(Associate Professor; Ph. D)
PhoneTel(Office):886-4-2473-0022 ext 11805
Interests in Research
Regulation of nitric oxide synthesis and gene expression in inflammatory disorders and tissue fibrosis by epigenetic mechanism.
Nitric oxide (NO) is a magic gas molecule critical to numerous biological processes, and acts an important host defense effector in the immune system. NO acts as a double-edged sword. NO produced by mammalian cells at an appropriate scale serves as a key signaling molecule in physiological processes; while excessive and unregulated NO synthesis has been implicated in pathophysiological conditions in human diseases, such as inflammatory disorders including glomerulonephritis (GN), chronic obstructive pulmonary disease (COPD), arthritis and so forth. Nitric oxide is a fairly short-lived molecule (with a half-life of a few seconds) produced from enzymes known as nitric oxide synthase (NOS). The major research activities of Dr. Ting-Hui Lin’s lab in the past years were to investigate the regulation of inducible nitric oxide synthase (iNOS) at transcriptional and post-translational levels in glomerular mesangial cells during glomerulonephritis and renal fibrosis.
Many of the physiological processes that are promoted by NO are mediated by the NO–cGMP signalling pathway. Moreover, NO signaling mediates physiolgocial functions by means of post--translational modification of proteins, mainly through S-nitrosylation of cysteine thiol residues. Therefore, NO also acts as a versatile epigenetic regulator. Epigenetics is defined as somatically heritable changes in gene activity and expression without alterations in the DNA sequences. The patterns of epigenetic modifications include DNA methylation, histone modifications, chromatin remodeling, and microRNAs. Epigenetics has become a central issue in many diseases during development and differentiation, or in response to environmental stimuli. The current research interests of Dr. Ting-Hui Lin’s lab are to investigate the epigenetic regulation of NO synthesis and gene expression during glomerulonephritis and renal fibrosis.
Publications (at most 7 publications in recent 5 years)
Upregulation of PRMT6 by LPS suppresses Klotho expression through interaction with NF-κB in glomerular mesangial cells. Journal of Cellular Boichemistry, 2017 Nov 13. doi: 10.1002/jcb.26511
- Novel findings of secreted cyclophilin A in diabetic nephropathy and its association with renal protection of dipeptidyl peptidase 4 inhibitor. Clinica Chimica Acta, 2016; 463, 181–192.
Galangin prevents acute hepato-renal Toxicity in novel propacetamol-induced acetaminophen-overdose mice. Journal of Medicinal Food, 2015; 18, 1187-1195.
Downregulation of connective tissue growth factor by LPS/IFN-γ-induced nitric oxide is reversed by aristolochic acid treatment in glomerular mesangial cells via STAT-1α and NF-κB signaling. Chemico-Biological Interactions, 2014; 210, 86-95.
- Differential effects of LY294002 and wortmannin on inducible nitric oxide synthase expression in glomerular mesangial cells. International Immunopharmacology, 2012; 12, 471-489.