Clifford Woolf

Clifford Woolf, MB, BCh, PhD

Professor of Neurology, Harvard Medical School

Adaptive and Maladaptive Plasticity in Sensory and Motor Systems

Neurons are subject to functional, chemical and structural plasticity. This plasticity is an important factor both in the normal function of the nervous system and in a vast range of neurological diseases.

The Woolf lab studies how different forms of neuronal plasticity contribute both to adaptive and maladaptive changes in the mammalian nervous system, particularly in relation to pain, regeneration and neurodegenerative diseases.

Most of our work is concentrated on primary sensory and motor neurons, and to the interaction of neurons and immune cells, using a multidisciplinary approach spanning stem cell, molecular and cell biology, electrophysiology, neuroanatomy, behavior and genetics. We have established functional and comparative genomic strategies using expression profiling, bioinformatics and gain- and loss-of-function approaches, to screen for novel genes that contribute to neuronal plasticity and disease phenotypes. Our group works closely with many academic groups and the pharmaceutical industry to model disease and identify molecular targets for novel analgesics, axonal growth determinants and neuroprotective agents.

Current research includes study of the transcriptional control and post-translational processing of receptors and ion channels that mediate pain hypersensitivity, selective silencing of defined neuronal populations, intracellular signal transduction cascades activated by peripheral inflammation and nerve injury, neuro-immune interactions, transcription factors as master regulators of pain, growth and survival programs, cell survival in injured sensory and motor neurons, and the contribution of intrinsic growth determinants in establishing regenerative capacity in the peripheral and central nervous system. We are an active part of the Harvard Stem Cell Institute and are investigating how sensory and motor neurons reprogrammed from patient fibroblasts can be used to study pain and motor neuron disease and to screen for new treatments.

Publications View
High basal expression and injury-induced down regulation of two regulator of G-protein signaling transcripts, RGS3 and RGS4 in primary sensory neurons.
Authors: Authors: Costigan M, Samad TA, Allchorne A, Lanoue C, Tate S, Woolf CJ.
Mol Cell Neurosci
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Selective up-regulation of the growth arrest DNA damage-inducible gene Gadd45 alpha in sensory and motor neurons after peripheral nerve injury.
Authors: Authors: Befort K, Karchewski L, Lanoue C, Woolf CJ.
Eur J Neurosci
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A conditional deletion of the NR1 subunit of the NMDA receptor in adult spinal cord dorsal horn reduces NMDA currents and injury-induced pain.
Authors: Authors: South SM, Kohno T, Kaspar BK, Hegarty D, Vissel B, Drake CT, Ohata M, Jenab S, Sailer AW, Malkmus S, Masuyama T, Horner P, Bogulavsky J, Gage FH, Yaksh TL, Woolf CJ, Heinemann SF, Inturrisi CE.
J Neurosci
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p38 mitogen-activated protein kinase is activated after a spinal nerve ligation in spinal cord microglia and dorsal root ganglion neurons and contributes to the generation of neuropathic pain.
Authors: Authors: Jin SX, Zhuang ZY, Woolf CJ, Ji RR.
J Neurosci
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No Nogo: now where to go?
Authors: Authors: Woolf CJ.
Neuron
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Peripheral nerve injury alters excitatory synaptic transmission in lamina II of the rat dorsal horn.
Authors: Authors: Kohno T, Moore KA, Baba H, Woolf CJ.
J Physiol
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The prostaglandin E2 receptor-1 (EP-1) mediates acid-induced visceral pain hypersensitivity in humans.
Authors: Authors: Sarkar S, Hobson AR, Hughes A, Growcott J, Woolf CJ, Thompson DG, Aziz Q.
Gastroenterology
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Exploiting microarrays to reveal differential gene expression in the nervous system.
Authors: Authors: Griffin RS, Mills CD, Costigan M, Woolf CJ.
Genome Biol
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Gabapentin-- actions on adult superficial dorsal horn neurons.
Authors: Authors: Moore KA, Baba H, Woolf CJ.
Neuropharmacology
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Can we conquer pain?
Authors: Authors: Scholz J, Woolf CJ.
Nat Neurosci
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