cell apoptosis. Chen (1993) has proved that the blue light with a fatal dose could inhibit the cytochrome oxidase irreversibly, and then lead to redistribution of chlorine and potassium in the inner and outer segments, damage to the mitochondria in the inner segments, edema in the inner and outer segments, and progressive degeneration of photoreceptor cells. So the dysfunction of cytochrome oxidase is the fuse to the cell apoptosis.

Based on above factors, the mechanism of LED treatment for light damage was speculated like that: Absorbing the NIL, the cytochrome c oxidase oxidizes its substrate cytochrome c and reduces the free radical oxygen to water and produces substantial deoxidize substance and ATP for the activity of the Na/K-ATPase to retain the physiological ions’ distribution, balance the intracellular osmotic pressure and prevent the cellular edema and apoptosis.

In the past decade, mitochondrial genomic instability was investigated as an important factor in mitochondrial impairment resulting in age-related changes and age-related pathology. Focused on the relationship between mitochondria and AMD, those researches found that the acquired mitochondrial (mt) DNA deletion (Barron et al. 2001) or damage (Wang et al. 2008) and mtDNA control region SNPs (Udar et al. 2009) increased with aging in the retina, particularly in the foveal region, which was consistent with the decline in mitochondrial function with age. Genomic alterations and the consequent events including altered mitochondrial translation, import of nuclear-encoded proteins, and ATP synthase activity would be the susceptibility factors underlying the development of AMD (Nordgaard et al. 2008). Since the LED treatment could enhance the mitochondrial function by stimulating the cytochrome oxidase to resist light damage, it probably could prevent or delay the age-related macular degeneration as a mitochondria-related disease.

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Chapter 43

BDNF Improves the Efficacy ERG Amplitude Maintenance by Transplantation of Retinal Stem Cells in RCS Rats

Chunyu Tian, Chuan Chuang Weng, and Zheng Qin Yin

Abstract The aim of this study was to evaluate the efficacy of subretinal transplantation of rat retinal stem cell when combined with Brain-derived neurotrophic factor (BDNF) in a rat model of retinal degeneration – Royal College of Surgeons (RCS) rats. Retinal stem cells were derived from embryonic day 17 Long-Evans rats and pre-labeled with fluorescence pigment-DiI prior to transplant procedures. RCS rats received injections of retinal stem cells, stem cells+BDNF, phosphate buffered saline or BNDF alone (n = 3 eyes for each procedure). At 1, 2 and 3 months after transplantation, the electroretinogram (ERG) was assessed and the outer nuclear layer thickness measured. The eyes receiving retinal stem cell and stem cell+BDNF transplants showed better photoreceptor maintenance than the other groups (P < 0.01) at all time points. One month after retina transplantation, the amplitudes of rod-ERG and Max-ERG b waves were significantly higher the eyes with stem cells+BDNF (P < 0.01), however, this difference was not seen at two and three months post transplantation. BDNF treatment alone group (without transplanted cells) had no effect when compared to buffer injections. The present results indicate that BDNF can enhance the short-term efficacy of the retinal stem cell transplantation in treating retinal degenerative disease.

43.1 Introduction

Brain-derived neurotrophic factor (BDNF) has been shown to regulate many aspects of neuronal development in the central neural system, including survival, axonal and dendritic growth and synapse formation. In the retina, BDNF can support the survival and maintenance of the dendritic morphology of retinal ganglion cells

Z.Q. Yin (B)

Southwest Hospital, Southwest Eye Hospital, Third Military Medical University, Chongqing 400038, People’s Republic of China

e-mail: qinzyin@yahoo.com.cn

The authors Chunyu Tian and Zheng Qin Yin contributed equally to this work.

Medicine and Biology 664, DOI 10.1007/978-1-4419-1399-9_43,C Springer Science+Business Media, LLC 2010