江信仲 助理教授

職級: 助理教授 Assistant Professor

辦公室Office/實驗室Lab : D404/D412

電話Tel：03-8565301 分機ext. 2426/2427

E-mail: sjjiang@mail.tcu.edu.tw

學歷/Education：

國立成功大學基礎醫學研究所博士

PhD, Institute of Basic Medical Sciences, Medical College, National Cheng Kung University, Taiwan

國立成功大學生物化學研究所碩士直攻

Master, Department of Biochemistry, National Cheng Kung University, Medical College, Taiwan

大同大學生物工程學系學士

Bachelor, Institute of Bioengineering, Tatung University, Taiwan

經歷/Work experience：

慈濟大學醫學系生化學科助理教授(2009/08 ~迄今)

Assistant Professor, Department of Biochemistry, School of Medicine, Tzu Chi University (2009/08 ~)

國立成功大學生物化學暨分子生物學研究所專案助理教授(2009/02 ~2009/07)

Project Assistant Professor, Department of Biochemistry and Molecular Biology, Medical College, National Cheng Kung University (2009/02 ~2009/07)

國立成功大學心血管研究中心博士後研究員(2008/08 ~2009/02)

Postdoctor, Cardiovascular Research Center, National Cheng Kung University (2008/08 ~2009/02)

博士後研究員University of Washington, Department of Pathobiology, USA, Postdoc Fellow (2005/10 ~2008/05)

中央研究院分子生物研究所博士後研究員(2004/9 ~2005/09)

Academia Sinica, Institute of Molecular Biology, Taiwan, Postdoc Fellow (2004/9 ~2005/09)

研究興趣/Research interest:

l   血管生物功能探討

l   Vascular biology and functional study

進行中之研究/Current research:

1. 研究CD93在血管發炎的生物功能探討/ biological functions of CD93 on vascular inflammation

2. 抗血管發炎藥物之篩選/ screening the anti-inflammatory drugs

說明:

動脈粥狀硬化是一種疾病，涉及的血管壁脂質蓄積，慢性炎症，細胞死亡，血栓形成。CD93是一種新的調控細胞吞噬功能和細胞粘附發炎相關的調節子。然而，它的分子功能是未知的。 CD93是一種位在細胞表面，與細胞膜聯結的醣蛋白，這些細胞參與在發炎反應的過程中，包括內皮細胞和髓系細胞。血液中可偵測到可溶性形式的CD93，並且在發炎的過程中其濃度會逐漸升高。研究結果表明，CD93是一種發炎相關的因子，可活化單核細胞，藉由刺激粘附分子的表達，結合並且穿過內皮細胞。單核細胞粘連在血管的發炎反應加上跨內皮細胞的遷移，是血管發炎反應最初且必要的步驟，並且在整個動脈粥樣硬化過程中不斷發生。因此，破解CD93調節發炎反應的分子機制，於急性和慢性的病理具有廣泛的適用性。本實驗室在研究CD93在血管發炎的生物功能探討以及抗血管發炎藥物之篩選。

Atherosclerosis is a disease of the vessel wall involving lipid accumulation, chronic inflammation, cell death, and thrombosis. CD93 is a novel regulator of inflammation involved in the regulation of phagocytosis and cell adhesion. However, its molecular function is unknown. CD93 exists as a membrane associated glycoprotein on the surface of cells involved in the inflammatory cascade, including endothelial and myeloid cells. A soluble form (sCD93) is detectable in blood and is elevated with inflammation. Our research findings suggest that CD93 is an inflammatory-associated factor and activates the monocytes bind and transmigrate to endothelial cells via adhesion molecules expression. The adhesions of monocytes to endothelial cells coupled with transendothelial migration are initial and essential steps of inflammatory response in vasculature, and occur continuously throughout the entire atherogenic process. Therefore, deciphering the molecular mechanisms that CD93 regulated inflammatory cascade has wide applicability to acute and chronic pathology. Our lab aims at studying the biological functions of CD93 on vascular inflammation and screening the anti-inflammatory drugs.

研究著作/Publications:

1. Jiang SJ, Hsu SY, Deng CR, Huang HC, Liu SL, Shi GY, Wu HL. Dextromethorphan attenuates LPS-induced adhesion molecule expression in human endothelial cells. Microcirculation. 2013;20:190-201. (SCI)

2. Kao YC, Jiang SJ*, Pan WA, Wang KC, Chen PK, Wei HJ, Chen WS, Chang BI, Shi GY, Wu HL. The epidermal growth factor-like domain of CD93 is a potent angiogenic factor. PLoS One. 2012;7:e51647. (SCI) (*co-authors)

3. Liu SL, Li YH, Shi GY, Tang SH, Jiang SJ, Huang CW, Liu PY, Hong JS, Wu HL. Dextromethorphan reduces oxidative stress and inhibits atherosclerosis and neointima formation in mice. Cardiovasc Res. 2009;82:161-169. (SCI)

4. Jiang SJ, Kuo CC, Berry MW, Lee AW, Campbell LA. Identification and characterization of Chlamydia pneumoniae specific antigens which activate TNF-a production in RAW 264.7 murine macrophages. Infect. Immun. 2008; 76: 1558-1564. (SCI)

5. Jiang SJ, Campbell LA, Berry MW, Rosenfeld ME, Kuo CC. Retinoic acid prevents Chlamydia pneumoniae induced foam cell development in a mouse model of atherosclerosis. Microbes Infect. 2008;10(12-13):1393-1397. (SCI)

6. Kuo CC, Lee A, Jiang SJ, Yaraei K, Campbell LA. Inoculation of Chlamydia pneumoniae or Chlamydia trachomatis with ligand that inhibit attachment to host cells reduces infectivity in the mouse model of lung infection: implication for anti-adhesive therapy. Microbes Infect. 2007;9:1139-1141. (SCI)

7. Jiang SJ, Lin TM, Shi GY, Eng HL, Chen HY, Wu HL. Inhibition of bovine herpesvirus-4 replication in endothelial cells by arsenite. Antiviral Res. 2004;63:167-175. (SCI)

8. Jiang SJ, Lin TM, Shi GY, Eng HL, Chen HY, Wu HL. Inhibition of bovine herpesvirus-4 replication by arsenite through downregulation of the extracellular signal-regulated kinase signaling pathway. J Biomed Sci. 2004;11:500-510. (SCI)

9. Huang HC, Shi GY, Jiang SJ, Shi CS, Wu CM, Yang HY, Wu HL. Thrombomodulin-mediated cell adhesion: involvement of its lectin-like domain. J Biol Chem. 2003;278:46750-46759. (SCI)

10. Jiang SJ, Lin TM, Wu HL, Han HS, Shi GY. Decrease of fibrinolytic activity in human endothelial cells by arsenite. Thromb Res. 2002;105:55-62. (SCI)

11. Lin TM, Shi GY, Jiang SJ, Tsai CF, Hwang BJ, Hsieh CT, Wu HL. Persistent infection of bovine herpesvirus type4 in bovine endothelial cell cultures. Vet Microbiol. 1999;70:41-53. (SCI)