Erythropoietin protects against cisplatin-induced nephrotoxicity by attenuating endoplasmic reticulum stress-induced apoptosis

Kong, Deyang; Li, Zhuo; Gao, Changlu; Shi, Suozhu; Wang, Nan; Huang, Zhiyong; Li, Wenge; Hao, Lirong

doi:10.5301/jn.5000177

Cited by 52 publications

(31 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ER stress pathway has been implicated to play an important role in CP-induced apoptosis. 34,35 In cells, ER dysfunction can trigger ER stress, resulting in the accumulation and aggregation of unfolded proteins in ER lumen, and prolonged ER stress will initiate the apoptotic pathway. 14,15 Three ER transmembrane receptors including PERK, inositol-requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6) regulate the complicated network of physiological responses to ER stress.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate protects against cisplatin-induced nephrotoxicity by inhibiting endoplasmic reticulum stress-induced apoptosis

Chen

Zou

et al. 2015

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Cisplatin (CP)-induced nephrotoxicity hampers its application in clinic. Green tea, particularly its predominant polyphenolic constituent epigallocatechin-3-gallate (EGCG), possesses anti-inflammatory, antioxidant, and anti-apoptotic properties. The present study was designed to investigate the protective effects of EGCG against CP-induced nephrotoxicity in mice. Male C57/BL6 mice in different groups received single injection of CP (20 mg/kg) and EGCG (100 mg/kg) in various sets and kidney tissues and blood were collected after killing. Then, samples were used for biochemical and immunohistochemical assay. Our results showed EGCG decreased biochemical factors and immunohistochemical damage induced by CP. Besides, expression of phosphorylatedextracellular signal-regulated kinase (p-ERK), glucose-regulated protein 78 (GRP78), caspase-12, and apoptosis of kidney were decreased by EGCG via inhibition of endoplasmic reticulum (ER) stress-induced apoptosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-gallate protects against cisplatin-induced nephrotoxicity by inhibiting endoplasmic reticulum stress-induced apoptosis

Chen

Zou

et al. 2015

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

show abstract

“…Injection of recombinant human erythropoietin (rHuEPO) was shown to enhance the recovery from cisplatin-induced acute kidney injury (AKI) in rats by relieving renal functional impairment and exerting significant anti-apoptotic effects. However, rHuEPO inhibited cisplatin-induced AKI through a mechanism possibly involving phosphatidylinositol-3 kinase̸Akt activation and inhibition of ER stress-mediated apoptosis (29).…”

Section: Er Stress Is Involved In Cisplatin-induced Cell Death and Ismentioning

confidence: 99%

A new strategy of promoting cisplatin chemotherapeutic efficiency by targeting endoplasmic reticulum stress

Wang

2013

Molecular and Clinical Oncology

View full text Add to dashboard Cite

Abstract. Cisplatin (cis-diamminedichloroplatinum II, CDDP) is one of the most effective chemotherapeutic agents and is widely used in the treatment of solid tumors. However, its side effects and acquired resistance gained during the course of treatment may limit its usage. It is generally considered to be a cytotoxic drug that kills cancer cells by damaging their DNA and inhibiting DNA synthesis to induce apoptosis via the mitochondrial death pathway or through plasma membrane disruption, triggering the Fas death receptor pathway. The endoplasmic reticulum (ER) is one of the most important protein-folding compartments within the cell and an intracellular Ca 2+ storage organelle. The ER contains a number of molecular chaperones, which may play an important role in determining cellular sensitivity to ER stress and apoptosis. The aim of this review was to summarize our current understanding regarding the mechanisms of ER stress response by which cisplatin induces cell death and the basis for cisplatin resistance. Various aspects were addressed, including the two-way regulation of ER stress, the involvement of ER stress in cisplatin-induced cell death and drug resistance and the drugs enhancing cisplatin-induced cell death by interfering with ER stress. An understanding of how ER stress signaling pathways regulate cisplatin-induced cell death may enable the development of more effective therapeutic strategies for the treatment of cancer.

show abstract

“…All these abnormalities were reversed by EPO administration (7). Moreover, administration of rhEPO (5000 U/kg) 15 minutes and 2 days before and 2 days after cisplatin administration was effective for inhibiting the cisplatininduced nephrotoxicity by a possible mechanism involving activation of the PI3K/Akt pathway, which is involved in endoplasmic reticulum stress-mediated apoptosis (18). Rjiba-Touati et al demonstrated that pre-administration, co-administration or even post-administration of rhEPO especially in cases of pretreatment with EPO protected the rats against cisplatin-induced renal OS and nephrotoxicity via reduction of malondialdehyde and protein carbonyl levels and prevention of glutathione depletion (19).…”

Section: Epo and Nephrotoxicity Induced By Cisplatinmentioning

confidence: 86%

“…However, it has several side effects such as nephrotoxicity or AKI. Furthermore, the clinical administration of cisplatin is limited due to the increase of dose-dependent nephrotoxicity in about thirty percent of patients (18). In an experimental study by Mohamed et al, 60 rats were divided into three groups including control group (normal saline), cisplatin group (9.0 mg/ kg) and EPO/cisplatin group (100 IU/kg/d).…”

Section: Epo and Nephrotoxicity Induced By Cisplatinmentioning

confidence: 99%

Beyond hematopoietic property; administration of erythropoietin for nephroprotection

Bahadorimonfared¹,

Alirezaei²,

Zare³

et al. 2017

J Renal Inj Prev

View full text Add to dashboard Cite

This review paper showed that erythropoietin (EPO) is suitable as a nephroprotective agent. The nephroprotective efficacy of EPO is associated with its direct and indirect antioxidant properties. The activities of EPO are mediated by binding to EPO-receptor and the positive role of EPO in the kidney is related to presence of functional EPO-receptor in renal mesangial cells and renal tubular epithelial cells. These findings revealed an association between administration of EPO and reduction of renal injuries, induced by cisplatin, gentamicin, rhabdomyolysis, vancomycin and amikacin in rats and renal ischemia/reperfusion injury (IRI) as one of the most common causes of acute kidney injury. Previous studies and this review showed the encouraging results on potential therapeutic impact of EPO in acute kidney injury. Acute kidney injury (AKI) is defined as an abrupt or rapid decline in renal filtration function. Erythropoietin (EPO) as a hematopoietic and multifunctional hormone is produced primarily by kidney. Many investigations have shown that EPO as an antioxidant agent has shown several effects such as anti-apoptotic, antioxidant, and anti-inflammatory and also angiogenic activities. The biological activities of EPO are mediated by binding to its receptor (EPOR). The potential role of EPO in kidney is related to the presence of functional EPOR in renal mesangial cells, tubular epithelial cells and the glomerulus. Antioxidants and reactive oxygen species (ROS) scavengers such as EPO, can protect the kidneys against conditions that induce nephrotoxicity. Most studies in the field of renoprotective effects of EPO have focused on AKI models. In this paper we sought to review the ameliorative effects of EPO against various agents or conditions that induce nephrotoxicity including ischemia/reperfusion injury (IRI), cisplatin, gentamicin, rhabdomyolysis, amikacin and vancomycin. Please cite this paper as: A R T I C L E I N F O Keywords: Erythropoietin Review A B S T R A C T ReviewIntroduction Erythropoietin (EPO) is a glycoprotein and cytoprotective multifunctional hormone. More than 90% of systemic EPO is produced primarily by peritubular interstitial fibroblasts in renal cortex and outer medulla of the kidney in adults and is secreted in order to increase the rate of production of red blood cells in the bone marrow by stimulating the proliferation of erythroid progenitors and precursors, in response to hypoxia in the renal tissues

show abstract

Erythropoietin protects against cisplatin-induced nephrotoxicity by attenuating endoplasmic reticulum stress-induced apoptosis

Cited by 52 publications

References 0 publications

Epigallocatechin-3-gallate protects against cisplatin-induced nephrotoxicity by inhibiting endoplasmic reticulum stress-induced apoptosis

Epigallocatechin-3-gallate protects against cisplatin-induced nephrotoxicity by inhibiting endoplasmic reticulum stress-induced apoptosis

A new strategy of promoting cisplatin chemotherapeutic efficiency by targeting endoplasmic reticulum stress

Beyond hematopoietic property; administration of erythropoietin for nephroprotection

Contact Info

Product

Resources

About