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Gladys Ko

Associate Professor

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Phone: (979) 845-1797

Mailstop: 4458

Department: VIBS

Photo of Ko, Gladys

Education

  • Ph.D. Neuroscience in Biomedical Sciences, Kent State U. affiliated w/ N.E. Ohio U Col. Med. 1996
  • M.S. Anatomical Sciences, National Yang-Ming Medical College, Taiwan 1991
  • B.S. Biology, National Chang-Kung University, Taiwan 1989

Research

  • Cell Biology
  • Toxicology
  • Neuroscience

Interdisciplinary Activities

  • Neuroscience
  • Toxicology

Scholarly Interests

Diabetic retinopathy (DR) is the leading cause of blindness among the American working population with a projected prevalence of more than 11 million patients by 2030 in the US. Once the disease starts, it cannot be stopped simply by controlling the blood glucose (glycemic) levels strictly through diets and exercise. While DR is a disorder with two major problems, the vascular complications and the neural retina degeneration, the current treatments mainly target the vascular complications without treating the neural retina. The first-line gold standard treatments for DR is regular injections with anti-VEGF agents into the eyes. However, roughly 30% of DR patients do not respond well to these treatments. Often these non-responders are identified months after the treatments have started. Therefore, discovering new ways to treat or prevent DR are a major health issue, which is also the research focus in our laboratory. Interestingly, diabetic patients with retinitis pigmentosa, a congenital blindness with degenerated retinal photoreceptors, rarely develop DR. This suggests that the neural retina, especially the photoreceptors contribute to the development of DR. Our laboratory has been investigated the molecular mechanisms that regulate photoreceptor physiology over 11 years. More specifically, we have been investigating how metabolism and energy expenditure of photoreceptors are regulated throughout the course of 24 hours. We employ different techniques, including electroretinogram (ERG) recordings, fundus angiography, electrophysiological patch-clamp recordings, various biochemical and molecular assays, and cellular imaging, and now focus on how early diabetic conditions trigger changes in photoreceptors that might lead to DR. In addition, we have recently discovered a new bioactive peptide, peptide Lv. This peptide not only regulates photoreceptor physiology, it also modulates cardiovascular functions. We now further elucidate the molecular mechanisms of peptide Lv's bioactivities, as well as its other unknown function.

Publications

Phosphatidylinositol 3 kinase-Akt signaling serves as a circadian output in the retina.
Ko ML, Jian K, Shi L, Ko GY
J Neurochem. 2009 Mar; 108(6):1607-20.
Somatostatin peptides produce multiple effects on gating properties of native cone photoreceptor cGMP-gated channels that depend on circadian phase and previous illumination.
Chen SK, Ko GY, Dryer SE
J Neurosci. 2007 Nov; 27(45):12168-75.
Tyrosine phosphorylation of cGMP-gated ion channels is under circadian control in chick retina photoreceptors.
Chae KS, Ko GY, Dryer SE
Invest Ophthalmol Vis Sci. 2007 Feb; 48(2):901-6.
Circadian and cAMP-dependent modulation of retinal cone cGMP-gated channels does not require protein synthesis or calcium influx through L-type channels.
Ko GY, Ko M, Dryer SE
Brain Res. 2004 Sep; 1021(2):277-80.
Circadian regulation of cGMP-gated channels of vertebrate cone photoreceptors: role of cAMP and Ras.
Ko GY, Ko ML, Dryer SE
J Neurosci. 2004 Feb; 24(6):1296-304.
Circadian phase-dependent modulation of cGMP-gated channels of cone photoreceptors by dopamine and D2 agonist.
Ko GY, Ko ML, Dryer SE
J Neurosci. 2003 Apr; 23(8):3145-53.
Peptide Lv augments L-type voltage-gated calcium channels through vascular endothelial growth factor receptor 2 (VEGFR2) signaling.
Shi L, Ko S, Ko ML, Kim AJ, Ko GY
Biochim Biophys Acta. 1853(5):1154-64.
High-Fat Diet-Induced Retinal Dysfunction.
Chang RC, Shi L, Huang CC, Kim AJ, Ko ML, Zhou B, Ko GY
Invest Ophthalmol Vis Sci. 56(4):2367-80.


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