Responses of retinal and brain microvasculature to streptozotocin induced diabetes revealed by global expression profiling.
- Publisher:
- SAGE PUBLICATIONS LTD
- Publication Type:
- Journal Article
- Citation:
- Diab Vasc Dis Res, 2023, 20, (1), pp. 14791641221147533
- Issue Date:
- 2023
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Li, Y | |
dc.contributor.author |
Faiz, A https://orcid.org/0000-0003-1740-3538 |
|
dc.contributor.author | Moshage, H | |
dc.contributor.author | Schilling, L | |
dc.contributor.author | Kamps, JA | |
dc.date.accessioned | 2024-01-16T06:15:18Z | |
dc.date.available | 2024-01-16T06:15:18Z | |
dc.date.issued | 2023 | |
dc.identifier.citation | Diab Vasc Dis Res, 2023, 20, (1), pp. 14791641221147533 | |
dc.identifier.issn | 1479-1641 | |
dc.identifier.issn | 1752-8984 | |
dc.identifier.uri | http://hdl.handle.net/10453/174604 | |
dc.description.abstract | This study aims to determine the effects of diabetes in the retinal and brain microvasculature through gene expression profiling. Twelve male Wistar rats were randomly divided into two groups: streptozotocin-induced diabetic rats and time-matched nondiabetic rats. The retinal microvessels (RMVs) and brain microvessels (BMVs) were mechanically isolated from individual rats. Differentially expressed genes (DEGs) in diabetic and nondiabetic microvessels were identified by cDNA microarrays analysis. In RMVs, we identified 43 DEGs, of which 20 were upregulated while 23 were downregulated by diabetes. In BMVs, 35 genes DEGs were identified, of which 22 were upregulated and 13 were downregulated by diabetes. Altered expression of the Nars, Gars, Mars, Iars, Yars, Bcl2, Nqo1, NR4A3, Gpd1, Stc1, Tsc22d3, Tnfrsf21 mRNA as observed in the microarray analyses, was confirmed by quantitative RT-PCR. The aminoacyl-tRNA synthetases (aaRSs) pathway in RMVs was significantly overrepresented as compared to BMVs. Our study demonstrates for the first time that in the brain microvasculature multiple compensatory mechanisms exists, serving to protect brain tissue from diabetic insults, whereas these mechanisms are not activated in the retinal microvasculature. This provides new insights as to why brain microvasculature is less susceptible to diabetes. | |
dc.format | ||
dc.language | eng | |
dc.publisher | SAGE PUBLICATIONS LTD | |
dc.relation.ispartof | Diab Vasc Dis Res | |
dc.relation.isbasedon | 10.1177/14791641221147533 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 1103 Clinical Sciences, 1115 Pharmacology and Pharmaceutical Sciences, 1116 Medical Physiology | |
dc.subject.classification | Endocrinology & Metabolism | |
dc.subject.classification | 3202 Clinical sciences | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Male | |
dc.subject.mesh | Rats | |
dc.subject.mesh | Brain | |
dc.subject.mesh | Diabetes Mellitus, Experimental | |
dc.subject.mesh | Diabetic Retinopathy | |
dc.subject.mesh | Microvessels | |
dc.subject.mesh | Rats, Wistar | |
dc.subject.mesh | Retinal Vessels | |
dc.subject.mesh | Streptozocin | |
dc.subject.mesh | Retinal Vessels | |
dc.subject.mesh | Brain | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Rats | |
dc.subject.mesh | Rats, Wistar | |
dc.subject.mesh | Diabetic Retinopathy | |
dc.subject.mesh | Diabetes Mellitus, Experimental | |
dc.subject.mesh | Streptozocin | |
dc.subject.mesh | Male | |
dc.subject.mesh | Microvessels | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Male | |
dc.subject.mesh | Rats | |
dc.subject.mesh | Brain | |
dc.subject.mesh | Diabetes Mellitus, Experimental | |
dc.subject.mesh | Diabetic Retinopathy | |
dc.subject.mesh | Microvessels | |
dc.subject.mesh | Rats, Wistar | |
dc.subject.mesh | Retinal Vessels | |
dc.subject.mesh | Streptozocin | |
dc.title | Responses of retinal and brain microvasculature to streptozotocin induced diabetes revealed by global expression profiling. | |
dc.type | Journal Article | |
utslib.citation.volume | 20 | |
utslib.location.activity | England | |
utslib.for | 1103 Clinical Sciences | |
utslib.for | 1115 Pharmacology and Pharmaceutical Sciences | |
utslib.for | 1116 Medical Physiology | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | /University of Technology Sydney/Centre for Health Technologies (CHT) | |
pubs.organisational-group | /University of Technology Sydney/Strength - CFI - Centre for Inflammation | |
utslib.copyright.status | open_access | * |
dc.date.updated | 2024-01-16T06:15:14Z | |
pubs.issue | 1 | |
pubs.publication-status | Published | |
pubs.volume | 20 | |
utslib.citation.issue | 1 |
Abstract:
This study aims to determine the effects of diabetes in the retinal and brain microvasculature through gene expression profiling. Twelve male Wistar rats were randomly divided into two groups: streptozotocin-induced diabetic rats and time-matched nondiabetic rats. The retinal microvessels (RMVs) and brain microvessels (BMVs) were mechanically isolated from individual rats. Differentially expressed genes (DEGs) in diabetic and nondiabetic microvessels were identified by cDNA microarrays analysis. In RMVs, we identified 43 DEGs, of which 20 were upregulated while 23 were downregulated by diabetes. In BMVs, 35 genes DEGs were identified, of which 22 were upregulated and 13 were downregulated by diabetes. Altered expression of the Nars, Gars, Mars, Iars, Yars, Bcl2, Nqo1, NR4A3, Gpd1, Stc1, Tsc22d3, Tnfrsf21 mRNA as observed in the microarray analyses, was confirmed by quantitative RT-PCR. The aminoacyl-tRNA synthetases (aaRSs) pathway in RMVs was significantly overrepresented as compared to BMVs. Our study demonstrates for the first time that in the brain microvasculature multiple compensatory mechanisms exists, serving to protect brain tissue from diabetic insults, whereas these mechanisms are not activated in the retinal microvasculature. This provides new insights as to why brain microvasculature is less susceptible to diabetes.
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