Ru-Rong Ji

Ru-Rong Ji
Distinguished Professor of Anesthesiology, in the School of Medicine
CMB - Clinical/Other
Third Year Mentor - Anesthesiology, Surgery, and Environmental Physiology Study Program (ASEP)

Chronic pain is a major health problem in the US, affecting 100 million Americans. The long-term goal of the lab is to identify molecular and cellular mechanisms that underlie the genesis of chronic pain and, furthermore, to develop novel pain therapeutics that can target these mechanisms. We are interested in the following questions. (1) How do neuroinflammation and activation of glial cells (microglia and astrocytes) regulate pain and spinal cord synaptic plasticity via neuro-glial and neuro-immune interactions? (2) How do secreted miRNAs regulate neuronal signaling and synaptic transmission and pain as novel neuromodulators and pain mediators? (3) How do pro-resolution lipid mediators such as resolvins and protectin control pain via GPCR and arrestin signaling? (4) Do pain and itch share similar mechanisms? (5) How does Toll-like receptor (TLR) signaling in primary sensory neurons regulate pain and itch? (6) How can bone marrow stem cells produce long-term pain relief via secreting anti-inflammatory and trophic factors? We employ a multidisciplinary approach that covers in vitro, ex vivo, and in vivo electrophysiology, neuronal and glial cell biology, transgenic mice, and behaviors.

Education and Training

  • Chinese Academy of Sciences (China), Ph.D. 1990

Publications

Activation of JNK pathway in persistent pain

The c-Jun N-terminal kinase (JNK) is a stress-activated member of MAP kinase family. JNK activation has been strongly implicated in inflammatory responses, neurodegeneration, and apoptosis.

Pages