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autophagy renal ischemia

Mingyi Zhao, Ping Zhu, Masayuki Fujino, Yoshiaki Nishio, Jimei Chen, Hidenori Ito, Kiwamu Takahashi, Motowo Nakajima, Tohru Tanaka, Lingling Zhao, Jian Zhuang, Xiao-Kang Li
BACKGROUND: Hypoxia causes cardiac disease via oxidative stress and mitochondrial dysfunction. 5-Aminolevulinic acid in combination with sodium ferrous citrate (ALA/SFC) has been shown to up-regulate heme oxygenase-1 (HO-1) and decrease macrophage infiltration and renal cell apoptosis in renal ischemia injury mice. However, its underlying mechanism remains largely unknown. The aim of this study was to investigate whether ALA/SFC could protect cardiomyocytes from hypoxia-induced apoptosis by autophagy via HO-1 signaling...
October 28, 2016: Biochemical and Biophysical Research Communications
Reem Alshaman, Luan Truong, Adebayo Oyekan
Despite the presence of many studies on the role of mechanistic target of rapamycin (mTOR) in cardiorenal tissues, the definitive role of mTOR in the pathogenesis of renal injury subsequent to ischemia-reperfusion (IR) remains unclear. The aims of the current study were to characterize the role of mTOR in normal kidney function and to investigate the role of mTOR activation in IR-induced kidney injury. In euvolemic anesthetized rats, treatment with the mTOR inhibitor rapamycin increased blood pressure (121±2 to 144±3 mmHg; P<0...
August 24, 2016: Clinical and Experimental Pharmacology & Physiology
Yi Fang, Hui Zhang, Yihong Zhong, Xiaoqiang Ding
Prolyl hydroxylase domain protein 2 (PHD2) is a key oxygen sensor, setting low steady-state level of hypoxia-inducible factor-α (HIF-α). Here, we showed that treatment of cobalt chloride (CoCl2), a hypoxia mimic, in HK-2 tubular epithelial cells induced PHD2 and HIF-1/2α expression as well as cell apoptosis and autophagy activation. Three methyladenine (3-MA), the autophagy inhibitor, blocked autophagy and protected HK-2 cells from CoCl2. Significantly, siRNA knockdown of PHD2 also protected HK-2 cells from CoCl2,possibly via increasing HIF-1α expression...
August 5, 2016: Oncotarget
Wenjing Zhang, Shuo Yang, Liyan Cui, Jie Zhang
This study aimed to explore the influence of neutrophil gelatinase-associated lipocalin on autophagy and its role in ischemia/reperfusion injury in human kidney-2 (HK-2) cells during acute kidney injury (AKI). HK-2 cells were given hypoxia/reoxygenation treatment for different times to simulate ischemia/reperfusion injury. Autophagy was evaluated by western blot and immunofluorescence of GFP-LC3. Cell viability was tested to reflect the degree of cell damage. The autophagy inhibitor 3-MA was used to inhibit autophagy and determine the role of autophagy in ischemia/reperfusion injury...
August 2016: Renal Failure
Steven C Borkan
B-cell lymphoma 2 (BCL-2) family proteins gather at the biologic cross-roads of renal cell survival: the outer mitochondrial membrane. Despite shared sequence and structural features, members of this conserved protein family constantly antagonize each other in a life-and-death battle. BCL-2 members innocently reside within renal cells until activated or de-activated by physiologic stresses caused by common nephrotoxins, transient ischemia, or acute glomerulonephritis. Recent experimental data not only illuminate the intricate mechanisms of apoptosis, the most familiar form of BCL-2-mediated cell death, but emphasizes their newfound roles in necrosis, necroptosis, membrane pore transition regulated necrosis, and other forms of acute cell demise...
May 2016: Seminars in Nephrology
Andrea Havasi, Zheng Dong
Many common renal insults such as ischemia and toxic injury primarily target the tubular epithelial cells, especially the highly metabolically active proximal tubular segment. Tubular epithelial cells are particularly dependent on autophagy to maintain homeostasis and respond to stressors. The pattern of autophagy in the kidney has a unique spatial and chronologic signature. Recent evidence has shown that there is complex cross-talk between autophagy and various cell death pathways. This review specifically discusses the interplay between autophagy and cell death in the renal tubular epithelia...
May 2016: Seminars in Nephrology
Jeremy S Leventhal, Jie Ni, Morgan Osmond, Kyung Lee, G Luca Gusella, Fadi Salem, Michael J Ross
Sepsis related acute kidney injury (AKI) is a common in-hospital complication with a dismal prognosis. Our incomplete understanding of disease pathogenesis has prevented the identification of hypothesis-driven preventive or therapeutic interventions. Increasing evidence in ischemia-reperfusion and nephrotoxic mouse models of AKI support the theory that autophagy protects renal tubular epithelial cells (RTEC) from injury. However, the role of RTEC autophagy in septic AKI remains unclear. We observed that lipopolysaccharide (LPS), a mediator of gram-negative bacterial sepsis, induces RTEC autophagy in vivo and in vitro through TLR4-initiated signaling...
2016: PloS One
Gur P Kaushal, Sudhir V Shah
Autophagy is a conserved multistep pathway that degrades and recycles damaged organelles and macromolecules to maintain intracellular homeostasis. The autophagy pathway is upregulated under stress conditions including cell starvation, hypoxia, nutrient and growth-factor deprivation, endoplasmic reticulum stress, and oxidant injury, most of which are involved in the pathogenesis of acute kidney injury (AKI). Recent studies demonstrate that basal autophagy in the kidney is vital for the normal homeostasis of the proximal tubules...
April 2016: Kidney International
Mingjun Shi, Brianna Flores, Nancy Gillings, Ao Bian, Han Jun Cho, Shirley Yan, Yang Liu, Beth Levine, Orson W Moe, Ming Chang Hu
AKI confers increased risk of progression to CKD. αKlotho is a cytoprotective protein, the expression of which is reduced in AKI, but the relationship of αKlotho expression level to AKI progression to CKD has not been studied. We altered systemic αKlotho levels by genetic manipulation, phosphate loading, or aging and examined the effect on long-term outcome after AKI in two models: bilateral ischemia-reperfusion injury and unilateral nephrectomy plus contralateral ischemia-reperfusion injury. Despite apparent initial complete recovery of renal function, both types of AKI eventually progressed to CKD, with decreased creatinine clearance, hyperphosphatemia, and renal fibrosis...
August 2016: Journal of the American Society of Nephrology: JASN
Hatem A Alnasser, Qiunong Guan, Fan Zhang, Martin E Gleave, Christopher Y C Nguan, Caigan Du
Cellular autophagy is a prosurvival mechanism in the kidney against ischemia-reperfusion injury (IRI), but the molecular pathways that activate the autophagy in ischemic kidneys are not fully understood. Clusterin (CLU) is a chaperone-like protein, and its expression is associated with kidney resistance to IRI. The present study investigated the role of CLU in prosurvival autophagy in the kidney. Renal IRI was induced in mice by clamping renal pedicles at 32°C for 45 min. Hypoxia in renal tubular epithelial cell (TEC) cultures was induced by exposure to a 1% O2 atmosphere...
January 15, 2016: American Journal of Physiology. Renal Physiology
Arpita Baisantry, Sagar Bhayana, Song Rong, Esther Ermeling, Christoph Wrede, Jan Hegermann, Petra Pennekamp, Inga Sörensen-Zender, Hermann Haller, Anette Melk, Roland Schmitt
Evidence suggests that autophagy promotes the development of cellular senescence. Because cellular senescence contributes to renal aging and promotes the progression from AKI to CKD, we investigated the potential effect of tubular autophagy on senescence induction. Compared with kidneys from control mice, kidneys from mice with conditional deletion of autophagy-related 5 (Atg5) for selective ablation of autophagy in proximal tubular S3 segments (Atg5(Δ) (flox/) (Δ) (flox)) presented with significantly less tubular senescence, reduced interstitial fibrosis, and superior renal function 30 days after ischemia/reperfusion injury...
June 2016: Journal of the American Society of Nephrology: JASN
Bhavya B Chandrika, Cheng Yang, Yang Ou, Xiaoke Feng, Djamali Muhoza, Alexandrea F Holmes, Sue Theus, Sarika Deshmukh, Randy S Haun, Gur P Kaushal
We examined whether endoplasmic reticulum (ER) stress-induced autophagy provides cytoprotection from renal tubular epithelial cell injury due to oxidants and chemical hypoxia in vitro, as well as from ischemia-reperfusion (IR) injury in vivo. We demonstrate that the ER stress inducer tunicamycin triggers an unfolded protein response, upregulates ER chaperone Grp78, and activates the autophagy pathway in renal tubular epithelial cells in culture. Inhibition of ER stress-induced autophagy accelerated caspase-3 activation and cell death suggesting a pro-survival role of ER stress-induced autophagy...
2015: PloS One
Xiu-Juan Liu, Quan Hong, Zhen Wang, Yan-Yan Yu, Xin Zou, Li-Hong Xu
BACKGROUND: Acute kidney injury (AKI) is traditionally described as a condition leading to rapid damage to kidney function, eventually becoming a significant healthcare concern with a high mortality rate. Autophagy deficiency in the tubular epithelial cells is the main cause of AKI; however, the underlying molecular mechanism remains to be defined. MicroRNAs (miRNAs) are related to autophagy in many diseases. This study was aimed at investigating the relationship between miRNA expression and autophagic activity in the pathogenesis of AKI...
2015: American Journal of Nephrology
Xiujuan Liu, Quan Hong, Zhen Wang, Yanyan Yu, Xin Zou, Lihong Xu
Renal ischemia-reperfusion (I/R) is one of the main causes of the acute kidney injury (AKI) that usually occurs during clinical surgery. Autophagy plays an important role in recovery from acute ischemic kidney injury. MicroRNA-21 (miR-21) was reported to inhibit autophagy in several diseases. However, the molecular mechanism of miR-21 on autophagy during renal I/R is still unclear. For the in vitro study, NRK-52E cells were transfected with miR-21 mimics and subjected to I/R. Results showed that miR-21 mimics inhibited cell viability and induced cell apoptosis in NRK-52E cells...
October 15, 2015: Experimental Cell Research
Daniel Patschan, Katrin Schwarze, Elvira Henze, Susann Patschan, Gerhard Anton Müller
BACKGROUND: Autophagy enables cells to digest endogenous/exogenous waste products, thus potentially prolonging the cellular lifespan. Early endothelial progenitor cells (eEPCs) protect mice from ischemic acute kidney injury (AKI). The mid-term prognosis in AKI critically depends on vascular rarefication and interstitial fibrosis with the latter partly being induced by mesenchymal transdifferentiation of endothelial cells (EndoMT). This study aimed to determine the impact of eEPC preconditioning with different autophagy inducing agents [suberoylanilide hydroxamic acid (SAHA)/temsirolimus] in ischemic AKI...
October 2016: Journal of Nephrology
Jean-Paul Decuypere, Laurens J Ceulemans, Patrizia Agostinis, Diethard Monbaliu, Maarten Naesens, Jacques Pirenne, Ina Jochmans
Autophagy, an evolutionary conserved intracellular lysosome-dependent catabolic process, is an important mechanism for cellular homeostasis and survival during pathologic stress conditions in the kidney, such as ischemia-reperfusion injury (IRI). However, stimulation of autophagy has been described to both improve and exacerbate IRI in the kidney. We summarize the current understanding of autophagy in renal IRI and discuss possible reasons for these contradictory findings. Furthermore, we hypothesize that autophagy plays a dual role in renal IRI, having both protective and detrimental properties, depending on the duration of the ischemic period and the phase of the IRI process...
October 2015: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
Mai Taniguchi, Hiderou Yoshida
PURPOSE OF REVIEW: Recently, a number of papers have reported that endoplasmic reticulum (ER) stress is involved in the onset of various kidney diseases, but the pathological mechanisms responsible have not been clarified. In this review, we summarize recent findings on this issue and try to clarify the pathology of ER stress-induced kidney diseases. RECENT FINDINGS: ER stress is evoked in various kidney diseases, including diabetic nephropathy, renal fibrosis, inflammation or osmolar contrast-induced renal injury, ischemia-reperfusion, genetic mutations of renal proteins, proteinuria and cyclosporine A treatment...
July 2015: Current Opinion in Nephrology and Hypertension
Xuejing Guan, Yingying Qian, Yue Shen, Lulu Zhang, Yi Du, Huili Dai, Jiaqi Qian, Yucheng Yan
BACKGROUND/AIMS: Autophagy is a dynamic catabolic process that maintains cellular homeostasis. Whether it plays a role in promoting cell survival or cell death in the process of renal ischemia/reperfusion (I/R) remains controversial, partly because renal autophagy is usually examined at a certain time point. Therefore, monitoring of the whole time course of autophagy and apoptosis may help better understand the role of autophagy in renal I/R. METHODS: Autophagy and apoptosis were detected after mice were subjected to bilateral renal ischemia followed by 0-h to 7-day reperfusion, exposure of TCMK-1 cells to 24-h hypoxia, and 2 to 24-h reoxygenation...
2015: Cellular Physiology and Biochemistry
Tatsuki Matsumoto, Madoka Urushido, Haruna Ide, Masayuki Ishihara, Kazu Hamada-Ode, Yoshiko Shimamura, Koji Ogata, Kosuke Inoue, Yoshinori Taniguchi, Takafumi Taguchi, Taro Horino, Shimpei Fujimoto, Yoshio Terada
BACKGROUND: Heat shock protein beta-1 (HSPB1, also known as HSP27) is a small heat shock protein involved in many cellular processes and reportedly protects cells against oxidative stress. Autophagy protects cells from many types of stress and is thought to play a key role in preventing stress in acute kidney injury (AKI). However, little is known about the role of HSPB1 in autophagy and apoptosis in the pathogenesis of AKI. METHODS: We used a rat ischemia/reperfusion AKI model and cultured renal tubular cells as an in vitro model...
2015: PloS One
Ya-Li Zhang, Jie Zhang, Li-Yan Cui, Shuo Yang
Ischemia-reperfusion (I/R) injury is a leading cause of acute kidney injury (AKI), which is a common clinical complication but lacks effective therapies. This study investigated the role of autophagy in renal I/R injury and explored potential mechanisms in an established rat renal I/R injury model. Forty male Wistar rats were randomly divided into four groups: Sham, I/R, I/R pretreated with 3-methyladenine (3-MA, autophagy inhibitor), or I/R pretreated with rapamycin (autophagy activator). All rats were subjected to clamping of the left renal pedicle for 45 min after right nephrectomy, followed by 24 h of reperfusion...
December 2015: Experimental Biology and Medicine
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