TY - JOUR
T1 - Resistance to retinopathy development in obese, diabetic and hypertensive ZSF1 rats
T2 - an exciting model to identify protective genes
AU - Caolo, Vincenza
AU - Roblain, Quentin
AU - Lecomte, Julie
AU - Carai, Paolo
AU - Peters, Linsey
AU - Cuijpers, Ilona
AU - Robinson, Emma Louise
AU - Derks, Kasper
AU - Sergeys, Jurgen
AU - Noel, Agnes
AU - Jones, Elizabeth A. V.
AU - Moons, Lieve
AU - Heymans, Stephane
PY - 2018/8/9
Y1 - 2018/8/9
N2 - Diabetic retinopathy (DR) is one of the major complications of diabetes, which eventually leads to blindness. Up to date, no animal model has yet shown all the co-morbidities often observed in DR patients. Here, we investigated whether obese 42 weeks old ZSF1 rat, which spontaneously develops diabetes, hypertension and obesity, would be a suitable model to study DR. Although arteriolar tortuosity increased in retinas from obese as compared to lean (hypertensive only) ZSF1 rats, vascular density pericyte coverage, microglia number, vascular morphology and retinal thickness were not affected by diabetes. These results show that, despite high glucose levels, obese ZSF1 rats did not develop DR. Such observations prompted us to investigate whether the expression of genes, possibly able to contain DR development, was affected. Accordingly, mRNA sequencing analysis showed that genes (i.e. Npy and crystallins), known to have a protective role, were upregulated in retinas from obese ZSF1 rats. Lack of retina damage, despite obesity, hypertension and diabetes, makes the 42 weeks of age ZSF1 rats a suitable animal model to identify genes with a protective function in DR. Further characterisation of the identified genes and downstream pathways could provide more therapeutic targets for the treat DR.
AB - Diabetic retinopathy (DR) is one of the major complications of diabetes, which eventually leads to blindness. Up to date, no animal model has yet shown all the co-morbidities often observed in DR patients. Here, we investigated whether obese 42 weeks old ZSF1 rat, which spontaneously develops diabetes, hypertension and obesity, would be a suitable model to study DR. Although arteriolar tortuosity increased in retinas from obese as compared to lean (hypertensive only) ZSF1 rats, vascular density pericyte coverage, microglia number, vascular morphology and retinal thickness were not affected by diabetes. These results show that, despite high glucose levels, obese ZSF1 rats did not develop DR. Such observations prompted us to investigate whether the expression of genes, possibly able to contain DR development, was affected. Accordingly, mRNA sequencing analysis showed that genes (i.e. Npy and crystallins), known to have a protective role, were upregulated in retinas from obese ZSF1 rats. Lack of retina damage, despite obesity, hypertension and diabetes, makes the 42 weeks of age ZSF1 rats a suitable animal model to identify genes with a protective function in DR. Further characterisation of the identified genes and downstream pathways could provide more therapeutic targets for the treat DR.
KW - OXYGEN-INDUCED RETINOPATHY
KW - NEUROPEPTIDE-Y RECEPTORS
KW - RETINAL NEOVASCULARIZATION
KW - ENDOTHELIAL-CELLS
KW - GAMMA-CRYSTALLIN
KW - VASCULAR LEAKAGE
KW - ALPHA-CRYSTALLIN
KW - BETA-CRYSTALLIN
KW - B-CRYSTALLIN
KW - MOUSE MODEL
U2 - 10.1038/s41598-018-29812-w
DO - 10.1038/s41598-018-29812-w
M3 - Article
C2 - 30093686
SN - 2045-2322
VL - 8
JO - Scientific Reports
JF - Scientific Reports
IS - 1
M1 - 11922
ER -