Huijuan Hu
Rutgers University-New Brunswick, NJ·Neuroscience
Chronic itch and neuropathic pain are hard to treat because the nervous system itself becomes altered. It begins sending persistent itch or pain signals.
- Fields
Neuroscience
Pharmacology
Physiology
- Topics
chronic itch
pruritus
neuropathic pain
- Grants
- 2 known grants, through Mar 2028
What they work on
- Determine whether deleting or knocking down STIM2, a calcium-store sensor, in the mouse spinal cord reduces chronic itch in models of chronic itch, including DNFB- and DCP-induced dermatitis.
- Examine how STIM2 expression and function change in spinal neurons and astrocytes under chronic itch conditions.
- Investigate how STIM2 supports itch transmission through the GRP receptor GRPR in excitatory neurons and through TLR4–STAT3 signaling in astrocytes.
- Test whether restoring DS-lncRNA, a long noncoding RNA in the dorsal root ganglion, prevents neuropathic pain after nerve injury, and whether lowering it causes pain in uninjured mice.
- Determine whether nerve injury lowers DS-lncRNA by reducing the gene activator Pou4f3, increasing RALY–RNA polymerase II binding and raising expression of the pain-related enzyme G9a.
More about the research
The two projects look for the molecules behind these changes. One focuses on the spinal cord's role in chronic itch. The other focuses on the dorsal root ganglion (DRG), a cluster of sensory nerve cells next to the spinal cord, and its role in pain after nerve injury. Both use mouse models, and both aim to find molecules that could become new treatment targets.
Why it matters
Chronic itch and neuropathic pain are debilitating and poorly managed. Identifying STIM2 as a key controller of itch signaling in the spinal cord could point to a new drug target for people with chronic itch. Showing that restoring DS-lncRNA in sensory ganglia relieves nerve-injury pain could provide a new target for neuropathic pain. Because virus-delivered gene therapy is already in clinical trials, this approach could eventually be explored as a treatment.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Murali Prakriya
Northwestern University, IL·Neuroscience
Map the binding interface between the Orai1 channel and the calcium sensor STIM1. Use photocrosslinking with unnatural amino acids that can be locked in place by light.
Bin Pan
University of Texas Medical Branch at Galveston, TX·Neuroscience
Establish whether CaMKII activity in peripheral sensory neurons suppresses pain, testing the hypothesis that reduced CaMKII signaling in dorsal root ganglion neurons maintains chronic pain in preclinical neuropathic and osteoarthritic pain models.
Francesca Bartolini
Columbia University, NY·Neuroscience
Test whether unrelated CIPN-causing chemotherapy drugs share a mechanism of altering tubulin post-translational modifications early, before neuropathy symptoms appear, using cellular and preclinical models.
The school
Rutgers University-New Brunswick: 57 labs on PI Pages, $837M a year on research, 713 research doctorates a year.
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