Anne-Marie Malfait
Rush University, IL·Neuroscience
Chronic pain from joints, muscles and connective tissue is among the most common causes of disability worldwide. Current painkillers work on only a few targets and often give poor long-term relief.
- Fields
Neuroscience
Medicine & Clinical Research
Pharmacology
- Topics
chronic pain
osteoarthritis
Ehlers-Danlos syndrome
- Grants
- 4 known grants, through Jul 2029
What they work on
- Map nerve fibers and gene activity in skin from classic Ehlers-Danlos syndrome patients versus controls, using tissue staining and Visium spatial transcriptomics, which measures gene activity across tissue slices.
- Test whether fibroblasts with type V collagen (Col5a1) defects make sensory neurons overexcitable or overgrown, using microfluidic co-cultures of mouse DRG neurons and of patient fibroblasts with human stem-cell-derived neurons.
- Map where NP1 nociceptors, the pain-sensing fibers that carry the Mrgprd receptor, grow in osteoarthritic mouse knees and in human knee tissue from donors and knee-replacement surgery.
- Test whether Mrgprd-blocking drugs reduce the excitability and sprouting of NP1 neurons and relieve osteoarthritis pain, using electrophysiology, GCaMP calcium imaging and axon-growth microchips.
- Determine which knee and DRG cells express NGF (nerve growth factor) and its receptor TrkA during osteoarthritis, using reporter mice, single-cell RNA sequencing and RNAscope.
- Test whether NGF-TrkA signaling protects joints after injury, by deleting Ngf or Ntrk1 from sensory neurons, immune cells, bone cells or cartilage cells in mice and by treating mice with anti-NGF antibodies.
More about the research
The lab studies how pain-sensing nerve fibers, called nociceptors, change in diseased tissue. Its focus is on osteoarthritis, the wear-related joint disease, and a connective-tissue disorder called Ehlers-Danlos syndrome. In both conditions, nociceptors can become overly sensitive and grow into places they normally do not reach. The projects use mouse models, human tissues and nerve-cell cultures to find which nerve populations and signals drive that change. The aim is to find new, safer treatment targets.
Why it matters
Osteoarthritis and Ehlers-Danlos syndrome cause chronic pain that current drugs treat poorly, and patients urgently need non-opioid options. Pinpointing NP1 nociceptors and the Mrgprd receptor could yield new drug targets for osteoarthritis pain. Clarifying how NGF blockade harms joints could guide safer anti-NGF therapies. Fibroblast-nerve findings could point to new treatments for EDS pain and other skin-related pain conditions.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Chia-Lung Wu
University of Rochester, NY·Biomedical Engineering
Determine how mechanical loading switches on WNT16 in chondrocytes through the force-sensing calcium channel TRPV4, by loading human stem cell-derived and hip chondrocytes in agarose gels and sequencing their genetic and epigenetic controls.
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.
Sylvia Suadicani
Albert Einstein College of Medicine, NY·Neuroscience
Test whether bladder or colon injury enhances signaling between dorsal root ganglia (DRG) sensory neurons and their wrapping satellite glial cells, using established mouse models of direct bladder and colon insult with behavioral, functional and molecular measures.
The school
Rush University: 7 labs on PI Pages, $139M a year on research, 26 research doctorates a year.
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