Sung Jun Jung
한양대학교 의과대학 생리학교실 · 의학
Sung Jun Jung 교수의 연구실은 신경성 통증의 분자 기전을 규명하고자 하며, 특히 TRPV1 채널과 TLR4 수용체 간의 상호작용, I(h) 채널의 기능적 역할, 그리고 에ugenol이 신경세포에서 작용하는 이он 채널 조절 메커니즘을 중심으로 연구를 진행하고 있습니다. 통증 수용체의 활성화 및 조절 메커니즘, 특히 생리적 자극과 병리적 상태에서의 이온 채널 기능 변화를 다루며, 신약 타겟 탐색과 통증 완화를 위한 천연물질의 약리학적 기전 규명을 목표로 하고 있습니다. 특히 TRPV1의 내재적 활성화자인 디아실글리세롤과 염증 수용체 TLR4와의 상호작용, 그리고 에ugenol의 다중 작용 메커니즘을 통한 통증 조절 기전에 초점을 맞추고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The capsaicin receptor, known as transient receptor potential channel vanilloid subtype 1 (TRPV1), is activated by a wide range of noxious stimulants and putative ligands such as capsaicin, heat, pH, anandamide, and phosphorylation by protein kinase C (PKC). However, the identity of endogenous activators for TRPV1 under physiological condition is still debated. Here, we report that diacylglycerol (DAG) directly activates TRPV1 channel in a membrane-delimited manner in rat dorsal root ganglion (D
Our data show that direct association between TRPV1 and TLR4 through the TIR domain enhances TRPV1 activity by blocking activation-induced TRPV1 desensitization.
Mechanical allodynia is a common symptom found in neuropathic patients. Hyperpolarization-activated cyclic nucleotide-gated channels and their current, I(h), have been suggested to play an important role in neuropathic pain, especially in mechanical allodynia and spontaneous pain, by involvement in spontaneous ectopic discharges after peripheral nerve injury. Thus, I(h) blockers may hold therapeutic potential for the intervention of mechanical allodynia under diverse neuropathic conditions. Here
Eugenol has sedative, antioxidant, anti-inflammatory, and analgesic effects, but also serves as an irritant through the regulation of a different set of ion channels. Activation of gamma aminobutyric acid (GABA) receptors on sensory neurons leads to the stabilization of neuronal excitability but contributes to formalin-induced inflammatory pain. In this study, we examined the effect of eugenol on the GABA-induced current in rat trigeminal ganglia (TG) neurons and in human embryonic kidney (HEK)
Modulation of the function of somatosensory neurons is an important analgesic strategy, requiring the proposal of novel molecular targets. Many G-protein-coupled receptors (GPRs) have been deorphanized, but the receptor locations, outcomes due to their activations, and their signal transductions remain to be elucidated, regarding the somatosensory nociceptor function. Here we report that GPR171, expressed in a nociceptor subpopulation, attenuated pain signals via Gi/o-coupled modulation of the a
The generation of pain signals from primary afferent neurons is explained by a labeled-line code. However, this notion cannot apply in a simple way to cutaneous C-fibers, which carry signals from a variety of receptors that respond to various stimuli including agonist chemicals. To represent the discharge patterns of C-fibers according to different agonist chemicals, we have developed a quantitative approach using three consecutive spikes. By using this method, the generation of pain in response
Cyclooxygenase metabolizes dihomo-γ-linolenic acid and arachidonic acid to form prostaglandin (PG) E, including PGE1 and PGE2, respectively. Although PGE2 is well known to play an important role in the development and maintenance of hyperalgesia and allodynia, the role of PGE1 in pain is unknown. We confirm whether PGE1 induced pain using orofacial pain behavioral test in mice and determine the target molecule of PGE1 in TG neurons with whole-cell patch-clamp and immunohistochemistry. Intraderma
In this study, we observed quantal changes in single synapse excitatory postsynaptic currents to characterize N-methyl-D-aspartate receptor-mediated silent synapses between primary afferents and spinal substantia gelatinosa neurons. The failure rate of primary afferent quantal excitatory postsynaptic currents was lower at depolarized holding potentials than at hyperpolarized potentials. This lower failure rate at depolarized potentials was due to the activation of N-methyl-D-aspartate receptor-m
Riboflavin, also known as vitamin B<sub>2</sub>, isfound in foods and is used as a dietary supplement. Its deficiency (also called ariboflavinosis) results in some skin lesions and inflammations, such as stomatitis, cheilosis, oily scaly skin rashes, and itchy, watery eyes. Various therapeutic effects of riboflavin, such as anticancer, antioxidant, anti-inflammatory, and anti-nociceptive effects, are well known. Although some studies have identified the clinical effect of riboflavin on skin prob