Restraint stress aggravates rat kidney injury caused by a crush injury through endoplasmic reticulum stress

2013 ◽  
Vol 75 (5) ◽  
pp. 798-806 ◽  
Author(s):  
Jing Geng ◽  
Xiao Jing Zhang ◽  
Chun Ling Ma ◽  
Ying Min Li ◽  
Guo Zhong Zhang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Restraint Stress ◽  
Rat Kidney ◽  
Kidney Injury ◽  
Crush Injury

scholarly journals Recombinant α-Klotho Protein Alleviated Acute Cardiorenal Injury in a Mouse Model of Lipopolysaccharide-Induced Septic Cardiorenal Syndrome Type 5

2019 ◽  
Vol 2019 ◽  
pp. 1-12
Author(s):  
Xi Liu ◽  
Yangyang Niu ◽  
Xiaoqin Zhang ◽  
Yingying Zhang ◽  
Ying Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Interleukin 1 ◽  
Kidney Injury ◽  
Left Ventricular ◽  
Control Group ◽  
Renal Tubules ◽  
Protective Function ◽  
Klotho Protein

Background and Aims. Klotho is an aging-suppressor gene mainly expressed in the renal tubules. The klotho gene encodes the α-klotho protein, which has many functions. Previous studies have found that α-klotho protein has a cardiorenal protective function. α-Klotho deficiency renders the kidney more susceptible to injury and results in cardiovascular calcification and left ventricular hypertrophy in chronic kidney disease. However, the role of α-klotho in acute heart injury and acute kidney injury with sepsis remains unknown. This study aimed to investigate the effects and mechanisms of α-klotho in septic cardiorenal injury. Methods. Male 8-week-old C57BL/6 mice were randomly assigned to the control group, lipopolysaccharide (LPS; 10 mg/kg) group, LPS (10 mg/kg)+α-klotho (0.01 mg/kg) group, and LPS (10 mg/kg)+α-klotho (0.02 mg/kg) group. Recombinant α-klotho was intraperitoneally injected an hour before LPS injection. Mice were euthanized at 24 h after LPS injection. The serum troponin, brain natriuretic peptide (BNP), neutrophil gelatinase-associated lipocalin (NGAL), and creatinine levels were measured in all groups at 24 h. Biomarkers of mice heart apoptosis, inflammation, oxidative stress, and endoplasmic reticulum stress, such as caspase-3, interleukin 1 (IL-1), reactive oxygen species (ROS), and glucose-regulated protein 78 (GRP78), were also measured. Results. α-Klotho was mainly expressed in mice kidneys and was undetectable in the control mice hearts. α-Klotho substantially decreased after LPS injection. In the LPS group, the serum troponin levels significantly increased as early as 6 h (p<0.05) after LPS injection, while the BNP, NGAL, and creatinine levels significantly increased at 24 h (p<0.05). Pretreatment with α-klotho significantly ameliorated acute cardiorenal injury. In the LPS+α-klotho (0.01 mg/kg) group, the levels of apoptosis, inflammation, and oxidative stress were decreased, while the level of endoplasmic reticulum stress was elevated. Conclusions. α-Klotho significantly alleviates acute cardiorenal injury in LPS-induced septic cardiorenal injury due to the inhibition of apoptosis, inflammation, and oxidation, as well as the regulation of endoplasmic reticulum stress levels.

scholarly journals Shiga Toxin 2-Induced Endoplasmic Reticulum Stress Is Minimized by Activated Protein C but Does Not Correlate with Lethal Kidney Injury

Toxins ◽  
2015 ◽  
Vol 7 (1) ◽  
pp. 170-186 ◽  
Author(s):  
Caitlin Parello ◽  
Chad Mayer ◽  
Benjamin Lee ◽  
Amanda Motomochi ◽  
Shinichiro Kurosawa ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Shiga Toxin ◽  
Protein C ◽  
Activated Protein C ◽  
Kidney Injury ◽  
Shiga Toxin 2

Indomethacin induces endoplasmic reticulum stress, but not apoptosis, in the rat kidney

2015 ◽  
Vol 761 ◽  
pp. 199-205 ◽  
Author(s):  
Arumugam Suriyam Nagappan ◽  
Joe Varghese ◽  
Jithu V. James ◽  
Molly Jacob
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Rat Kidney

scholarly journals A Weak Response to Endoplasmic Reticulum Stress Is Associated With Postoperative Organ Failure in Patients Undergoing Cardiac Surgery With Cardiopulmonary Bypass

2021 ◽  
Vol 7 ◽  
Author(s):  
Thomas Clavier ◽  
Zoé Demailly ◽  
Xavier Semaille ◽  
Caroline Thill ◽  
Jean Selim ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Endoplasmic Reticulum Stress ◽  
Organ Failure ◽  
Plasma Levels ◽  
Invasive Mechanical Ventilation ◽  
Kidney Injury ◽  
Total Blood ◽  
Expression Of Genes

Introduction: Endoplasmic reticulum stress (ERS) is involved in inflammatory organ failure. Our objective was to describe ERS, its unfolded protein response (UPR) expression/kinetics during cardiac surgery with cardiopulmonary bypass (CPB) and its association with postoperative organ failure (OF).Methods: Prospective study conducted on patients undergoing cardiac surgery with CPB. Blood samples were taken before (Pre-CPB), 2 h (H2-CPB) and 24 h (H24-CPB) after CPB. Plasma levels of 78 kDa Glucose- Regulated Protein (GRP78, final effector of UPR) were evaluated by ELISA. The expression of genes coding for key elements of UPR (ATF6, ATF4, sXBP1, CHOP) was evaluated by quantitative PCR performed on total blood. OF was defined as invasive mechanical ventilation and/or acute kidney injury and/or hemodynamic failure requiring catecholamines.Results: We included 46 patients, GRP78 was decreased at H2-CPB [1,328 (878–1,730) ng/ml vs. 2,348 (1,655–3,730) ng/ml Pre-CPB; p &lt; 0.001] but returned to basal levels at H24-CPB [2,068 (1,436–3,005) ng/ml]. The genes involved in UPR had increased expression at H2 and H24. GRP78 plasma levels in patients with OF at H24-CPB (n = 10) remained below Pre-CPB levels [−27.6 (−51.5; −24.2)%] compared to patients without OF (n = 36) in whom GRP78 levels returned to basal levels [0.6 (−28.1; 26.6)%; p &lt; 0.01]. H24-CPB ATF6 and CHOP expressions were lower in patients with OF than in patients without OF [2.3 (1.3–3.1) vs. 3.0 (2.7–3.7), p &lt; 0.05 and 1.3 (0.9–2.0) vs. 2.2 (1.7–2.9), p &lt; 0.05, respectively].Conclusions: Low relative levels of GRP78 and weak UPR gene expression appeared associated with postoperative OF. Further studies are needed to understand ERS implication during acute organ failure in humans.

scholarly journals Huaier Extract Attenuates Acute Kidney Injury to Chronic Kidney Disease Transition by Inhibiting Endoplasmic Reticulum Stress and Apoptosis via miR-1271 Upregulation

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Jing-Ying Zhao ◽  
Yu-Bin Wu
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury

Endoplasmic reticulum stress (ERS) is strongly associated with acute kidney injury (AKI) to chronic kidney disease (CKD) transition. Huaier extract (HE) protects against kidney injury; albeit, the underlying mechanism is unknown. We hypothesized that HE reduces kidney injury by inhibiting ERS. In this study, using an AKI-CKD mouse model of ischemia-reperfusion injury (IRI), we evaluated the effect of HE on AKI-CKD transition. We also explored the underlying molecular mechanisms in this animal model and in the HK-2 human kidney cell line. The results showed that HE treatment improved the renal function, demonstrated by a significant decrease in serum creatinine levels after IRI. HE appreciably reduced the degree of kidney injury and fibrosis and restored the expression of the microRNA miR-1271 after IRI. Furthermore, HE reduced the expression of ERS markers glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) and inhibited apoptosis in the IRI group. This in vivo effect was supported by in vitro results in which HE inhibited apoptosis and decreased the expression of CHOP and GRP78 induced by ERS. We demonstrated that CHOP is a target of miR-1271. In conclusion, HE reduces kidney injury, probably by inhibiting apoptosis and decreasing the expression of GRP78 and CHOP via miR-1271 upregulation.

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