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Current Research:

My laboratory studies normal and diseased craniofacial muscles, focusing on the extraocular muscles, and optic nerve injury and regeneration. My research has two main areas of focus.

Duchenne muscular dystrophy (DMD) is a devastating disease for which there is currently no effective treatment. The clinical sparing of the EOM in DMD patients is an enigma. We are examining several aspects of the EOM that may play a role in this sparing. It may be that the myogenic precursor cell population in the EOM is different or more diverse than in limb skeletal muscles. We are studying the myogenic precursor population in the EOM to determine if these muscles contain more “multipotent precursor cells” than seen in limb skeletal muscles. It appears that there may be a unique population within the EOM that is both more “primitive” and also better able to survive injury than similar populations derived from limb skeletal muscle. In turn this leads to us to ask whether the myogenic precursor cells from EOM may be a better alternative for myoblast transfer for DMD than those cell derived from limb, which have been done with extremely limited success. In addition, EOM do not suffer changes seen in aging of limb skeletal muscle. The main hypothesis we are testing is that the myogenic precursor cell populations in the extraocular muscles are intrinsically different from those in limb muscle, and that these intrinsic differences may be, at least in part, responsible for the sparing of EOM in Duchenne muscular dystrophy and aging.

Ischemic optic neuropathy (ION) is a devastating ocular disease caused by disruption in arterial blood supply to the optic nerve head. This loss of oxygenation by interruption of the blood supply results in ischemic injury to the retinal ganglion cells and their axons, resulting in loss of visual field and decrease of visual acuity. The incidence of this disease is 2.3-10.3 per 100,000 in the US. The risk for development of ION on the fellow eye in affected patients is estimated to be 15-25%. There is no effective treatment for this condition. In addition, while the etiology of glaucoma is not well understood, there is increasing evidence that blood flow at the optic nerve head plays a role in development and progression of disease pathophysiology. Risk of disease is increased when ophthalmic artery flow rates decrease. We use a rodent model shown to produce a transient ischemia in the retina and optic nerve. These injuries result in significant but transient oxygen loss of the optic nerve, and by 5 months over half of the optic axons degenerate. Intranasal drug application produces almost instant drug delivery to brain structures with little evidence of systemic spread. It is non-invasive, easy to perform, and was effective for the treatment of an animal model of stroke. We are examining if intranasal administration of insulin growth factor-1 and/or erythropoietin can rescue retinal ganglion cells and optic axons that have been exposed to transient ischemia.