Yung-Chih (Inge) earned his Ph.D degree in Biochemical Sciences at National Taiwan University in 2011. During his Ph.D, he worked on the function of Toll-like receptor (TLR) in central nervous system. He identified a specific TLR ligand, 3’-poly-G-tailed ODNs, induces neuronal cell death and neurite retraction in embryonic neuron cells, and proved this neuronal cell death is due to inhibition of an extracellular matrix protein, F-spondin, which is expressed in neuron cell for axon guidance. Accordingly, this research work suggests F-spondin plays an important role in neuronal survival and has potential role in promoting neuron regeneration.
As a pharmacologist and neurophysiologist, I am interested in the study of the molecular mechanisms underlying neuropathic pain and other neurodegenerative diseases with the goal of identifying novel targets for therapeutic development. In particular, I would like to develop treatments selectively targeting diseased neurons by exploiting changes in neuronal function that occur due to injury and neurodegeneration.
In November 2011, Yung-Chih joined Clifford Woolf’s lab to start postdoctoral training for pursuing his research interesting in neuroscience. As a molecular neurobiologist, his research works focus on identifying molecular mechanism that drives neuron regeneration and neuronal survival. Understanding molecular mechanism that orchestrate complex processes to promote regeneration and survival of peripheral nervous system could have a broad range of applications in nerve injuries or neurodegenerative diseases in central nervous system. Yung-Chih has already established a platform for drug screening to identify potential compounds that induce neurite outgrowth of dorsal root ganglion (DRG) neuron. Additionally, he is interested in utilizing CRISPR/Cas9 genome editing technique to generate a series of transgenic mouse lines to perform gain- and loss-of-function of target candidates that are known from human studies to alter the pain phenotype. These will establish if the specific role of the targets in producing neuropathic pain is mediated by altering the function of primary sensory neurons. This strategy is aimed at enabling a reverse engineering platform from human gene target identification to mouse mechanistic studies for testing new neuropathic pain treatments.
- Michio W Painter, Amanda Brosius Lutz, Yung-Chih Cheng, Alban Latremoliere, Kelly Duong, Christine M Miller, Sean Posada, Enrique J Cobos, Alice X Zhang, Amy J Wagers, Leif A Havton, Ben Barres, Takao Omura, Clifford J Woolf. Diminished Schwann Cell Repair Responses Underlie Age-Associated Impaired Axonal Regeneration. Neuron 07/2014; 83(2):331-343.
- Yung-Chih Cheng, Tai-An Chen, Chih-Yuan Chen, Chi-Ming Liang, Shu-Mei Liang. 3'poly-G-tailed ODNs inhibit F-spondin to induce cell death and neurite retraction in rat embryonic neurons. Molecular Neurobiology 05/2012; 45(3):536-49.
- C. Ravindran*, Yung-Chih Cheng*, Shu-Mei Liang. CpG-ODNs induces up-regulated expression of chemokine CCL9 in mouse macrophages and microglia. Cellular Immunology 01/2010
- Yung-Chih Cheng, Chi-Ming Liang, Yen-Po Chen, Inn-Ho Tsai, Cheng-Chin Kuo, Shu-Mei Liang. F-spondin plays a critical role in murine neuroblastoma survival by maintaining IL-6 expression. Journal of Neurochemistry 07/2009; 110(3):947-55.
- Sheng-Chin Liao, Yung-Chih Cheng, Yo-Ching Wang, Chiung-Wen Wang, San-Ming Yang, Chun-Keung Yu, Chi-Chang Shieh, Kuo-Chen Cheng, Meng-Feng Lee, Shyh-Ren Chiang, Jiunn-Min Shieh, Ming-Shi Chang. IL-19 induced Th2 cytokines and was up-regulated in asthma patients. The Journal of Immunology 01/2005; 173(11):6712-8.