategies targeted at restoring TNF-α receptor-B mediated expression of PDGF-B may improve cardiac microvascular function and provide novel approaches for treatment and possible prevention of cardiovascular disease in older individuals.
aging, heart, endothelial, phage display, functional genomics
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【期刊论文】Parvalbumin Expression Is Downregulated in Rat Fast-Twitch Skeletal Muscles during Aging
蔡冬青, D. Q. Cai, * M. Li, * K. K. H. Lee, † K. M. Lee, ‡ L. Qin, * and K. M. Chan*,
Archives of Biochemistry and Biophysics Vol.387, No.2, March 15, pp. 202-208, 2001,-0001,():
-1年11月30日
In this study, the protein expression pro
two-dimensional electrophoresis, parvalbumin, aging, exercise, water-soluble muscle protein.,
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【期刊论文】Translation of PDGF Cardioprotective Pathways
蔡冬青, Jay M. Edelberg, * Dongqing Cai, and Munira Xaymardan
Cardiovascular Toxicology (2003) 03 27-35,-0001,():
-1年11月30日
Vascular function in the aging heart is impaired and may underlie the increased morbidity and mortality associated with ischemic heart disease in older individuals. This vascular dysfunction is due, in part, to impairment of plateletderived growth factor (PDGF)-mediated pathways in senescent cardiac microvascular endothelial cells. Restoration of these pathways by intramyocardial injection of growth factor transiently rescues senescent cardiac angiogenesis. Longer-term reconstitution can be achieved experimentally by transplantation of young bone marrow-derived stem cells to promote enescent cardiac angiogenic function in the murine host. Moreover, enhancement of PDGF pathways is cardioprotective, markedly reducing the extent of myocardial injury following coronary occlusion. The clinical translation of these findings for treatment of ischemic heart diseases must overcome the limitation of the proatherosclerotic actions of PDGF, as well as the generation of autologous stem/precursor cell approaches, for the aging cardiovascular system. Strategies targeting growth factor and/or stem-cell homing to gene products downstream of PDGF in the cardiac microvasculature may provide positive feedback loops to enhance cardiac angiogenesis and protection from myocardial infarction and may offer a foundation for developing novel therapies for the prevention and treatment of cardiovascular disease associated with aging.
Heart, angiogenesis, myocardial infarction, stem cells, plateletderived growth factor.,
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蔡冬青, Ming Li, * Kaiming Chan, *, Dongqing Cai, * Pingchun Leung, * Chunyiu Cheng, * Kwongman Lee, † Kenneth Kaho Lee‡
Archives of Biochemistry and Biophysics Vol.384, No.2, December 15, pp. 263-268, 2000,-0001,():
-1年11月30日
The limited ability of damaged muscle to regenerate after gross injuries is a major clinical problem. To date, there is no effective therapeutic treatment for muscle injuries. In the present study, we have examined the ability of crude and fractionated human skeletal muscle extracts to promote myogenic cell proliferation and differentiation. It was found that the crude muscle extract could signi
myogenic factor, myogenic cell proliferation,, muscle healing.,
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【期刊论文】Functions of the Growth Arrest Specific 1 Gene in the Development of the Mouse Embryo
蔡冬青, K. K. H. Lee, *, , A. K. C. Leung, * M. K. Tang, * D. Q. Cai, †, C. Schneider, ‡ C. Brancolini, ‡ and P. H. Chow*
Developmental Biology 234, 188-203(2001),-0001,():
-1年11月30日
The growth arrest specific 1 (gas1) gene is highly expressed in quiescent mammalian cells (Schneider et al., 1988, Cell 54, 787-793). Overexpression of gas1 in normal and some cancer cell lines could inhibit G0/G1 transition. Presently, we have examined the functions of this gene in the developing mouse embryo. The spatial-temporal expression patterns for gas1 were established in 8.5-to 14.5-day-old embryos by immunohistochemical staining and in situ hybridization. Gas1 was found heterogeneously expressed in most organ systems including the brain, heart, kidney, limb, lung, and gonad. The antiproliferative effects of gas1 on 10.5 and 12.5 day limb cells were investigated by flow cytometry. In 10.5 day limbs cells, gas1 overexpression could not prevent G0/G1 progression. It was determined that gas1 could only induce growth arrest if p53 was also coexpressed. In contrast, gas1 overexpression alone was able to induce growth arrest in 12.5 day limb cells. We also examined the cell cycle profile of gas1-expressing and nonexpressing cells by immunochemistry and flow cytometry. For 10.5 day Gas1-expressing heart and limb cells, we did not find these cells preferentially distributed at G0/G1, as compared with Gas1-negative cells. However, in the 12.5 day heart and limb, we did find significantly more Gas1-expressing cells distributed at G0/G1 phase than Gas1-negative cells. These results implied that Gas1 alone, during the early stages of development, could not inhibit cell growth. This inhibition was only established when the embryo grew older. We have overexpressed gas1 in subconfluent embryonic limb cells to determine the ability of gas1 to cross-talk with various response elements of important transduction pathways. Specifically, we have examined the interaction of gas1 with Ap-1, NFkB, and c-myc responsive elements tagged with a SEAP reporter. In 10.5 day limb cells, gas1 overexpression had little effect on Ap-1, NFkB, and c-myc activities. In contrast, gas1 overexpression in 12.5 day limb cells enhanced AP-1 response while it inhibited NFkB and c-myc activities. These responses were directly associated with the ability of gas1 to induce growth arrest in embryonic limb cells. In the 12.5 day hindlimb, gas1 was found strongly expressed in the interdigital tissues. We overexpressed gas1 in these tissues and discovered that it promoted interdigital cell death. Our in situ hybridization studies of limb sections and micromass cultures revealed that, during the early stages of chondrogenesis, only cells surrounding the chondrogenic condensations expressed gas1. The gene was only expressed by chondrocytes after the cartilage started to differentiate. To understand the function of gas1 in chondrogenesis, we overexpressed the gene in limb micromass cultures. It was found that cells overexpressing gas1/GFP could not participate in cartilage formation, unlike cells that just express the GFP reporter. We speculated that the reason gas1 was expressed outside the chondrogenic nodules was to restrict cells from being recruited into the nodules and thereby defining the boundary between chondrogenic and nonchondrogenic forming regions.
growth arrest specific 1 gene, mouse embryo, cell cycle, signal transduction.,
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