著作: [西村 賢二]/Taguchi Kensei/[岸 誠司]/Brooks Craig R/Ochi Arisa/Kadoya Hiroyuki/[池田 康将]/Miyoshi Masashi/[田蒔 昌憲]/Abe Hideharu/Aihara Ken-Ichi/Kashihara Naoki/Nagai Kojiro/Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury./[Biochemical and Biophysical Research Communications]
(英) Dual disruption of eNOS and ApoE gene accelerates kidney fibrosis and senescence after injury.
(英) mice (DKO) were obtained by breeding. Unilateral ureteral obstruction (UUO) was performed on 8-10 week old male mice and the degree of renal tubular injury, fibrosis and kidney senescence were evaluated. DKO manifested elevated blood pressure, higher total cholesterol and lower HDL than WT. DKO showed sustained kidney injury molecule-1 protein expression. Kidney fibrosis was significantly higher in ApoEKO and DKO. mRNA expression of genes related to kidney fibrosis was the highest in DKO. The mRNA expression of Zinc-α2-Glycoprotein and heme oxygenase-1 were significantly decreased in DKO. Furthermore, mRNA expression of p53, p21 and p16 were increased both in ApoEKO and DKO, with DKO being the highest. Senescence associated β-gal positive tubule area was significantly increased in DKO. Increased DNA damage and target of rapamycin-autophagy spatial coupling compartments (TASCCs) formation was found in DKO. Mice with endothelial dysfunction and dyslipidemia developed kidney fibrosis and accelerated senescence even in young mice after injury. These data highlight the fact managing lifestyle-related diseases from a young age is important for CKD prevention.
Biochemical and Biophysical Research Communications([Elsevier])
|年月日||必須||2021年 4月 9日|