About Dr. Kavelaars
Annemieke Kavelaars is a researcher in the field of neuroimmunology. She began her work in the areas of brain, behavior and immunity as a graduate student. She has worked extensively with experimental animal models of pain and of acute and chronic inflammatory diseases, has used biochemical and cell biology techniques, and has performed multiple translational studies.
The main focus of Dr. Kavelaars' work in the pain field is on mechanisms underlying the transition from acute to chronic pain. She has worked extensively with various experimental animal models of pain in mice, including inflammatory and nerve damage models. Her lab was the first to identify a key role for the kinase GRK2 in regulating transition from acute to chronic pain. She showed that GRK2 in nociceptors prevents transition from acute to chronic pain by controlling the activity of the cAMP sensor Epac1. In addition, she investigated the role of monocytes and macrophages in the transition from acute to chronic pain. Using mice with cell-specific deletion of GRK2, she demonstrated that GRK2 in monocytes and macrophages is required to prevent chronic inflammatory pain. In cell transfer studies, she demonstrated that resolution of inflammatory pain depends on IL-10 production by monocytes and macrophages. More recently, she is using a combination of models of reflexive and spontaneous pain and also a novel test we developed to study numbness because this is frequently reported by patients treated for cancer.
Dr. Kavelaars has also begun working on chemotherapy-induced neuropathic pain. Her group is identifying novel targets for treatment and investigating the contribution of the immune system to recovery from pain. She uses behavioral measures to determine sensitivity to pain and its comorbidities, such as depression-like behavior, as well as cellular and molecular methods for analysis of the underlying mechanisms.
Department Chair ad interim, Department of Symptom Research, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
Professor, Department of Symptom Research, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX
Professor, School of Behavioral and Brain Sciences, The University of Texas at Dallas, Dallas, TX
Associate Professor, Division of Laboratory of Neuroimmunology and Developmental Origins of Disease (NIDOD), University Medical Center Utrecht, Utrecht
Professor, The University of Texas Graduate School of Biomedical Sciences at Houston (GSBS), Houston, TX
|1990||Utrecht University, Utrecht, PHD, Infection and Immunity|
|1986||Utrecht University, Utrecht, MSc, Biology|
|1990-1997||Research Fellowship, Psychoneuroimmunology, University Medical Center Utrecht, Utrecht|
|1986-1990||PhD Student Training, Pediatric Immunology, Section of Psychoneuroimmunology, Wilhelmina Children's Hospital, Utrecht University, Utrecht|
Institutional Committee Activities
Member, Genetically Engineered Mouse Facility (GEMF) Advisory Committee, 2016 - Present
|2017||Robert M. Chamberlain Distinguished Mentor Award, The University of Texas MD Anderson Cancer Center|
|2012||Norman Cousins Award, Psychoneuroimmunology Research Society|
|2001||Bob Ader New Investigator Award, Psychoneuroimmunology Research Society|
- Krukowski K, Ma J, Golonzhka O, Laumet GO, Gutti T, van Duzer JH, Mazitschek R, Jarpe MB, Heijnen CJ, Kavelaars A. HDAC6 inhibition effectively reverses chemotherapy-induced peripheral neuropathy. Pain 158(6):1126-1137, 2017. e-Pub 2017. PMID: 28267067.
- Chiu GS, Maj MA, Rizvi S, Dantzer R, Vichaya EG, Laumet G, Kavelaars A, Heijnen CJ. Pifithrin-µ prevents cisplatin-induced chemobrain by preserving neuronal mitochondrial function. Cancer Res 77(3):742-752, 2017. e-Pub 2016. PMID: 27879267.
- Maj MA, Ma J, Krukowski KN, Kavelaars A, Heijnen CJ. Inhibition of mitochondrial p53 accumulation by PFT-μ prevents cisplatin-induced peripheral neuropathy. Front Mol Neurosci 10:108, 2017. e-Pub 2017. PMID: 28458631.
- Baameur F, Singhmar P, Zhou Y, Hancock JF, Cheng X, Heijnen CJ, Kavelaars A. Epac1 interacts with importin β1 and controls neurite outgrowth independently of cAMP and Rap1. Sci Rep 6:36370, 2016. e-Pub 2016. PMID: 27808165.
- Krukowski K, Eijkelkamp N, Laumet G, Hack CE, Li Y, Dougherty PM, Heijnen CJ, Kavelaars A. CD8+ T cells and endogenous IL-10 are required for resolution of chemotherapy-induced neuropathic pain. J Neurosci 36(43):11074-11083, 2016. PMID: 27798187.
- Singhmar P, Huo X, Eijkelkamp N, Berciano SR, Baameur F, Mei FC, Zhu Y, Cheng X, Hawke D, Mayor F, Murga C, Heijnen CJ, Kavelaars A. Critical role for Epac1 in inflammatory pain controlled by GRK2-mediated phosphorylation of Epac1. Proc Natl Acad Sci U S A 113(11):3036-41, 2016. e-Pub 2016. PMID: 26929333.
- Vichaya EG, Molkentine JM, Vermeer DW, Walker AK, Feng R, Holder G, Luu K, Mason RM, Saligan L, Heijnen CJ, Kavelaars A, Mason KA, Lee JH, Dantzer R. Sickness behavior induced by cisplatin chemotherapy and radiotherapy in a murine head and neck cancer model is associated with altered mitochondrial gene expression. Behav Brain Res 297:241-50, 2016. e-Pub 2015. PMID: 26475509.
- Krukowski K, Nijboer CH, Huo X, Kavelaars A, Heijnen CJ. Prevention of chemotherapy-induced peripheral neuropathy by the small-molecule inhibitor pifithrin-μ. Pain 156(11):2184-92, 2015. PMID: 26473292.
- Laumet G, Zhou W, Dantzer R, Edralin JD, Huo X, Budac DP, O'Connor JC, Lee AW, Heijnen CJ, Kavelaars A. Upregulation of neuronal kynurenine 3-monooxygenase mediates depression-like behavior in a mouse model of neuropathic pain. Brain Behav Immun. e-Pub 2017. PMID: 28709913.
|Title:||A Novel Molecular Switch Regulating Transition from Acute to Chronic Pain|
|Title:||A Novel Neuroimmune Risk Factor for Comorbid Depression and Chronic Pain|
|Title:||Adult Mesenchymal Stem Cells (MSC) to Regenerate the Neonatal Brain|
|Funding Source:||ZonMW, Translational Adult Stemcell Research (TASo)|
|Title:||NEUROBID: Neuroscience on Barriers in Development|
|Funding Source:||European Community; FP-7 EU|
|Title:||Faculty Science and Technology Acquisition and Retention (STARS) Program|
|Funding Source:||The University of Texas System|