지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2016.1
- 수록면
- 1,252 - 1,259 (8page)
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Purpose: Diabetic nephropathy (DN) is a prevalent chronic microvascular complication of diabetes mellitus involving disturbancesin electrolytes and the acid-base balance caused by a disorder of glucose metabolism. NHE1 is a Na+/H+ exchanger responsiblefor keeping intracellular pH (pHi) balance and cell growth. Our study aimed to investigate roles of NHE1 in high glucose (HG)-induced apoptosis in renal tubular epithelial cells.
Materials and Methods: Renal epithelial tubular cell line HK-2 was cultured in medium containing 5 mM or 30 mM glucose. Then, cell apoptosis, oxidative stress, NHE1 expression, and pHi were evaluated. NHE1 siRNA and inhibitor were used to evaluate its role in cell apoptosis.
Results: HG significantly increased cell apoptosis and the production of reactive oxygen species (ROS) and 8-OHdG (p<0.05). Meanwhile, we found that HG induced the expression of NHE1 and increased the pHi from 7.0 to 7.6 after 48 h of incubation. However,inhibiting NHE1 using its specific siRNA or antagonist DMA markedly reduced cell apoptosis stimulated by HG. In addition, suppressing cellular oxidative stress using antioxidants, such as glutathione and N-acetyl cysteine, significantly reduced the productionof ROS, accompanied by a decrease in NHE1. We also found that activated cyclic GMP-Dependent Protein Kinase Type I (PKG) signaling promoted the production of ROS, which contributed to the regulation of NHE1 functions.
Conclusion: Our study indicated that HG activates PKG signaling and elevates the production of ROS, which was responsible for the induction of NHE1 expression and dysfunction, as well as subsequent cell apoptosis, in renal tubular epithelial cells.
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참고문헌 (23)
참고문헌 신청
Okada H / 2015 / Senescence marker protein-30/gluconolactonase deficiency exacerbates diabetic nephropathy through tubular injury in a mouse model of type 1 diabetes / J Diabetes Investig 6:35~43
Kumar D / 2004 / Evidence of apoptosis in human diabetic kidney / Mol Cell Biochem 259:67~70
Karki P / 2010 / Overexpression of the NHE1 isoform of the Na(+)/H (+) exchanger causes elevated apoptosis in isolated cardiomyocytes after hypoxia/reoxygenation challenge / Mol Cell Biochem 338:47~57
Ng LL / 1994 / Abnormal Na+/H+ antiporter phenotype and turnover of immortalized lymphoblasts from type 1 diabetic patients with nephropathy / J Clin Invest 93:2750~2757
Li P / 2016 / Inhibition of NA(+)/H(+) exchanger 1 attenuates renal dysfunction induced by advanced glycation end products in rats / J Diabetes Res 2016:1802036
Kumar D / 2004 / Evidence of apoptosis in human diabetic kidney / Mol Cell Biochem 259:67~70
Karki P / 2010 / Overexpression of the NHE1 isoform of the Na(+)/H (+) exchanger causes elevated apoptosis in isolated cardiomyocytes after hypoxia/reoxygenation challenge / Mol Cell Biochem 338:47~57
Ng LL / 1994 / Abnormal Na+/H+ antiporter phenotype and turnover of immortalized lymphoblasts from type 1 diabetic patients with nephropathy / J Clin Invest 93:2750~2757
Li P / 2016 / Inhibition of NA(+)/H(+) exchanger 1 attenuates renal dysfunction induced by advanced glycation end products in rats / J Diabetes Res 2016:1802036
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