Telephone: +44 (0) 121 204 4828 Email: firstname.lastname@example.org Room: MB354
Office Hours: Normal working hours
I joined Aston University as a lecturer in neuroscience in 2017. Prior to that, I was a lecturer at the University of Aberdeen after a period of independent research funded by an MRC new investigator award at the University of Cambridge. I carried out my postdoctoral research at the University of Cambridge after received a Ph.D degree in China.
FHEA, Aston University, 2018
Ph.D Tongji Medical College, Huazhong University of Science and Technology, China, 2001
2002-2008, Postdoctoral research fellow, University of Cambridge
I am interested in the molecular mechanisms of pain and itch. Pain is one of the most common medical conditions affecting quality of life of many patients. Pain signals are generated by specialized sensory receptors (or nociceptors) on peripheral sensory nerve endings followed by transmission via afferent nerve fibres to the brain where pain is interpreted. Damage to and interference with the pain pathway can markedly affect pain sensation, leading to either enhanced pain (hyperalgesia) or pain inhibition (analgesia). Notably, a family of Transient Receptor Potential (TRP) ion channels (e.g. TRPV1, TRPA1) have emerged as critical sensory nociceptors responsible for detecting noxious thermal, chemical and mechanical stimuli. TRP ion channels have thus become targets for analgesics. The first line of my research is to investigate the function and modulation of TRP ion channels in sensory neurons under physiological and disease conditions, and how they contribute to hyperalgesia. This research has led to several high impact publications, such as Neuron, Nature Cell Biology, EMBO J and Journal of Neuroscience. They have promoted our understanding of molecular underpinnings of pain with therapeutic implications.
The second aspect of my research is to decipher the molecular links between the pain signalling system and the metabolic system. Pain sensitivity is influenced by the body metabolic status. Indeed, pain is often reported in old people known to have a lower metabolic rate. Metabolic disorders such as diabetic neuropathy are often associated with enhanced pain sensitivity. Reciprocally, pain signalling modulates body metabolism and promotes diet-induced obesity. Understanding how pain sensitivity is determined by the metabolic status offers a unique means to unravel the mechanisms of pain and to identify novel therapeutic targets.
The third area of interest is to understand the mechanisms of itch (pruritus). Itch is another somatic sensation and is a common symptom associated with many diseases such as cholestatic liver disease and diabetes. Itch is closely linked to pain, but is transduced via distinct neural pathways. Interestingly, TRP ion channels, such as TRPV1 and TRPA1, not only mediate pain, but also carry itch. We are interested in the molecules and signalling pathways that mediate itch.
We use electrophysiology, molecular biology, protein biochemistry and imaging combined with behavioural approaches to address our queries.
Acute pain warns animals of danger allowing animals to initiate protective behaviours. Acute pain is therefore beneficial for survival. However, when acute pain is transitioned to chronic stage, it is debilitating and harmful to health. Indeed, chronic pain is a common medical complication to many diseases such as arthritis, cancer, diabetes and heart diseases, and is a major public health problem, incurring enormous medical costs and productivity loss in the workplace. In fact, chronic pain is one of the most prominent causes of disability worldwide, and affects over one third of the population in the UK. Developing effective pain therapies will therefore have significant economic and societal impact. We aim to understand how pain signals are generated and transduced, and how pain is transitioned, modulated and maintained, with a view to devising novel therapies for the effective treatment of pain.
We are particularly interested in the general inflammatory pain, arthritis pain, diabetic neuropathic pain. Our questions are: what are the common grounds among these different types of pain? What mechanisms are unique to an individual pain type? How acute pain is transitioned to chronic pain? How pain is collectively controlled by different body systems? Our ambitions are to find out the molecules and pathways critical to these processes and to develop new strategies to target these molecules and pathways for pain therapy.
Medical Research Council
Hasan R & Zhang X. Ca2+ regulation of TRP ion channels. Int J Mol Sci 2018, 19 (4). E1256
Hasan R, Leeson-Payne AT, Jaggar JH and Zhang X. Calmodulin is responsible for Ca2+-dependent regulation of damage sensing TRPA1 ion channels. Scientific Reports 2017 7, 45098.Pubmed.
Zhang X. Molecular sensor and modulators of thermoreception. Channels (Austin) 2015, 9(2): 73-81. Pubmed
Zhang X. Targeting TRP ion channels for itch relief. Journal Archives of Pharmacology (Naunyn-Schmiedeberg) 2015, 388(4): 389-399. Pubmed
Li L, Hasan R and Zhang X. The basal thermal sensitivity of the TRPV1 ion channel is determined by PKCII. Journal of Neuroscience 2014, 34(24): 8246-58. Pubmed
Than JY, Lin Li, Hasan R and Zhang X. Excitation and modulation of TRPV1, TRPM8 and TRPA1 ion channel expressing sensory neurons by the pruritogen chloroquine. Journal of Biological Chemistry. 2013, 288(18):12818-27.Pubmed
Lin Li and Zhang X. Differential inhibition of the TRPM8 ion channel by Gq and G11. Channels. 2013. 18, 7(2): 115-8. Pubmed
Zhang X*, Mak S, Li L, Martin AP, Denlinger B, Belmonte C and McNaughton PA*. Direct inhibition of the cold-activated TRPM8 ion channel by Gq. Nature Cell Biology 2012, 14(8): 8518. ( * co-senior author). Pubmed
Fan H-C, Zhang X and McNaughton PA. Activation of TRPV4 ion channel is enhanced by phosphorylation. Journal of Biological Chemistry.2009, 284(41): 27884-91.Pubmed.
Mak S, Zhang X and McNaughton PA. Temperature sensation. Encyclopaedia of Life Sciences (2009).
Zhang X, Li L and McNaughton PA. Pro-inflammmatory mediators modulate the heat-gated ion channel TRPV1 via scaffolding protein AKAP79/150. Neuron 2008, 59(3): 450-61.Pubmed
Smith ES, Zhang X, Cadiou H and McNaughton PA. Proton binding sites involved in the activation of acid-sensing ion channel ASIC2a. Neuroscience Letters 2007, 426(1): 12-7. Pubmed
Huang J, Zhang X, McNaughton PA. Modulation of temperature-sensitive TRP channels. Semin Cell Dev Biol, 2006; 17(6): 638-45. Pubmed
Zhang X, McNaughton PA. Why pain gets worse: the mechanisms of heat hyperalgesia. J Gen Physiol, 2006; 128(5): 491-3. Pubmed
Huang J, Zhang X, McNaughton PA. Inflammatory pain: the cellular basis of heat hyperalgesia. Current Neuropharmacology, 2006; 4, 197-206. Pubmed
Zhang X, Huang J and McNaughton PA. NGF rapidly increases membrane expression of TRPV1 heat-gated ion channels. EMBO Journal, 2005; 24(24): 4211-23. Featured in “Nature Research Highlights”, Nature 2005, 438(15): p893. Pubmed
Zhang X, Deng Z, Qu Z and Ni J. Oxidized low density lipoprotein and very low density lipoprotein induce the expression of macrophage inflammatory protein-1 in human peripheral blood monocytes. Chinese Journal of Atheroclerosis 2001, 9(3):198-202.
Zhang X, Deng Z, Qu Z and Ni J. Oxidized low density lipoprotein and very low density lipoprotein induce the expression of macrophage inflammatory protein-1alpha in human peripheral blood monocytes. Chinese Journal of Atheroclerosis 2001, 9(3):198-202.
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