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autophagy renal ischemia

Yang Zhou, Ting Cai, Jing Xu, Lei Jiang, Jining Wu, Qi Sun, Ke Zen, Junwei Yang
Uncoupling protein 2 (UCP2) plays critical roles in energy metabolism and cell survival. Previous investigations showed that UCP2 regulated the production of extracellular matrix and renal fibrosis. However, little is known about UCP2 in acute kidney injury. Here, we used UCP2 knockout mice to investigate the role of UCP2 in AKI model generated by renal ischemia/reperfusion (I/R) injury. The UCP2 global knockout mice were born and growth normal without kidney histological abnormality or renal dysfunctions. As compared with littermates, deletion of UCP2 exacerbated I/R-induced AKI while increase of UCP2 by conjugated linoleic acid (CLA) attenuated I/R injury...
April 19, 2017: American Journal of Physiology. Renal Physiology
Jiaqi Liu, Meiqing Liu, Linxi Chen
Apelin is the endogenous peptide APJ receptor, while APJ is a member of the G protein-coupled receptors family. Recent evidence strongly suggests that Apelin/APJ system influences apoptosis in various diseases through different signal pathways. In this review, we discuss the possible mechanisms by which the Apelin/APJ system inhibits apoptosis, including the phosphatidylinositol-3-kinase (PI3K)/Akt, ERK1/2, caspase signaling, and autophagy pathway. We also summarize the role of Apelin/APJ system in apoptosis in myocardial ischemia-reperfusion (I/R) injury, pulmonary artery hypertension, retinal neovascular disease, acute renal injury, skeletal homeostasis, and gastrointestinal diseases...
April 12, 2017: Acta Biochimica et Biophysica Sinica
Stanislovas S Jankauskas, Irina B Pevzner, Nadezda V Andrianova, Ljubava D Zorova, Vasily A Popkov, Denis N Silachev, Nataliya G Kolosova, Egor Y Plotnikov, Dmitry B Zorov
In young rats, ischemic preconditioning (IPC), which consists of 4 cycles of ischemia and reperfusion alleviated kidney injury caused by 40-min ischemia. However,old rats lost their ability to protect the ischemic kidney by IPC. A similar aged phenotype was demonstrated in 6-month-old OXYS rats having signs of premature aging. In the kidney of old and OXYS rats, the levels of acetylated nuclear proteins were higher than in young rats, however, unlike in young rats, acetylation levels in old and OXYS rats were further increased after IPC...
March 15, 2017: Scientific Reports
Huiping Sun, Shuangfa Zou, Keith A Candiotti, Yanhua Peng, Qinya Zhang, Weiqiang Xiao, Yiyun Wen, Jiao Wu, Jinfeng Yang
Octreotide exerts a protective effect in hepatic ischemia-reperfusion (HIR) injury. However, whether octreotide preconditioning could also reduce acute kidney injury (AKI) after HIR is unknown. This study was designed to investigate the role of octreotide in AKI after HIR. Male Sprague-Dawley rats were pretreated with octreotide or octreotide combined with 3-methyladenine (autophagy inhibitor, 3MA). Plasma creatinine, inflammation markers (e.g., TNF-α and IL-6 etc.), apoptosis, autophagy and phosphorylation of protein kinase B/mammalian target of rapamycin/p70 ribosomal S6 kinase (Akt/mTOR/p70S6K) in the kidney were measured after 60 minutes of liver ischemia and 24 hours of reperfusion for each rat...
February 16, 2017: Scientific Reports
Ding-Su Bao, Yu-Ke Wu, Shi-Jie Fu, Guo-You Wang, Si-Jin Yang, Guo-Biao Liang, Zhi-Hui Xie, Song Rong
BACKGROUND Ischemia-reperfusion injury (IRI) is a clinically common pathologic process defined as the inability to improve neuronal function. This study aimed to investigate the pathological mechanism of IRI and to explore effects of hyperbaric oxygenation (HBO) on autophagy and inflammatory response in IRI. MATERIAL AND METHODS Ninety Sprague-Dawley (SD) rats were randomly divided into a Sham group, a kidney transplant group (Trans), and a kidney transplant plus HBO treatment group (Trans+HBO). The kidney was harvested from the donor and transplanted to recipient rats according to a previously reported study...
February 10, 2017: Annals of Transplantation: Quarterly of the Polish Transplantation Society
Takeshi Yamamoto, Yoshitsugu Takabatake, Atsushi Takahashi, Tomonori Kimura, Tomoko Namba, Jun Matsuda, Satoshi Minami, Jun-Ya Kaimori, Isao Matsui, Taiji Matsusaka, Fumio Niimura, Motoko Yanagita, Yoshitaka Isaka
Excessive fat intake contributes to the progression of metabolic diseases via cellular injury and inflammation, a process termed lipotoxicity. Here, we investigated the role of lysosomal dysfunction and impaired autophagic flux in the pathogenesis of lipotoxicity in the kidney. In mice, a high-fat diet (HFD) resulted in an accumulation of phospholipids in enlarged lysosomes within kidney proximal tubular cells (PTCs). In isolated PTCs treated with palmitic acid, autophagic degradation activity progressively stagnated in association with impaired lysosomal acidification and excessive lipid accumulation...
December 8, 2016: Journal of the American Society of Nephrology: JASN
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 23, 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
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