Pericyte Loss in the Diabetic Retina

2009 ◽  
pp. 61-78 ◽  
Author(s):  
Frederick Pfister ◽  
Jihong Lin ◽  
Hans-Peter Hammes
Keyword(s):  
Diabetic Retina ◽  
Pericyte Loss

Pericyte Loss in the Diabetic Retina

2008 ◽  
pp. 245-264
Author(s):  
Frederick Pfister ◽  
Yuxi Feng ◽  
Hans-Peter Hammes
Keyword(s):  
Diabetic Retina ◽  
Pericyte Loss

scholarly journals Reduced Levels of Drp1 Protect against Development of Retinal Vascular Lesions in Diabetic Retinopathy

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1379
Author(s):  
Dongjoon Kim ◽  
Hiromi Sesaki ◽  
Sayon Roy
Keyword(s):  
Diabetic Retinopathy ◽  
Cell Loss ◽  
Vascular Lesions ◽  
Protective Effects ◽  
Diabetic Mice ◽  
Wild Type ◽  
Apoptotic Genes ◽  
Retinal Vascular Lesions ◽  
Acellular Capillaries ◽  
Pericyte Loss

High glucose (HG)-induced Drp1 overexpression contributes to mitochondrial dysfunction and promotes apoptosis in retinal endothelial cells. However, it is unknown whether inhibiting Drp1 overexpression protects against the development of retinal vascular cell loss in diabetes. To investigate whether reduced Drp1 level is protective against diabetes-induced retinal vascular lesions, four groups of mice: wild type (WT) control mice, streptozotocin (STZ)-induced diabetic mice, Drp1+/− mice, and STZ-induced diabetic Drp1+/− mice were examined after 16 weeks of diabetes. Western Blot analysis indicated a significant increase in Drp1 expression in the diabetic retinas compared to those of WT mice; retinas of diabetic Drp1+/− mice showed reduced Drp1 level compared to those of diabetic mice. A significant increase in the number of acellular capillaries (AC) and pericyte loss (PL) was observed in the retinas of diabetic mice compared to those of the WT control mice. Importantly, a significant decrease in the number of AC and PL was observed in retinas of diabetic Drp1+/− mice compared to those of diabetic mice concomitant with increased expression of pro-apoptotic genes, Bax, cleaved PARP, and increased cleaved caspase-3 activity. Preventing diabetes-induced Drp1 overexpression may have protective effects against the development of vascular lesions, characteristic of diabetic retinopathy.

scholarly journals Analysis of Lipid Peroxidation by UPLC-MS/MS and Retinoprotective Effects of the Natural Polyphenol Pterostilbene

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 168
Author(s):  
Isabel Torres-Cuevas ◽  
Iván Millán ◽  
Miguel Asensi ◽  
Máximo Vento ◽  
Camille Oger ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Diabetic Retinopathy ◽  
Redox Homeostasis ◽  
Ultra Performance Liquid Chromatography ◽  
Protective Effects ◽  
Diabetic Retina ◽  
Key Factor ◽  
Adrenic Acid ◽  
Diabetic Rabbits ◽  
High Level

The loss of redox homeostasis induced by hyperglycemia is an early sign and key factor in the development of diabetic retinopathy. Due to the high level of long-chain polyunsaturated fatty acids, diabetic retina is highly susceptible to lipid peroxidation, source of pathophysiological alterations in diabetic retinopathy. Previous studies have shown that pterostilbene, a natural antioxidant polyphenol, is an effective therapy against diabetic retinopathy development, although its protective effects on lipid peroxidation are not well known. Plasma, urine and retinas from diabetic rabbits, control and diabetic rabbits treated daily with pterostilbene were analyzed. Lipid peroxidation was evaluated through the determination of derivatives from arachidonic, adrenic and docosahexaenoic acids by ultra-performance liquid chromatography coupled with tandem mass spectrometry. Diabetes increased lipid peroxidation in retina, plasma and urine samples and pterostilbene treatment restored control values, showing its ability to prevent early and main alterations in the development of diabetic retinopathy. Through our study, we are able to propose the use of a derivative of adrenic acid, 17(RS)-10-epi-SC-Δ15-11-dihomo-IsoF, for the first time, as a suitable biomarker of diabetic retinopathy in plasmas or urine.

scholarly journals Mild traumatic brain injury induces microvascular injury and accelerates Alzheimer-like pathogenesis in mice

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Yingxi Wu ◽  
Haijian Wu ◽  
Jianxiong Zeng ◽  
Brock Pluimer ◽  
Shirley Dong ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Vascular Connection ◽  
Microvascular Injury ◽  
Amyloid Pathology ◽  
Blood Flow Reduction ◽  
5Xfad Mouse ◽  
Time Courses ◽  
5Xfad Mice ◽  
Pericyte Loss

Abstract Introduction Traumatic brain injury (TBI) is considered as the most robust environmental risk factor for Alzheimer’s disease (AD). Besides direct neuronal injury and neuroinflammation, vascular impairment is also a hallmark event of the pathological cascade after TBI. However, the vascular connection between TBI and subsequent AD pathogenesis remains underexplored. Methods In a closed-head mild TBI (mTBI) model in mice with controlled cortical impact, we examined the time courses of microvascular injury, blood–brain barrier (BBB) dysfunction, gliosis and motor function impairment in wild type C57BL/6 mice. We also evaluated the BBB integrity, amyloid pathology as well as cognitive functions after mTBI in the 5xFAD mouse model of AD. Results mTBI induced microvascular injury with BBB breakdown, pericyte loss, basement membrane alteration and cerebral blood flow reduction in mice, in which BBB breakdown preceded gliosis. More importantly, mTBI accelerated BBB leakage, amyloid pathology and cognitive impairment in the 5xFAD mice. Discussion Our data demonstrated that microvascular injury plays a key role in the pathogenesis of AD after mTBI. Therefore, restoring vascular functions might be beneficial for patients with mTBI, and potentially reduce the risk of developing AD.

Evidence for a dysfunction and disease-promoting role of the circadian clock in the diabetic retina

2021 ◽  
Vol 211 ◽  
pp. 108751
Author(s):  
Patrick Vancura ◽  
Laura Oebel ◽  
Simon Spohn ◽  
Ute Frederiksen ◽  
Kristina Schäfer ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Diabetic Retina

scholarly journals Angiotensin II Type 1 Receptor Signaling Contributes to Synaptophysin Degradation and Neuronal Dysfunction in the Diabetic Retina

Diabetes ◽  
2008 ◽  
Vol 57 (8) ◽  
pp. 2191-2198 ◽  
Author(s):  
T. Kurihara ◽  
Y. Ozawa ◽  
N. Nagai ◽  
K. Shinoda ◽  
K. Noda ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Neuronal Dysfunction ◽  
Receptor Signaling ◽  
Diabetic Retina

scholarly journals Prolonged systemic hyperglycemia does not cause pericyte loss and permeability at the mouse blood-brain barrier

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Maarja Andaloussi Mäe ◽  
Tian Li ◽  
Giacomo Bertuzzi ◽  
Elisabeth Raschperger ◽  
Michael Vanlandewijck ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Mouse Blood ◽  
Blood Brain ◽  
Pericyte Loss

Fractal analysis of region-based vascular change in the normal and non-proliferative diabetic retina

2002 ◽  
Vol 24 (4) ◽  
pp. 274-280 ◽  
Author(s):  
Arpenik Avakian ◽  
Robert E. Kalina ◽  
E. Helene Sage ◽  
Avni H. Rambhia ◽  
Katherine E. Elliott ◽  
...  
Keyword(s):  
Fractal Analysis ◽  
Vascular Change ◽  
Diabetic Retina

scholarly journals Tribbles Homolog 3 Mediates the Development and Progression of Diabetic Retinopathy

2021 ◽  
Author(s):  
Priyamvada M. Pitale ◽  
Irina V. Saltykova ◽  
Yvonne Adu-Agyeiwaah ◽  
Sergio Li Calzi ◽  
Takashi Satoh ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Functional Restoration ◽  
Dramatic Reduction ◽  
Vegf Expression ◽  
Inflammatory Gene Expression ◽  
Hypoxic Conditions ◽  
Molecular Events ◽  
Glucose Flux ◽  
Pericyte Loss

The current understanding of molecular pathogenesis of diabetic retinopathy does not provide a mechanistic link between early molecular changes and the subsequent progression of the disease. In this study, we found that human diabetic retinas overexpressed TRIB3 and investigated the role of TRIB3 in diabetic retinal pathobiology in mice. We discovered that TRIB3 controlled major molecular events in early diabetic retinas via HIF1α-mediated regulation of retinal glucose flux, reprograming cellular metabolism, and governing inflammatory gene expression. These early molecular events further defined the development of neurovascular deficit observed in mice with diabetic retinopathy. TRIB3 ablation in STZ-induced mouse model led to significant RGC survival and functional restoration accompanied by a dramatic reduction in pericyte loss and acellular capillary formation. Under hypoxic conditions, TRIB3 contributed to advanced proliferative stages by significant upregulation of GFAP and VEGF expression, thus controlling gliosis and aberrant vascularization in OIR mouse retinas. Overall, our data reveal that TRIB3 is a master regulator of diabetic retinal pathophysiology that may accelerate the onset and progression of diabetic retinopathy to proliferative stages in humans and present TRIB3 as a potentially novel therapeutic target for diabetic retinopathy.

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