Andrew Shepherd (0000-0002-8440-6192)

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I received my Bachelors’ degree in Molecular Cell Biology in 2003 from the University of Manchester Institute of Science and Technology in the UK.

I received my PhD in Neuroimmunomodulation in 2006 at the nearby University of Manchester – where I investigated the impact of sensory innervation and neuropeptide release in a rodent model of allergic inflammation. Following a brief postdoc in the same institution studying folate metabolism in the development of hydrocephalus, I relocated to the newly-established lab of Durga ‘DP’ Mohapatra in the Department of Pharmacology at the University of Iowa in 2008. During this time, I developed an interest in G-protein coupled receptor-based modulation of ion channel activity in the central and peripheral nervous system, particularly in relation to pain associated with bone-metastasized prostate cancer.

Since becoming a research-track faculty member of the Department of Anesthesiology at Washington University in St. Louis in 2015, I have developed research related to macrophage involvement in chronic inflammatory and neuropathic pain. In particular, I am currently focusing on the pain-promoting effects of obesity and the renin-angiotensin system in the exacerbation of such pain states.

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The University of Texas MD Anderson Cancer Center: Houston, Texas, US

2018-12-18 to present | Assistant Professor (Symptom Research)

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Andrew Shepherd

https://orcid.org/0000-0002-8440-6192

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Employment (5)

The University of Texas MD Anderson Cancer Center: Houston, Texas, US

Washington University in Saint Louis: Saint Louis, MO, US

University of Iowa: Iowa City, IA, US

University of Iowa: Iowa City, IA, US

University of Manchester: Manchester, Greater Manchester, GB

Education and qualifications (2)

University of Manchester: Manchester, Greater Manchester, GB

University of Manchester: Manchester, Greater Manchester, GB

Professional activities (4)

International Association for the Study of Pain: Seattle, WA, US

American Pain Society: Chicago, Illinois, US

American Heart Association: TX, TX, US

Society for Neuroscience: Washington, DC, US

Funding (9)

Targeting Angiotensin-Based Neuroimmune Cross Talk for Treatment of Neuromuscular Trauma

Targeting STAT3 Signaling to Promote Recovery from Neuropathic Pain

Validation of Fibroblast-Derived PI16 as a Novel Target for pain Treatment

Neuro-Immuno Modulating Analgesic (NiMA) Nanomedicine Platform for Treatment of Diabetic Neuropathy

Non-addictive Angiotensin AT2 inhibitors for neuropathic pain relief

Non-addictive Angiotensin AT2 inhibitors for neuropathic pain relief

PQ12 Targeting HDAC6 for Chemotherapy-Induced Neuropathy and Chemobrain

Angiotensin Links Osteoarthritis Pain to Obesity via Macrophages and TRPA1

Mesenchymal Stem Cells to Repair Chemobrain

Works (38)

Intrinsic adaptive plasticity in mouse and human sensory neurons

Animal models of neuropathic pain

Single-cell analysis of age-related changes in leukocytes of diabetic mouse hindpaws

Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

Role of Src kinase in regulating protein kinase C mediated phosphorylation of TRPV1

Targeting Neuroimmune Interactions in Diabetic Neuropathy with Nanomedicine

Tracking macrophages in diabetic neuropathy with two-color nanoemulsions for near-infrared fluorescent imaging and microscopy

Drug targeting to sites of oxidative stress using the Baeyer-Villiger reaction

Tracking Macrophages in Diabetic Neuropathy With Two-Color Nanoemulsions for Near-Infrared Fluorescent Imaging and Microscopy

Astrocytes improve neuronal health after cisplatin treatment through mitochondrial transfer

Attenuation of Unevoked Mechanical and Cold Pain Hypersensitivities Associated With Experimental Neuropathy in Mice by Angiotensin II Type-2 Receptor Antagonism.

Macrophage angiotensin II type 2 receptor triggers neuropathic pain.

Angiotensin II Triggers Peripheral Macrophage-to-Sensory Neuron Redox Crosstalk to Elicit Pain

Deficits in Burrowing Behaviors Are Associated With Mouse Models of Neuropathic but Not Inflammatory Pain or Migraine.

Parathyroid hormone-related peptide activates and modulates TRPV1 channel in human DRG neurons.

Parathyroid Hormone-Related Peptide Elicits Peripheral TRPV1-dependent Mechanical Hypersensitivity.

Pharmacological validation of voluntary gait and mechanical sensitivity assays associated with inflammatory and neuropathic pain in mice.

Inflammation and nerve injury minimally affect mouse voluntary behaviors proposed as indicators of pain.

Macrophage-to-sensory neuron crosstalk mediated by Angiotensin II type-2 receptor elicits neuropathic pain

Neuropathic Pain: Central vs. Peripheral Mechanisms

Nociceptive TRP Channels: Sensory Detectors and Transducers in Multiple Pain Pathologies.

The Complement System Component C5a Produces Thermal Hyperalgesia via Macrophage-to-Nociceptor Signaling That Requires NGF and TRPV1.

Convergent phosphomodulation of the major neuronal dendritic potassium channel Kv4.2 by pituitary adenylate cyclase-activating polypeptide.

Induction of thermal and mechanical hypersensitivity by parathyroid hormone-related peptide through upregulation of TRPV1 function and trafficking.

Sensory TRP channels: the key transducers of nociception and pain.

Localization and expression of CaBP1/caldendrin in the mouse brain.

Chemokine co-receptor CCR5/CXCR4-dependent modulation of Kv2.1 channel confers acute neuroprotection to HIV-1 glycoprotein gp120 exposure.

Competition between α-actinin and Ca²⁺-calmodulin controls surface retention of the L-type Ca²⁺ channel Ca(V)1.2.

Disruption of the non-canonical Wnt gene PRICKLE2 leads to autism-like behaviors with evidence for hippocampal synaptic dysfunction.

Distinct modifications in Kv2.1 channel via chemokine receptor CXCR4 regulate neuronal survival-death dynamics.

The C-type natriuretic peptide induces thermal hyperalgesia through a noncanonical Gβγ-dependent modulation of TRPV1 channel.

Immunostaining of Voltage-Gated Ion Channels in Cell Lines and Neurons – Key Concepts and Potential Pitfalls

Tissue preparation and immunostaining of mouse sensory nerve fibers innervating skin and limb bones.

Regulator of G protein signaling 6 (RGS6) protein ensures coordination of motor movement by modulating GABAB receptor signaling.

RGS6, a modulator of parasympathetic activation in heart.

Addressing a folate imbalance in fetal cerebrospinal fluid can decrease the incidence of congenital hydrocephalus.

Without nerves, immunology remains incomplete -in vivo veritas.

Mobilisation of specific T cells from lymph nodes in contact sensitivity requires substance P.

Peer review (6 reviews for 5 publications/grants)