Dr. Chen, Chien-Chang 陳建璋 博士

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Dr. Chen, Chien-Chang
陳建璋 博士

Research Fellow
研究員

  • Ph.D., University of Illinois, Urbana-Champaign

  • 02-2652-3944 (Lab) (Room No: N713)
  • 02-2652-3522
  • 02-2782-7654
    備註: 實驗室位於生醫所N713室 (Fax)
Specialty:
  • Calcium Channel
  • Cardiovascular Disease
  • Chronic Pain

RESEARCH

Increased intracellular calcium via calcium channels triggers a variety of physiological events. Compared to the high voltage-activated Ca2+ channel, the functions of the low voltage-activated or T-type Ca2+ channels are not completed understood. Three T-channel subunits have been identified: CaV3.1, CaV3.2 and CaV3.3, only CaV3.2 has been linked to human diseases. It has been demonstrated that mutations and polymorphisms in the human CaV3.2 gene are associated with childhood absence epilepsies, idiopathic generalized epilepsies, and autism spectrum disorders. In addition, CaV3.2-null mice display abnormal coronary artery, reduced peripheral pain and fail to develop pathological cardiac hypertrophy.

The long-term research goal of my laboratory is to understand the physiological and pathological function of T-type calcium channels in brain and cardiovascular system, especially related to human diseases such as cardiac ischemia-reperfusion injury, cardiac hypertrophy, platelet function and pain sensation. In the past 10 years, we demonstrated that CaV3.2 channels are upregulated and required during the development of pathological cardiac hypertrophy, tracheal cartilage formation, and pain sensation. We recently identified a novel link between chronic neuropathic pain and cardioprotection via a PVA-dependent parasympathetic pathway. We are currently investigating the role of CaV3.2 channels in cardiovascular diseases and central sensitization in chronic pain using tissue-specific KO mice, optogenetic and chemogenetic tools.

研究介紹

經由鈣離子通道所引起的細胞內鈣離子濃度增加能引發各種生理事件,例如肌肉收縮,激活各種需要鈣離子才能活化的酶,基因表達,神經元和心肌細胞的起搏活動。與高電壓激活的鈣離子通道相比,低電壓激活或T型鈣離子通道的功能尚未完全理解。目前已知的三個T型鈣離子通道:CaV3.1CaV3.2CaV3.3,人的CaV3.2基因中的突變和多態性與兒童時期的失神癲癇,特發性全身性癲癇和自閉症譜系障礙有關。此外,CaV3.2缺失小鼠顯示冠狀動脈異常,外周疼痛減輕,降低病理性心臟肥大的發生,並且有先天性的氣管軟骨環發育缺失。

本實驗室的長期目標是了解T型鈣離子通道在腦和心血管系統中的作用,特別是與心臟缺血再灌注損傷,心臟肥大,血小板功能和疼痛感等人類疾病有關。在過去的10年中,我們證明CaV3.2通道在病理性心臟肥大,氣管軟骨形成和疼痛感的發展過程中被上調和需要。我們最近在小鼠發現慢性神經病理性疼痛時室旁丘腦的前側核區(PVA)活動增加,進而增加副交感神經活動來保護心臟,減少心肌梗塞。我們目前正在研究使用單一組織CaV3.2剔除小鼠,光遺傳學和化學工具來研究CaV3.2通道在心血管疾病和慢性疼痛中樞致敏中的作用。

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