Yuanxiang Tao
· Vice Chair of Research/ProfessorRutgers University · Anesthesiology
Active 1994–2024
About
Yuanxiang Tao is a Full Professor with Tenure and Vice Chair of Research in the Department of Anesthesiology at Rutgers New Jersey Medical School. His research focuses on understanding the molecular and cellular mechanisms underlying chronic pain, opioid-induced hyperalgesia, and opioid tolerance. His laboratory investigates how neuronal PDZ domain-containing scaffolding proteins participate in the development and maintenance of chronic pain and opioid-related phenomena, as well as how peripheral noxious stimuli influence glutamate receptor trafficking at synaptic and extrasynaptic sites of dorsal horn neurons, which are required for chronic pain induction and expression. Professor Tao's work aims to uncover novel therapeutic strategies for the prevention and treatment of chronic pain and opioid-related disorders, addressing a significant public health problem. His research projects include identifying long noncoding RNAs involved in chronic pain, exploring translational regulation underlying opioid tolerance and hyperalgesia, examining gene transcriptional changes in chronic pain, and studying molecular mechanisms of sickle cell disease-associated pain. His methodologies encompass molecular biology, morphology, biochemistry, electrophysiology, and behavioral tests. Throughout his career, he has made notable contributions, including the development of patents related to his research.
Research topics
- Biology
- Neuroscience
- Medicine
- Anesthesia
- Internal medicine
- Pharmacology
- Endocrinology
- Genetics
- Biochemistry
- Chemistry
- Bioinformatics
- Cell biology
- Cancer research
- Anatomy
Selected publications
British Journal of Pharmacology · 2023 · 8 citations
Senior authorCorresponding- Medicine
- Neuroscience
- Anesthesia
BACKGROUND AND PURPOSE: Peripheral nerve trauma-induced dysregulation of pain-associated genes in the primary sensory neurons of dorsal root ganglion (DRG) contributes to neuropathic pain genesis. RNA-binding proteins participate in gene transcription. We hypothesized that RALY, an RNA-binding protein, participated in nerve trauma-induced dysregulation of DRG pain-associated genes and nociceptive hypersensitivity. METHODS AND RESULTS: Immunohistochemistry staining showed that RALY was expressed exclusively in the nuclei of DRG neurons. Peripheral nerve trauma caused by chronic constriction injury (CCI) of unilateral sciatic nerve produced time-dependent increases in the levels of Raly mRNA and RALY protein in injured DRG. Blocking this increase through DRG microinjection of adeno-associated virus 5 (AAV5)-expressing Raly shRNA reduced the CCI-induced elevation in the amount of eukaryotic initiation factor 4 gamma 2 (Eif4g2) mRNA and Eif4g2 protein in injured DRG and mitigated the development and maintenance of CCI-induced nociceptive hypersensitivity, without altering basal (acute) response to noxious stimuli and locomotor activity. Mimicking DRG increased RALY through DRG microinjection of AAV5 expressing Raly mRNA up-regulated the expression of Eif4g2 mRNA and Eif4g2 protein in the DRG and led to hypersensitive responses to noxious stimuli in the absence of nerve trauma. Mechanistically, CCI promoted the binding of RALY to the promoter of Eif4g2 gene and triggered its transcriptional activity. CONCLUSION AND IMPLICATIONS: Our findings indicate that RALY participates in nerve trauma-induced nociceptive hypersensitivity likely through transcriptionally triggering Eif4g2 expression in the DRG. RALY may be a potential target in neuropathic pain management.
A nerve injury–specific long noncoding RNA promotes neuropathic pain by increasing Ccl2 expression
Journal of Clinical Investigation · 2022 · 106 citations
Senior authorCorresponding- Medicine
- Neuroscience
- Bioinformatics
Maladaptive changes of nerve injury-associated genes in dorsal root ganglia (DRGs) are critical for neuropathic pain genesis. Emerging evidence supports the role of long noncoding RNAs (lncRNAs) in regulating gene transcription. Here we identified a conserved lncRNA, named nerve injury-specific lncRNA (NIS-lncRNA) for its upregulation in injured DRGs exclusively in response to nerve injury. This upregulation was triggered by nerve injury-induced increase in DRG ELF1, a transcription factor that bound to the NIS-lncRNA promoter. Blocking this upregulation attenuated nerve injury-induced CCL2 increase in injured DRGs and nociceptive hypersensitivity during the development and maintenance periods of neuropathic pain. Mimicking NIS-lncRNA upregulation elevated CCL2 expression, increased CCL2-mediated excitability in DRG neurons, and produced neuropathic pain symptoms. Mechanistically, NIS-lncRNA recruited more binding of the RNA-interacting protein FUS to the Ccl2 promoter and augmented Ccl2 transcription in injured DRGs. Thus, NIS-lncRNA participates in neuropathic pain likely by promoting FUS-triggered DRG Ccl2 expression and may be a potential target in neuropathic pain management.
Advanced Science · 2021 · 69 citations
Senior authorCorresponding- Cell biology
- Medicine
- Biology
Nerve injury-induced maladaptive changes of gene expression in dorsal root ganglion (DRG) neurons contribute to neuropathic pain. Long non-coding RNAs (lncRNAs) are emerging as key regulators of gene expression. Here, a conserved lncRNA is reported, named DRG-specifically enriched lncRNA (DS-lncRNA) for its high expression in DRG neurons. Peripheral nerve injury downregulates DS-lncRNA in injured DRG due, in part, to silencing of POU domain, class 4, transcription factor 3, a transcription factor that interacts with the DS-lncRNA gene promoter. Rescuing DS-lncRNA downregulation blocks nerve injury-induced increases in the transcriptional cofactor RALY-triggered DRG Ehmt2 mRNA and its encoding G9a protein, reverses the G9a-controlled downregulation of opioid receptors and Kcna2 in injured DRG, and attenuates nerve injury-induced pain hypersensitivities in male mice. Conversely, DS-lncRNA downregulation increases RALY-triggered Ehmt2/G9a expression and correspondingly decreases opioid receptor and Kcna2 expression in DRG, leading to neuropathic pain symptoms in male mice in the absence of nerve injury. Mechanistically, downregulated DS-lncRNA promotes more binding of increased RALY to RNA polymerase II and the Ehmt2 gene promoter and enhances Ehmt2 transcription in injured DRG. Thus, downregulation of DS-lncRNA likely contributes to neuropathic pain by negatively regulating the expression of RALY-triggered Ehmt2/G9a, a key neuropathic pain player, in DRG neurons.
Advanced Science · 2020 · 89 citations
Senior authorCorresponding- Medicine
- Endocrinology
- Internal medicine
Abstract Nerve injury‐induced change in gene expression in primary sensory neurons of dorsal root ganglion (DRG) is critical for neuropathic pain genesis. N 6 ‐methyladenosine (m 6 A) modification of RNA represents an additional layer of gene regulation. Here, it is reported that peripheral nerve injury increases the expression of the m 6 A demethylase fat‐mass and obesity‐associated proteins (FTO) in the injured DRG via the activation of Runx1, a transcription factor that binds to the Fto gene promoter. Mimicking this increase erases m 6 A in euchromatic histone lysine methyltransferase 2 ( Ehmt2 ) mRNA (encoding the histone methyltransferase G9a) and elevates the level of G9a in DRG and leads to neuropathic pain symptoms. Conversely, blocking this increase reverses a loss of m 6 A sites in Ehmt2 mRNA and destabilizes the nerve injury‐induced G9a upregulation in the injured DRG and alleviates nerve injury‐associated pain hypersensitivities. FTO contributes to neuropathic pain likely through stabilizing nerve injury‐induced upregulation of G9a, a neuropathic pain initiator, in primary sensory neurons.
Neurotherapeutics · 2020 · 44 citations
Senior authorCorresponding- Pharmacology
- Medicine
- Cancer research
European Journal of Pain · 2020 · 36 citations
- Medicine
- Anesthesia
- Anatomy
BACKGROUND: The dorsal root (DRG) and trigeminal (TG) ganglia contain cell bodies of sensory neurons of spinal and trigeminal systems, respectively. They are homologs of each other; however, differences in how the two systems respond to injury exist. Trigeminal nerve injuries rarely result in chronic neuropathic pain (NP). To date, no genes involved in the differential response to nerve injury between the two systems have been identified. We examined transcriptional changes involved in the development of trigeminal and spinal NP. METHODS: Trigeminal and spinal mononueropathies were induced by chronic constriction injury to the infraorbital or sciatic nerve. Expression levels of 84 genes in the TG and DRG at 4, 8 and 21 days post-injury were measured using real-time PCR. RESULTS: We found time-dependent and ganglion-specific transcriptional regulation that may contribute to the development of corresponding neuropathies. Among genes significantly regulated in both ganglia Cnr2, Grm5, Htr1a, Il10, Oprd1, Pdyn, Prok2 and Tacr1 were up-regulated in the TG but down-regulated in the DRG at 4 days post-injury; at 21 days post-injury, Adora1, Cd200, Comt, Maob, Mapk3, P2rx4, Ptger1, Tnf and Slc6a2 were significantly up-regulated in the TG but down-regulated in the DRG. CONCLUSIONS: Our findings suggest that spinal and trigeminal neuropathies due to trauma are differentially regulated. Subtle but important differences between the two ganglia may affect NP development. SIGNIFICANCE: We present distinct transcriptional alterations in the TG and DRG that may contribute to differences observed in the corresponding mononeuropathies. Since the trigeminal system seems more resistant to developing NP following trauma our findings lay ground for future research to detect genes and pathways that may act in a protective or facilitatory manner. These may be novel and important therapeutic targets.
Experimental Neurology · 2020 · 15 citations
Senior authorCorresponding- Neuroscience
- Medicine
- Bioinformatics
Recent grants
Role of dorsal root ganglion FTO, a RNA demethylase, in neuropathic pain
NIH · $2.5M · 2019–2025
Epigenetic regulation of neuropathic pain: Role of native KV1.2 antisense RNA
NIH · $1.4M · 2013–2017
Epigenetic regulation of neuropathic pain: Role of DRG histone methyltransferase G9a
NIH · $2.0M · 2016–2023
Discovery and validation of a new long noncoding RNA as a novel target for neuropathic pain
NIH · $3.5M · 2019–2024
NIH · $1.4M · 2013
Frequent coauthors
- 114 shared
Roger A. Johns
Johns Hopkins Medicine
- 68 shared
Alex Bekker
- 63 shared
Srinivasa N. Raja
- 59 shared
Shaogen Wu
Stanford University
- 45 shared
Feng Tao
- 45 shared
Ronald S. Petralia
National Institute on Deafness and Other Communication Disorders
- 43 shared
Myron Yaster
Johns Hopkins University
- 40 shared
Lingli Liang
Xi'an Jiaotong University
Education
- 1986
M.D.
Nanjing Medical University
- 1992
M.S.
Nanjing Medical University
- 1997
Ph.D.
Shanghai Brain Research Institute, Chinese Academy of Science
Awards & honors
- Outstanding PhD Student from the Chinese Academy of Sciences…
- Beckman Outstanding Young Scientist Award from BECKMAN Instr…
- Remarkable Contribution to Nature and Science from the Chine…
- Rita Allen Foundation Pain Scholar, APS (2011)
- Faculty of the Year Award, NJMS, Rutgers, The State Universi…
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