Presenter Information

Jasmine FullerFollow

Presentation Title

Contrast Medium-Induced Apoptosis And Autophagy In Kidney Proximal Tubular Cells

Location

Nessmith-Lane Atrium

Session Format

Poster Presentation

Research Area Topic:

Natural & Physical Sciences - Biology

Abstract

Contrast medium-induced acute kidney injury (CM-AKI) is one of the leading causes of acute kidney failure during hospitalization. It has been defined as the occurrence of acute renal impairment within 2-7 days after administration of iodinated contrast medium in medical imaging. The mechanism of CM-AKI is not completely understood and there is no effective treatment for this disease. To study the mechanism, we administered various concentrations of contrast medium to rat proximal tubule cells (RPTC). Contrast medium induced apoptosis as shown by cell morphology and the cleavage of caspase-3 into active forms. Contrast medium also induced autophagy as shown by increased LC3II protein signal. Autophagy has been shown to play a protective role in acute kidney injury models such as cisplatin treatment and ischemia-reperfusion. During contrast medium treatment, inhibition of autophagy by chloroquoine enhanced apoptosis in RPTC, while activation of autophagy by rapamycin diminished apoptosis, further supporting a protective role of autophagy. Mammalian target of rapamycin (mTOR) is a major negative regulator of autophagy. Contrast medium treatment led to the activation of mTOR as shown by increased phosphorylation of P70s6kinase, suggesting that autophagy activation by contrast medium is not the result of mTOR suppression. These results reveal autophagy induction and its protective role during contrast medium treatment of kidney tubular cells.

Presentation Type and Release Option

Presentation (Open Access)

Start Date

4-16-2016 10:45 AM

End Date

4-16-2016 12:00 PM

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Apr 16th, 10:45 AM Apr 16th, 12:00 PM

Contrast Medium-Induced Apoptosis And Autophagy In Kidney Proximal Tubular Cells

Nessmith-Lane Atrium

Contrast medium-induced acute kidney injury (CM-AKI) is one of the leading causes of acute kidney failure during hospitalization. It has been defined as the occurrence of acute renal impairment within 2-7 days after administration of iodinated contrast medium in medical imaging. The mechanism of CM-AKI is not completely understood and there is no effective treatment for this disease. To study the mechanism, we administered various concentrations of contrast medium to rat proximal tubule cells (RPTC). Contrast medium induced apoptosis as shown by cell morphology and the cleavage of caspase-3 into active forms. Contrast medium also induced autophagy as shown by increased LC3II protein signal. Autophagy has been shown to play a protective role in acute kidney injury models such as cisplatin treatment and ischemia-reperfusion. During contrast medium treatment, inhibition of autophagy by chloroquoine enhanced apoptosis in RPTC, while activation of autophagy by rapamycin diminished apoptosis, further supporting a protective role of autophagy. Mammalian target of rapamycin (mTOR) is a major negative regulator of autophagy. Contrast medium treatment led to the activation of mTOR as shown by increased phosphorylation of P70s6kinase, suggesting that autophagy activation by contrast medium is not the result of mTOR suppression. These results reveal autophagy induction and its protective role during contrast medium treatment of kidney tubular cells.