| Academic Background:
Ph.D., Pharmaceutical
Sciences, University of Nebraska Medical Center, 1999
B.S., Medical Technology, University of Nebraska Medical Center, 1988
B.S., Computer Science, Winona State University, 1986
Professional Experience:
|
01/2004 –
present |
Assistant
Professor, Pharmacology, University Missouri-Kansas City |
|
10/1999 –
01/2004 |
Research
Associate/ Postdoctoral Fellow in the Pharmacology Department,
College of Medicine, University of Arizona - Tucson, AZ
|
|
07/1990 –
07/1993 |
Clinical
Instructor, Medical Technology Program, University of Nebraska
Medical Center (1990-1993) |
Research Interests:
Blood-brain barrier (BBB), inflammation, cytokines, tight junctions,
neurological diseases
Research interests in the Mark laboratory are focused on understanding
cellular signaling mechanisms and pathways of endothelial barrier
systems, especially the cerebral microvasculature, i.e., the blood-brain
barrier (BBB). In particular, our research investigates functional and
structural disturbances of the BBB due to stressors such as chronic
inflammation and the milieu of cytokines and mediators that are released
into the circulation as part of the pathology.
Our
research program examines intracellular mechanisms and pathways (i.e.,
signal transduction, gene regulation, protein expression, etc.) of
endothelial barrier systems that are stimulated by pathological insults,
which lead to perturbations of the BBB. This is particularly important
in several diseases with an inflammatory component where cerebral edema
and neurological dysfunction have been reported.
These research efforts are aimed to provide a better understanding of
the cellular mechanisms involved in the cytoskeleton and tight
junctional complexes (structural changes), changes of microvascular
barriers that result in disturbances in cellular homeostasis (i.e.,
altered transport, increased paracellular permeability, edema, and
multi-organ failure). Understanding the mechanisms by which these
pathological stressors induce endothelial cell alterations will
ultimately lead to improved pharmacological therapy for patients with
neurological dysfunction such as multiple sclerosis, ischemic stroke,
Alzheimer’s disease, and chronic inflammation such as liver fibrosis.
Models and techniques used in our laboratory include: in vitro
cell culture, Western blotting, permeability assays,
immunohistochemistry, RT-PCR, enzyme assays, and ELISA.
Representative Publications:
|
Huber, J.D., Campos, C.R., Mark, K.S., and
Davis, T.P., Alterations in Blood-brain Barrier ICAM-1
Expression and Brain Microglial Activation Following
l-carrageen-induced
Inflammatory Pain, Am J Physiol (Heart Circ Physiol),
290: H732-H740, (2006). |
| Witt,
K.A., Mark, K.S., Huber, J.D., and Davis, T.P.,
Hypoxia
Inducible Factor and Nuclear Factor Kappa-b
Activation in Blood-Brain Barrier Endothelium Under Hypoxic/Reoxygenation
Stress, J Neurochem, 92: 203-214, (2005). |
| Brown,
R.C., Mark, K.S., Egleton, R.D., and Davis, T.P.,
Protection
Against Hypoxia-Induced Blood-Brain Barrier Disruption: Changes
in Intracellular Calcium, Am J Physiol (Cell
Physiol), 286 (5): C1045-52 (2004). |
| Mark,
K.S.,
Burroughs, A.R., Brown, R.C., Huber, J.D., and Davis, T.P.,
Nitric Oxide Mediated Changes in Permeability During Hypoxia and Reoxygenation, Am J Physiol (Heart Circ Physiol), 286:
H174-H180, (2004). |
| Witt,
K.A., Mark, K.S., Hom, S., and Davis, T.P.,
Effects Of
Hypoxia-Reoxygenation On Rat Blood-Brain Barrier Permeability
And Tight Junctional Protein Expression, Am J
Physiol (Heart Circ Physiol), 285: H2820 - 2831 (2003). |
| Brown,
R.C., Mark, K.S., Egleton, R.D., Huber, J.D., Burroughs,
A.R., and Davis, T.P., Protection Against Hypoxia-induced
Increase in Blood-Brain Barrier Permeability: Role of Tight
Junction Proteins and NFkB,
J Cell Science, 16 (pt 4): 693-700 (2003). |
| Mark,
K.S.
and Davis, T.P., , Am J Physiol
(Heart Circ Physiol), 282 (4): H1485-1494 (2002). |
| Mark,
K.S.,
Trickler, W.J., and Miller, D.W.,
Tumor Necrosis Factor-a
Induces Cycyclooxygenase-2 Expression and Prostaglandin Release
in Brain Microvessel Endothelial Cells, JPET, 297 (3):
1051-1058 (2001). |
| Huber,
J.D., Witt, K.A., Hom, S., Egleton, R.D., Mark, K.S., and
T.P. Davis, Inflammatory Pain Alters Blood-brain Barrier
Permeability and Tight Junctional Protein Expression, Am J
Physiol (Heart Circ Physiol), 280 (3): H1241-H1248 (2001). |
| Mark,
K.S.
and Miller, D.W., Increased Permeability of Primary Cultured
Brain Microvessel Endothelial Cell Monolayers Following TNF-a
Exposure, Life Sci, 64 (21): 1941-1953 (1999). |
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