Endoplasmic reticulum stress participates in inflammation‐accelerated, lipid‐mediated injury of human glomerular mesangial cells

Yang, Haiping; Cui, Jingjing; Shi, Jing; Yang, Baohui; Wang, Mo; Wu, Daoqi; Zhang, Gaofu; Liu, Wei; Qiu, Li

doi:10.1111/nep.12748

Cited by 10 publications

(7 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, Zofia et al confirmed that podocytes are the major IL‐1β‐secreting cell among kidney cells, and NLRP3 inflammasome activation is main molecular mechanism of maturation and secretion of IL‐1β. In a previous study, we showed that IL‐1β aggravates lipid‐induced podocyte and mesangial cell injury during PNS by disrupting SREBP2‐SCAP‐LDL receptor signalling and inducing endoplasmic reticulum stress This supports the notion that IL‐17A induces podocyte injury by inducing secretion of IL‐1β via activation of the NLRP3 inflammasome. However, the conclusion was mainly confirmed by IL‐17A‐induced podocyte injury model in vitro, and there was still lack of adequate direct reference to clinical kidney diseases.…”

Section: Discussionsupporting

confidence: 73%

Interleukin‐17A participates in podocyte injury by inducing IL‐1β secretion through ROS‐NLRP3 inflammasome‐caspase‐1 pathway

Yan

Yang

et al. 2018

Scand J Immunol

View full text Add to dashboard Cite

Studies show that the Th17/IL-17A axis plays an important role in the pathogenesis of kidney diseases. Previously, we also showed that IL-17A may play a role in the pathogenesis of primary nephrotic syndrome; however, the underlying mechanism(s) is unclear. The aim of this study was to explore the molecular mechanism of IL-17A-inducing podocyte injury in vitro. In this study, the NLRP3 inflammasome activation and the morphology of podocytes were detected by Western blot and immunofluorescence. The results showed that podocytes persistently expressed IL-17A receptor and that NLRP3 inflammasome in these cells was activated upon exposure to IL-17A. Also, activity of caspase-1 and secretion of IL-1β increased in the presence of IL-17A. In addition, IL-17A disrupted podocyte morphology by decreasing expression of podocin and increasing expression of desmin. Blockade of intracellular ROS or inhibition of caspase-1 prevented activation of the NLRP3 inflammasome, thereby restoring podocyte morphology. Taken together, the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1β secretion and contributes to disruption of the kidney's filtration system.

show abstract

Section: Discussionsupporting

confidence: 73%

Interleukin‐17A participates in podocyte injury by inducing IL‐1β secretion through ROS‐NLRP3 inflammasome‐caspase‐1 pathway

Yan

Yang

et al. 2018

Scand J Immunol

View full text Add to dashboard Cite

show abstract

“…Researchers found that lipotoxicity induced ER stress via the protein arginine methyltransferase 1 (PRMT1), which exacerbated MC apoptosis. Interestingly, Yang et al [ 69 ] proved that inflammation accelerates lipid-induced MC injury through ER stress. Hence, strategies to mediate the expression of PRMT1 can be applied to prevent or limit DN.…”

Section: Roles Of Er Stress In Various Renal Cells In Dnmentioning

confidence: 99%

Endoplasmic Reticulum Stress in Diabetic Nephrology: Regulation, Pathological Role, and Therapeutic Potential

Yuan

2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Recent progress has been made in understanding the roles and mechanisms of endoplasmic reticulum (ER) stress in the development and pathogenesis of diabetic nephropathy (DN). Hyperglycemia induces ER stress and apoptosis in renal cells. The induction of ER stress can be cytoprotective or cytotoxic. Experimental treatment of animals with ER stress inhibitors alleviated renal damage. Considering these findings, the normalization of ER stress by pharmacological agents is a promising approach to prevent or arrest DN progression. The current article reviews the mechanisms, roles, and therapeutic aspects of these findings.

show abstract

“…CKD is involved with glomeruli [7, 8], tubules [9, 10], and interstitial tissue around the glomeruli and tubules [11]. CKD often results in glomerular injury because of the destruction of glomerular structure caused by high-level inflammatory cells [12, 13]. The result will prevent blood flow, resulting in the decrease in urine output and accumulation of uremic toxin.…”

Section: Introductionmentioning

confidence: 99%

Cordyceps militarisImproves Chronic Kidney Disease by Affecting TLR4/NF-κB Redox Signaling Pathway

Sun

Dong

Jiang

et al. 2019

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Cordyceps militaris may show good promise in protecting against chronic kidney disease (CKD) but the molecular mechanism remains unclear. CKD risk is associated with the Toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-κB) signaling pathway. Cordycepin is the main component of Cordyceps militaris and may affect the TLR4/NF-κB pathway. Cordycepin was prepared by preparative HPLC. CKD patients were assigned into Cordyceps militaris (COG, 100 mg daily) and placebo (CG) groups. Cordycepin activity was measured using human embryo kidney cells (HEK293T). Biochemical indices, the levels of TLR4, NF-κB, cyclooxygenase-2 (COX2), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), were measured by real-time qRT-PCR, or ELISA kits and or Western blot. After 3-month treatment, cordycepin reduced the levels of urinal protein, blood urea nitrogen (BUN), and creatinine by 36.7%±8.6%, 12.5%±3.2%, and 18.3%±6.6%, respectively (P<0.05). Cordyceps militaris improved lipid profile and redox capacity of CKD patients by reducing the serum levels of TG, TC, and LDL-C by 12.8%±3.6%, 15.7%±4.1%, and 16.5%±4.4% and increasing the HDL-C level by 10.1%±1.4% in the COG group when compared with the CG group, respectively (P<0.05). The serum levels of cystatin-C (Cys-C), myeloperoxidase (MPO), and malondialdehyde (MDA) were reduced by 14.0%±3.8%, 26.9%±12.3%, and 19.7%±7.9% while nitric oxide (NO) and superoxide dismutase (SOD) were increased by 12.5%±2.9% and 25.3%±13.4% in the COG group when compared with the CG group, respectively (P<0.05). Cordycepin reduced the levels of TLR4, NF-κB, COX2, TNF-α, and IL-1β in HEK293T cells too (P<0.05). However, cordycepin could not affect the levels anymore if TLR4 was silenced. Cordyceps militaris protected against CKD progression by affecting the TLR4/NF-κB lipid and redox signaling pathway via cordycepin.

show abstract

Endoplasmic reticulum stress participates in inflammation‐accelerated, lipid‐mediated injury of human glomerular mesangial cells

Abstract: These data provide evidence that ER stress participates in inflammation associated with lipid-induced injury of HMCs. Modulation of ER stress may be a novel therapeutic approach for combating lipid-induced injury of HMCs.

Cited by 10 publications

References 33 publications

Interleukin‐17A participates in podocyte injury by inducing IL‐1β secretion through ROS‐NLRP3 inflammasome‐caspase‐1 pathway

Interleukin‐17A participates in podocyte injury by inducing IL‐1β secretion through ROS‐NLRP3 inflammasome‐caspase‐1 pathway

Endoplasmic Reticulum Stress in Diabetic Nephrology: Regulation, Pathological Role, and Therapeutic Potential

Cordyceps militarisImproves Chronic Kidney Disease by Affecting TLR4/NF-κB Redox Signaling Pathway

Contact Info

Product

Resources

About