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
Pain TRPs.
Authors: Authors: Wang H, Woolf CJ.
Neuron
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ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model.
Authors: Authors: Zhuang ZY, Gerner P, Woolf CJ, Ji RR.
Pain
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Patients with chest pain and occult gastroesophageal reflux demonstrate visceral pain hypersensitivity which may be partially responsive to acid suppression.
Authors: Authors: Sarkar S, Thompson DG, Woolf CJ, Hobson AR, Millane T, Aziz Q.
Am J Gastroenterol
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Ionotropic and metabotropic receptors, protein kinase A, protein kinase C, and Src contribute to C-fiber-induced ERK activation and cAMP response element-binding protein phosphorylation in dorsal horn neurons, leading to central sensitization.
Authors: Authors: Kawasaki Y, Kohno T, Zhuang ZY, Brenner GJ, Wang H, Van Der Meer C, Befort K, Woolf CJ, Ji RR.
J Neurosci
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Adult neuron survival strategies--slamming on the brakes.
Authors: Authors: Benn SC, Woolf CJ.
Nat Rev Neurosci
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Axonal injury-dependent induction of the peripheral benzodiazepine receptor in small-diameter adult rat primary sensory neurons.
Authors: Authors: Karchewski LA, Bloechlinger S, Woolf CJ.
Eur J Neurosci
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Differential analgesic sensitivity of two distinct neuropathic pain models.
Authors: Authors: Decosterd I, Allchorne A, Woolf CJ.
Anesth Analg
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Peripheral noxious stimulation induces phosphorylation of the NMDA receptor NR1 subunit at the PKC-dependent site, serine-896, in spinal cord dorsal horn neurons.
Authors: Authors: Brenner GJ, Ji RR, Shaffer S, Woolf CJ.
Eur J Neurosci
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Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapy.
Authors: Authors: Woolf CJ.
Life Sci
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Pain: moving from symptom control toward mechanism-specific pharmacologic management.
Authors: Authors: Woolf CJ.
Ann Intern Med
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