Richard L. Benton, Ph.D.
Dr. Benton's research interests.
Assistant ProfessorPhone: 502-852-1333
Fax: 502-852-6228
My general research interests focus on the development of novel therapeutic strategies for the treatment of spinal cord injury (SCI). Working in collaboration with the faculty in the Kentucky Spinal Cord Injury Research Center (KSCIRC, www.kscirc.org), we continue to develop stem cell-based therapies facilitating neuronal replacement, spinal regeneration, and ex vivo gene therapy. More specifically, our recent efforts have been focused on better understanding vascular mechanisms of spinal cord injury.
Following traumatic SCI, the delicate microvascular network of the spinal cord is damaged and exhibits hyperacute pathology including petichial hemorrhage, leakiness, and endothelial cell death. Interestingly, the spinal microvasculature undergoes a second phase of dysfunction, which begins 3-7 days following the initial traumatic insult. Little is known about this second wave of microvascular pathology but it appears to be largely regulated by various cellular and molecular secondary injury cascades and ultimately results in further vascular destabilization and dysfunction, which contributes to the secondary loss of spinal tissue.
Thus,
we are actively advancing research focused on characterizing the
anatomy and physiology of spinal vessels in the evolving injury
epicenter, developing intravital tracing techniques to identify both
normal and pathologic spinal microvessels, and identify novel molecular
regulators of vascular pathology following SCI. Our ultimate goal is
the development of vascular-focused therapeutic strategies, both stem
cell-based and small molecule-centric, which will both stabilize
degenerating microvessels and promote the growth of functional
microvascular networks. We feel this is a promising area of research
that will one day lead to functional recovery following SCI.
Real-time video analysis of CNS angiogenesis in-vitro
Representative Publications:
Benton R.L.,
Ross C.D., and Miller KE. (2000) Spinal taurine levels are increased 7
and 30 days following methylprednisolone treatment of spinal cord
injury in rats. Brain Res. 893: 292-300.
Cao Q., Benton R.L., and Whittemore S.R. (2002) Stem cell repair of CNS injury. J. Neurosci. Res. 68(5): 501-510.
Benton R.L. and Whittemore SR. (2003) VEGF165 therapy exacerbates secondary damage following spinal cord injury. Neurochem. Res. 28(11): 1693-703.
Benton R.L.,
Woock J.P., Gozal E., Hetman M., and Whittemore S.R. (2005) Intraspinal
application of endothelin results in focal ischemic injury of spinal
gray matter and restricts the differentiation of engrafted neural stem
cells. Neurochem. Res. 30(7): 1-15.
Enzmann G.U.*, Benton R.L.*,
Woock J.P., Howard R.M., Tsoulfas P., and Whittemore S.R. (2005)
Consequences of noggin expression by neural stem, glial, and neuronal
precursor cells engrafted into the injured spinal cord. Exp. Neurol. 195:293-304.
Benton R.L., Enzmann G.U., and Whittemore S.R. (2006) Stem cell grafting and spinal cord injury. Chapter 16 in Synaptic Plasticity: basic mechanisms to clinical applications. M. Baudry ed. (in press).
Enzmann G.U., Benton R.L.,
Talbott J.F., Cao Q.L., and Whittemore S.R. (2006) Cellular, molecular,
and Functional considerations of stem cell transplantation therapy in
spinal cord repair. J. Neurotrauma (in press).
Lecturer In: Medical Microanatomy and Development
Professional Affiliations:
Society for Neuroscience (SFN)
International Brain Research Organization (IBRO)
American Association of Anatomists (AAA)
North American Vascular Biology Organization (NAVBO)
International Society on Oxygen Transport to Tissue (ISOTT)

