| Budget Amount *help |
¥19,240,000 (Direct Cost: ¥14,800,000、Indirect Cost: ¥4,440,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2013: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Outline of Final Research Achievements |
Heat shock protein beta-1 (HSPB1, also known as HSP27) is a small heat shock protein that is involved in many cellular processes and reportedly protects cells against oxidative stress. Autophagy is a mechanism that protects cells from many types of stress and is thought to play an important role in preventing stress in acute kidney injury (AKI). We used an in vivo rat ischemia/reperfusion AKI model and cultured renal tubular cells as an in vitro model. To elucidate the regulation of HSPB1, we evaluated the promoter activity and expression of HSPB1 in NRK-52E cells in the presence of H2O2. We showed that HSPB1 expression increased during oxidative stress in AKI. Incremental HSPB1 expression caused autophagy and inhibited apoptosis in renal tubular cells. These results indicate that upregulated HSPB1 plays a role in the pathophysiology of AKI.
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