The University of Osaka · 의학
이소 아츠미 교수의 연구실은 신장 질환과 대사성 질환에서의 폴리아민 대사, 비타민 D 시스템, 그리고 혈관 및 신장 석회화의 분자 기전을 중심으로 연구를 진행하고 있습니다. 특히, 폴리아민 조절 효소의 기능과 비타민 D의 신장세포 보호 작용, 그리고 페투인-A가 신장에서 석회화를 억제하는 메커니즘을 규명하고자 합니다. 실험 모델을 활용한 기전 연구를 바탕으로, 만성 신장질환의 예방 및 치료 전략 개발에 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
A cytosolic spermidine N-acetyltransferase has been partially purified from livers of rats treated with carbon tetrachloride or thioacetamide.This enzyme formed N'-acetylspermidine when incubated with spermidine and acetyl-coA.The enzyme was also able to acetylate spermine, norspermidine, norspermine and, at a much slower rate, 1,3-diaminopropane.Putrescine, cadaverine, homospermidine, and histones were not substrates ( ~2 % activity of spermidine) distinguishing this enzyme from a previously de
Combined use of two markers is useful for the risk stratification of renal outcome.
We demonstrated the breakdown of the vitamin D activation system in podocyte injury, and established a preventative role for vitamin D in podocyte injury.
Vascular calcification (VC) is a life-threatening complication of CKD. Severe protein restriction causes a shortage of essential amino acids, and exacerbates VC in rats. Therefore, we investigated the effects of dietary l-lysine, the first-limiting amino acid of cereal grains, on VC. Male Sprague-Dawley rats at age 13 weeks were divided randomly into four groups: low-protein (LP) diet (group LP), LP diet+adenine (group Ade), LP diet+adenine+glycine (group Gly) as a control amino acid group, and
Treatment of rats with dimethylnitrosamine (30 mg/kg) or diethylnitrosamine (200 mg/kg) produced a rapid increase in the activity of spermidine N1-acetyltransferase which peaked at values 7-fold greater than did control at 48 hr after exposure. This increase led to a small accumulation of N1-acetylspermidine in the liver but produced a more striking effect on putrescine which increased 30- to 40-fold after 2 days. Most of this increase appeared to be due to the conversion of N1-acetylspermidine
The serum glycoprotein fetuin-A is an important inhibitor of extraosseous calcification. The importance of fetuin-A has been confirmed in fetuin-A null mice, which develop widespread extraosseous calcification including the kidney. However, the mechanism how fetuin-A protects kidneys from nephrocalcinosis remains uncertain. Here, we demonstrate that intratubular fetuin-A plays a role in the prevention of nephrocalcinosis in the proximal tubules. Although normal rat kidney did not express mRNA fo
