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Mitoscriptome analysis to understand the pathogenesis of Diabetic Retinopathy using tissue microarray

ABSTRACT: Diabetic Retinopathy (DR) is a progressive disease affecting the structure and cellular composition of the microvasculature. Several factors like genetic, environmental and biochemical are involved in the development of DR. However, the inheritance pattern of this disease is multi factorial resulting from the interaction of one or more genes but the exact mechanism is not completely understood. Over the decade there has been alot of molecular genetics work done in nuclear genome for DR in different ethnic groups and identified several candidate genes involved in disease pathogenesis but the role of these genes in the development of disease is not yet clearly understood. Recently there are very few reports in determining the role of mitochondria in the pathogenesis of DR but no such studies are reported so far in India. The high relevance of mitochondria in the maintenance of cellular structure and function places mitoscriptome analysis as an important piece of the puzzle in understanding the pathogenesis of DR. Therefore we would like to focus on entire Human Mitoscriptome gene expression profile in relation to DR which could help us to identify new biomarker in health and disease condition.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53257 | GEO | 2015/04/02

SECONDARY ACCESSION(S): PRJNA231356

REPOSITORIES: GEO

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Project description:Functional decline and structural alterations of the brain microvasculature are associated with cognitive impairment and development of dementias such as Alzheimer’s disease during aging. Although mechanisms of leading to microvascular changes during aging are not clear, the loss of mitochondria and reduced efficiency of remaining mitochondria appear to play a major role. While pharmacological agents which target mitochondria such as SS-31 have been shown to be effective in beneficial during aging and diseases, the full extent on mitochondrial- and non-mitochondrial proteins in the brain microvasculature has not been examined. We tested the hypothesis that attenuation of aging-associated changes in the brain microvascular proteome via targeting mitochondria represents a therapeutic option in the aging brain. We used male, aged (>18 months) C57Bl6/J mice treated with a mitochondria-targeted tetrapeptide, SS-31 or vehicle saline. Baseline cerebral blood flow (CBF) was determined using laser speckle imaging during the two-week treatment period. Then, isolated cortical microvessels (MVs), composed of end arterioles, capillaries, and venules, were used for Orbitrap Eclipse Tribrid mass spectrometry. Baseline CBF was similar between the groups, whereas bioinformatic analysis revealed substantial differences in protein abundance of cortical MVs between SS-31 and vehicle groups. Specifically, we identified 6,266 proteins in our data set from which 12% were mitochondrial or mitochondria associated. 107 of these proteins were significantly differentially expressed between the treatment and vehicle groups, and were associated with the oxidative phosphorylation, metabolism, antioxidant defense system, or mitochondrial dynamics. Administration of SS-31 also affected many non-mitochondrial proteins. Our findings suggest that mitochondria in the microvasculature represent a therapeutic target in the aging brain, and widespread changes in the proteome may underlie the mechanisms of rejuvenating actions of SS-31 in the aging phenotype.

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Mitoscriptome analysis to understand the pathogenesis of Diabetic Retinopathy using tissue microarray

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