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Christine Wong

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Nanyang Assistant Professor Christine Siu Ling Wong 
Principal Investigator, Metabolic Disorders 
Research Programme: Metabolic/Vascular Diseases​


Dr Christine Wong is a Nanyang Assistant Professor at LKCMedicine. She obtained her PhD (Physiology) from the Chinese University of Hong Kong, where she focused on the role of cyclooxygenase-2 in endothelial dysfunction and vascular inflammation. She then joined Boston Children’s Hospital, Harvard Medical School, as a Postdoctoral Fellow to explore the impact of blood cells on vascular inflammation, and was later promoted to Instructor in Pediatrics. She found that diabetes predisposes individuals to form neutrophil extracellular traps (NETs), the cytotoxic chromatin released by activated neutrophils. She also identified the first detrimental implication of NETs in diabetes: impaired wound healing. Dr Wong was awarded numerous honors, including the Higher Education Outstanding Scientific Research Output Award (Second-Class Award), Ministry of Education, People’s Republic of China (2018), Young Investigator Award of the International Society on Thrombosis and Haemostasis (2013), and the prestigious Postgraduate Research Output Award of the Chinese University of Hong Kong (2010). Dr Wong was an invited speaker of conferences and seminars, including at the National Institutes of Health, USA (2018), and in the Heidelberg International Symposium on Diabetic Complications, Germany (2016). She is a co-inventor of a licensed patent on the use of anti-NET compounds in facilitating wound healing. 

Research Focus 

Originally described to trap and kill microbes, NETs are now also increasingly recognised to form in sterile inflammation. Being highly pro-coagulant and pro-inflammatory, NETs fuel thrombosis and cardiovascular disease - conditions that are prevalent in diabetics. In striking contrast to the rapidly expanding knowledge on the detrimental impact of NETs clinically, little is known about the cell biology of enhanced NET formation (NETosis) in chronic conditions such as diabetics, and how NETs contribute to diabetic complications. A lot of intriguing questions remain unresolved in this emerging field, including: By what mechanism is NETosis enhanced in diabetes? How do NETs interact with different body systems and what is the impact? Could NETs be of diagnostic and/or prognostic values in diabetic complications? Our research program is therefore structured into three main themes:

Cell biology of enhanced NETosis in diabetes
How diabetes enhances NETosis is unknown. Understanding the regulation of crucial cellular and molecular components in NETosis is important in order to uncover new targets to disrupt the NETosis pathway, and to minimize the unfavourable impact of NETs under diabetic conditions. The study may shed light on potential new targets for anti-NETosis inhibitors.

Pathophysiology of diabetic complications from the perspective of NETs
Diabetic nephropathy is one of the main causes of mortality in diabetics. However, glycemic and blood pressure control do not always prevent kidney damage and renal fibrosis. We will approach this issue from the perspective of neutrophils and NETs. NET formation may precede organ fibrosis. It would be clinically impactful if NET levels in blood or urine can be diagnostic and/or prognostic biomarkers for early detection (and hence early intervention) of diabetic renal complications and prediction of renal disease progression.

NET-microbiota interaction in metabolic disorders
NETs and gut microbiome contribute to chronic inflammation, but much remained unknown how they impact each other per se. Our study will provide the fundamental basis for the development of anti-NET therapies (i.e., whether gut microbiota would be affected by NET inhibition). Understanding the NET-gut microbiome interplay may also result in novel strategies to intervene the development of diabetes, metabolic disorders and their complications.
Our long-term research goal is to translate novel basic science findings to clinical applications, diagnostic and/or therapeutic, so as to promote healthy ageing by curtailing chronic inflammatory conditions, such as diabetes.

Selected Publications 

Demers M, Wong SL, Martinod K, Gallant M, Cabral JE, Wang Y, Wagner DD. Priming of neutrophils toward NETosis promotes tumor growth. Oncoimmunology. 2016;5(5):e1134073.

Wong SL, Demers M, Martinod K, Gallant M, Wang Y, Goldfine AB, Kahn CR, Wagner DD. Diabetes primes neutrophils to undergo NETosis, which impairs wound healing. Nat Med. 2015;21(7):815-9.

Yuen CY, Wong SL*, Lau CW, Tsang SY, Xu A, Zhu Z, Ng CF, Yao X, Kong SK, Lee HK, Huang Y. From skeleton to cytoskeleton: osteocalcin transforms vascular fibroblasts to myofibroblasts via angiotensin II and Toll-like receptor 4. Circ Res. 2012;111(3):e55-66. (*Co-first author)

Wong SL, Leung FP, Lau CW, Au CL, Yung LM, Yao X, Chen ZY, Vanhoutte PM, Gollasch M, Huang Y. Cyclooxygenase-2-derived prostaglandin F2alpha mediates endothelium-dependent contractions in the aortae of hamsters with increased impact during aging​. Circ Res. 2009;104(2):228-35.

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