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
Inhibition of the kinase WNK1/HSN2 ameliorates neuropathic pain by restoring GABA inhibition.
Authors: Authors: Kahle KT, Schmouth JF, Lavastre V, Latremoliere A, Zhang J, Andrews N, Omura T, Laganière J, Rochefort D, Hince P, Castonguay G, Gaudet R, Mapplebeck JC, Sotocinal SG, Duan J, Ward C, Khanna AR, Mogil JS, Dion PA, Woolf CJ, Inquimbert P, Rouleau GA.
Sci Signal
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A Systems-Level Analysis of the Peripheral Nerve Intrinsic Axonal Growth Program.
Authors: Authors: Chandran V, Coppola G, Nawabi H, Omura T, Versano R, Huebner EA, Zhang A, Costigan M, Yekkirala A, Barrett L, Blesch A, Michaelevski I, Davis-Turak J, Gao F, Langfelder P, Horvath S, He Z, Benowitz L, Fainzilber M, Tuszynski M, Woolf CJ, Geschwind DH.
Neuron
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Association of Joint Inflammation With Pain Sensitization in Knee Osteoarthritis: The Multicenter Osteoarthritis Study.
Authors: Authors: Neogi T, Guermazi A, Roemer F, Nevitt MC, Scholz J, Arendt-Nielsen L, Woolf C, Niu J, Bradley LA, Quinn E, Law LF.
Arthritis Rheumatol
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Lack of motor recovery after prolonged denervation of the neuromuscular junction is not due to regenerative failure.
Authors: Authors: Sakuma M, Gorski G, Sheu SH, Lee S, Barrett LB, Singh B, Omura T, Latremoliere A, Woolf CJ.
Eur J Neurosci
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Neuronal Circuits Modulate Antigen Flow Through Lymph Nodes.
Authors: Authors: Hanes WM, Olofsson PS, Talbot S, Tsaava T, Ochani M, Imperato GH, Levine YA, Roth J, Pascal MA, Foster SL, Wang P, Woolf C, Chavan SS, Tracey KJ.
Bioelectron Med
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CD11b+Ly6G- myeloid cells mediate mechanical inflammatory pain hypersensitivity.
Authors: Authors: Ghasemlou N, Chiu IM, Julien JP, Woolf CJ.
Proc Natl Acad Sci U S A
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Doublecortin-Like Kinases Promote Neuronal Survival and Induce Growth Cone Reformation via Distinct Mechanisms.
Authors: Authors: Nawabi H, Belin S, Cartoni R, Williams PR, Wang C, Latremolière A, Wang X, Zhu J, Taub DG, Fu X, Yu B, Gu X, Woolf CJ, Liu JS, Gabel CV, Steen JA, He Z.
Neuron
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The Stress-Induced Atf3-Gelsolin Cascade Underlies Dendritic Spine Deficits in Neuronal Models of Tuberous Sclerosis Complex.
Authors: Authors: Nie D, Chen Z, Ebrahimi-Fakhari D, Di Nardo A, Julich K, Robson VK, Cheng YC, Woolf CJ, Heiman M, Sahin M.
J Neurosci
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Silencing Nociceptor Neurons Reduces Allergic Airway Inflammation.
Authors: Authors: Talbot S, Abdulnour RE, Burkett PR, Lee S, Cronin SJ, Pascal MA, Laedermann C, Foster SL, Tran JV, Lai N, Chiu IM, Ghasemlou N, DiBiase M, Roberson D, Von Hehn C, Agac B, Haworth O, Seki H, Penninger JM, Kuchroo VK, Bean BP, Levy BD, Woolf CJ.
Neuron
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From Dish to Bedside: Lessons Learned While Translating Findings from a Stem Cell Model of Disease to a Clinical Trial.
Authors: Authors: McNeish J, Gardner JP, Wainger BJ, Woolf CJ, Eggan K.
Cell Stem Cell
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