scholarly journals A Decrease of Brain MicroRNA-122 Level Is an Early Marker of Cerebrovascular Disease in the Stroke-Prone Spontaneously Hypertensive Rat

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Rosita Stanzione ◽  
Franca Bianchi ◽  
Maria Cotugno ◽  
Simona Marchitti ◽  
Maurizio Forte ◽  
...  

Based on preliminary evidence that highlights microRNA-122 as a contributing factor to stroke pathogenesis, we aimed at assessing its expression level, along with the presence of early signs of cerebrovascular disease, in the brain of stroke-prone spontaneously hypertensive rat (SHRSP), a suitable model of human disease that accelerates stroke occurrence under a high sodium/low potassium (Japanese-style) diet (JD). After one month of JD, before stroke occurrence, brain microRNA-122 level was significantly decreased in SHRSP as compared to the stroke-resistant SHR (SHRSR). At this time, levels of markers of oxidative stress and inflammation, as well as of endothelial integrity and function, apoptosis and necrosis were differently modulated in the brains of JD-fed SHRSP as compared to SHRSR, pointing to a significant activation of all deleterious mechanisms underlying subsequent stroke development in SHRSP. We also showed that miR-122 improved survival of rat endothelial cerebral cells upon stress stimuli (excess NaCl, hydrogen peroxide). Our data suggest that a decrease of brain microRNA-122 level is deleterious and can be considered as an early marker of stroke in the SHRSP. Understanding the mechanisms by which microRNA-122 protects vascular cells from stress stimuli may provide a useful approach to improve preventive and treatment strategies against stroke.

1988 ◽  
Vol 29 (4) ◽  
pp. 562-562
Author(s):  
Hiroaki Tomori ◽  
Hiroshi Kawamura ◽  
Masahiro Maki ◽  
Hideaki Higashi ◽  
Kazuyoshi Tsukamoto ◽  
...  

2016 ◽  
Vol 7 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Jun Zhang ◽  
Mohammad Kazem Fallahzadeh ◽  
Peter A. McCullough

Background: Although there are some animal models for biomarkers of contrast-induced acute kidney injury (CI-AKI), for cardiorenal syndrome (CRS) and for acute renal failure, the interplay between CI-AKI and CRS has yet to be evaluated. Insight into the pathogenesis of CRS is urgently needed from animal models in order to foster the discovery and implementation of novel biomarkers for this disease. Specially designed animal models for type 1 and 3 CRS, particularly CI-AKI, have not yet emerged. Summary: We hypothesize that the aging male spontaneously hypertensive rat (SHR) is likely to be a suitable model. The SHR model is able to mimic risk factors for preclinical CRS that appears in the clinical setting, specifically hypertension, age, preexisting damage and dysfunction of the heart and kidney, endothelial dysfunction, increased level of reactive oxygen species, decreased level and bioavailability of nitric oxide (NO), impairment of the L-arginine-NO pathway, and insulin resistance. In the SHR, CI-AKI results in a different profile of AKI biomarkers than is seen with preexisting chronic kidney injury. Key Messages: The SHR model can be used to evaluate the interaction between CI-AKI and CRS type 1 and 3 and to verify neutrophil gelatinase-associated lipocalin (NGAL) as a reliable CI-AKI biomarker for clinical application. Further research is warranted with a large number of aging male SHRs to prove NGAL as a sensitive, specific, highly predictive, early biomarker for CI-AKI.


1982 ◽  
Vol 63 (s8) ◽  
pp. 339s-342s ◽  
Author(s):  
S. R. Winternitz ◽  
J. M. Wyss ◽  
J. R. Meadows ◽  
S. Oparil

1. High sodium intake results in an exacerbation of hypertension accompanied by evidence of increased peripheral sympathetic activity in the young spontaneously hypertensive rat (SHR) of the Okamoto strain. 2. To examine the hypothesis that high sodium intake increases peripheral sympathetic activity via an influence on central noradrenergic pathways involved in cardiovascular regulation, the effect of dietary sodium intake on noradrenaline stores of individual hypothalamic nuclei was examined in young SHR. 3. After 2 weeks of high sodium intake, the noradrenaline content of the anterior and dorsomedial hypothalamic nuclei of SHR was increased when compared with SHR receiving normal sodium intake. Increases in the noradrenaline content of anterior hypothalamic nucleus persisted at 4 weeks. No changes were seen in other regions examined. 4. These observations lend support to the hypothesis that sodium and the sympathetic nervous system have synergistic effects in the pathogenesis of hypertension in the SHR.


1996 ◽  
Vol 37 (4) ◽  
pp. 553-553
Author(s):  
Tomoji Mashimo ◽  
Yasuo Nara ◽  
Tomoko Tamada ◽  
Chiho Matsumoto ◽  
Katumi Ikeda ◽  
...  

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