Data associated with

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Data associated with "Retinal oxidative stress at the onset of diabetes determined by synchrotron FTIR widefield imaging: towards diabetes pathogenesis" and "Temporal diabetes-induced biochemical changes in distinctive layers of mouse retina"

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Description

This data folder is associated with the following publications in the Analyst journal and the Scientific Reports:

1. Retinal oxidative stress at the onset of diabetes determined by synchrotron FTIR widefield imaging: towards diabetes pathogenesis. (E. Aboualizadeh, et al. February 2017)

DOI: 10.1039/C6AN02603F

Citation: Aboualizadeh, E., Ranji, M., Sorenson, C. M., Sepehr, R., Sheibani, N., & Hirschmugl, C. J. (2017). Retinal oxidative stress at the onset of diabetes determined by synchrotron FTIR widefield imaging: towards diabetes pathogenesis. Analyst, 142(7), 1061-1072.

AND

2. Temporal diabetes-induced biochemical changes in distinctive layers of mouse retina. (E. Aboualizadeh, et al. January 2018)

DOI: 10.1038/s41598-018-19425-8

Citation: Aboualizadeh, E., Sorenson, C. M., Schofield, A. J., Unger, M., Sheibani, N., & Hirschmugl, C. J. (2018). Temporal diabetes-induced biochemical changes in distinctive layers of mouse retina. Scientific reports, 8(1), 1096.

Abstract of paper 1:

Diabetic retinopathy is a microvascular complication of diabetes that can lead to blindness. In the present study, we aimed to determine the nature of diabetes-induced, highly localized biochemical changes in the neuroretina at the onset of diabetes. High-resolution synchrotron Fourier transform infrared (s-FTIR) wide field microscopy coupled with multivariate analysis (PCA–LDA) was employed to identify biomarkers of diabetic retinopathy with spatial resolution at the cellular level. We compared the retinal tissue prepared from 6-week-old Ins2Akita/+ heterozygous (Akita/+, N = 6; a model of diabetes) male mice with the wild-type (control, N = 6) mice. Male Akita/+ mice become diabetic at 4-weeks of age. Significant differences (P < 0.001) in the presence of biomarkers associated with diabetes and segregation of spectra were achieved. Differentiating IR bands attributed to nucleic acids (964, 1051, 1087, 1226 and 1710 cm−1), proteins (1662 and 1608 cm−1) and fatty acids (2854, 2923, 2956 and 3012 cm−1) were observed between the Akita/+ and the WT samples. A comparison between distinctive layers of the retina, namely the photoreceptor retinal layer (PRL), outer plexiform layer (OPL), inner nucleus layer (INL) and inner plexiform layer (IPL) suggested that the photoreceptor layer is the most susceptible layer to oxidative stress in short-term diabetes. Spatially-resolved chemical images indicated heterogeneities and oxidative-stress induced alterations in the diabetic retina tissue morphology compared with the WT retina. In this study, the spectral biomarkers and the spatial biochemical alterations in the diabetic retina and in specific layers were identified for the first time. We believe that the conclusions drawn from these studies will help to bridge the gap in our understanding of the molecular and cellular mechanisms that contribute to the pathobiology of diabetic retinopathy.

Abstract of paper 2:

"To discover the mechanisms underlying the progression of diabetic retinopathy (DR), a more comprehensive understanding of the biomolecular processes in individual retinal cells subjected to hyperglycemia is required. Despite extensive studies, the changes in the biochemistry of retinal layers during the development of DR are not well known. In this study, we aimed to determine a more detailed understanding of the natural history of DR in Akita/+ (type 1 diabetes model) male mice with different duration of diabetes. Employing label-free spatially resolved Fourier transform infrared (FT-IR) chemical imaging engaged with multivariate analysis enabled us to identify temporal-dependent reproducible biomarkers of the individual retinal layers from mice with 6 weeks,12 weeks, 6 months, and 10 months of age. We report, for the first time, the nature of the biochemical alterations over time in the biochemistry of distinctive retinal layers namely photoreceptor retinal layer (PRL), inner nuclear layer (INL), and plexiform layers (OPL, IPL). Moreover, we present the molecular factors associated with the changes in the protein structure and cellular lipids of retinal layers induced by different duration of diabetes. Our paradigm provides a new conceptual framework for a better understanding of the temporal cellular changes underlying the progression of DR."

The data folder contains all the data that has been included in this publication. The data files are stored as OPUS files and DPT files. There are files based on the age of mice ranging from 6-weeks to 10 months old diabetic and wild-type mice. The bright field images are also stored in the data folder. The tables contain FT-IR spectra from diabetic and control retina at different duration of diabetes, where each column is one spectrum and the first column in each table shows the wavenumber range. The processed data in this folder are the processed OPUS data in Irydis software and they are saved as PXP file. We included all these data in these 2 mentioned publications. Please feel free to contact either Dr. Carol Hirschmugl (cjhirsch@uwm.edu) or Dr. Ebrahim Aboualizadeh (eabouali@ur.rochester.edu) for any questions or concerns regarding this data. This second article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder.

Publication Date

2-2017

Disciplines

Physics

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