A Low-Calorie Unrestricted Protein Diet Attenuates Kidney Damage in Uninephrectomized Spontaneously Hypertensive Rats

1999 ◽  
Vol 19 (3) ◽  
pp. 433-440 ◽  
Author(s):  
Efrain Reisin ◽  
Kimiyo Y. Harris ◽  
Silvia Azar ◽  
Bennett DeBoisblanc ◽  
Vashu Thakur ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Kidney Damage ◽  
Protein Diet ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Low Calorie

scholarly journals Brain Overexpression of Uncoupling Protein-2 (UCP2) Delays Renal Damage and Stroke Occurrence in Stroke-Prone Spontaneously Hypertensive Rats

2020 ◽  
Vol 21 (12) ◽  
pp. 4289
Author(s):  
Carla L. Busceti ◽  
Maria Cotugno ◽  
Franca Bianchi ◽  
Maurizio Forte ◽  
Rosita Stanzione ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Lentiviral Vector ◽  
Uncoupling Protein ◽  
Organ Damage ◽  
Kidney Damage ◽  
Uncoupling Protein 2 ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Protein Levels

The downregulation of uncoupling protein-2 (UCP2) is associated with increased brain and kidney injury in stroke-prone spontaneously hypertensive rats (SHRSP) fed with a Japanese style hypersodic diet (JD). Systemic overexpression of UCP2 reduces organ damage in JD-fed SHRSP. We examined the effect of brain-specific UCP2 overexpression on blood pressure (BP), stroke occurrence and kidney damage in JD-fed SHRSP. Rats received a single i.c.v. injection of a lentiviral vector encoding UCP2 (LV-UCP2), or an empty vector. The brain delivery of LV-UCP2 significantly delayed the occurrence of stroke and kidney damage. The large reduction of proteinuria observed after LV-UCP2 injection was unexpected, because BP levels were unchanged. At the time of stroke, rats treated with LV-UCP2 still showed a large UCP2 upregulation in the striatum, associated with increases in OPA1 and FIS1 protein levels, and reductions in PGC1-α, SOD2, TNFα mRNA levels and NRF2 protein levels. This suggested UCP2 overexpression enhanced mitochondrial fusion and fission and reduced oxidative damage and inflammation in the striatum of JD-fed SHRSP rats. Our data suggest the existence of central mechanisms that may protect against hypertension-induced organ damage independently of BP, and strengthen the suitability of strategies aimed at enhancing UCP2 expression for the treatment of hypertensive damage.

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