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
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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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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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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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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Progressive tactile hypersensitivity after a peripheral nerve crush: non-noxious mechanical stimulus-induced neuropathic pain.
Authors: Authors: Decosterd I, Allchorne A, Woolf CJ.
Pain
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Replicate high-density rat genome oligonucleotide microarrays reveal hundreds of regulated genes in the dorsal root ganglion after peripheral nerve injury.
Authors: Authors: Costigan M, Befort K, Karchewski L, Griffin RS, D'Urso D, Allchorne A, Sitarski J, Mannion JW, Pratt RE, Woolf CJ.
BMC Neurosci
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Hsp27 upregulation and phosphorylation is required for injured sensory and motor neuron survival.
Authors: Authors: Benn SC, Perrelet D, Kato AC, Scholz J, Decosterd I, Mannion RJ, Bakowska JC, Woolf CJ.
Neuron
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