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Macrophage angiotensin II type 2 receptor triggers neuropathic pain

by Shepherd, Andrew J. , Samineni, Vijay K. , Krause, Eric G. , Mohapatra, Durga P. , de Kloet, Annette D. , Mickle, Aaron D. , Gereau, Robert W. , Mack, Madison R. , Halabi, Carmen M. , Golden, Judith P. , Kim, Brian S.

in ACE inhibitors / Allografts / Angiotensin / Angiotensin II / Animals / Biocompatibility / Biological Sciences / Biomedical materials / Chronic Pain - genetics / Chronic Pain - metabolism / Chronic Pain - pathology / Clinical trials / Collagen / Collagen (type I) / Connective tissues / Danio rerio / Diagnostic systems / Disorders / Ehlers-Danlos syndrome / Genes / Genetic variability / Hematopoietic Stem Cell Transplantation / Macrophages / Macrophages - metabolism / Macrophages - pathology / Medical treatment / Mice / Mutation / Neuralgia / Neuralgia - genetics / Neuralgia - metabolism / Neuralgia - pathology / Neuropathology / Neuroscience / Osteogenesis imperfecta / Pain / Pain management / Pharmacology / Phenotypes / PNAS Plus / Receptor, Angiotensin, Type 2 - genetics / Receptor, Angiotensin, Type 2 - metabolism / Zebrafish

2018

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2018

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2018

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Journal Article

Macrophage angiotensin II type 2 receptor triggers neuropathic pain

Shepherd, Andrew J.,

Samineni, Vijay K.,

Krause, Eric G.,

Mohapatra, Durga P.,

de Kloet, Annette D.,

Mickle, Aaron D.,

Gereau, Robert W.,

Mack, Madison R.,

Halabi, Carmen M.,

Golden, Judith P.,

Kim, Brian S.

2018

Overview

Peripheral nerve damage initiates a complex series of structural and cellular processes that culminate in chronic neuropathic pain. The recent success of a type 2 angiotensin II (Ang II) receptor (AT2R) antagonist in a phase II clinical trial for the treatment of postherpetic neuralgia suggests angiotensin signaling is involved in neuropathic pain. However, transcriptome analysis indicates a lack of AT2R gene (Agtr2) expression in human and rodent sensory ganglia, raising questions regarding the tissue/cell target underlying the analgesic effect of AT2R antagonism. We show that selective antagonism of AT2R attenuates neuropathic but not inflammatory mechanical and cold pain hypersensitivity behaviors in mice. Agtr2-expressing macrophages (MΦs) constitute the predominant immune cells that infiltrate the site of nerve injury. Interestingly, neuropathic mechanical and cold pain hypersensitivity can be attenuated by chemogenetic depletion of peripheral MΦs and AT2R-null hematopoietic cell transplantation. Our study identifies AT2R on peripheral MΦs as a critical trigger for pain sensitization at the site of nerve injury, and therefore proposes a translatable peripheral mechanism underlying chronic neuropathic pain.

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Publisher

National Academy of Sciences

Subject

/ Animals

/ Biological Sciences