Relevance of megalin receptor injury with nuclear factor‐kappa B upregulation in acute kidney injury induced in rats

Elshaer, Shereen Saeid; Anwar, Hend Mohamed

doi:10.1002/jbt.22014

Cited by 5 publications

(3 citation statements)

References 34 publications

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“…Akther et al proved that human leukocytes submitted to oxidative stress had higher TLR 4 expression at the mRNA and protein level [ 31 ]. Similarly, the mRNA of TLR 4 and NF- κ B were overexpressed in Sprague Dawley rats with acute kidney injury aggravated by oxidative stress [ 32 ]. Another important observation in the study by Akther et al was that TLR 4 ligand lipopolysaccharide—that is a pathogen-derived compound—was responsible for the additional increase in receptor expression and depended on the TLR4/MyD88 signaling pathway [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of Toll-Like Receptors in the Animal Model of Bladder Outlet Obstruction

Niemczyk

Fus

Czarzasta

et al. 2020

BioMed Research International

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Introduction. Bladder outlet obstruction (BOO) occurs in more than 20 percent of the adult population and may lead to changes in the structure and function of the bladder. The main objective of the study was to evaluate the expression of Toll-like receptor 4 (TLR 4) and Toll-like receptor 9 (TLR 9) in the animal model of BOO as potential triggers of the inflammation phase in the bladder. In addition, the modulating effect of alpha-1 adrenergic antagonist (tamsulosin) on TLR 4 and TLR 9 expression and inflammatory markers was assessed. Material and Methods. Thirty-two male, 9-week-old Sprague Dawley rats were randomly divided into 4 groups: SOP—sham-operated rats with a placebo (water); SOB—sham-operated rats with an alpha-1 adrenergic antagonist; BOOP—rats with BOO and a placebo; and BOOB—rats with BOO and an alpha-1 adrenergic antagonist. The rats were given a placebo or alpha-1 adrenergic antagonist for 15 days. Next, urine and the bladder were collected from the rats for histopathological and biochemical study. Results. Histopathological analysis showed chronic inflammation without acute inflammation in the bladder. TLR 4 showed positive cytoplasmic reactivity in the urothelium and the smooth muscles of the bladder. TLR 9 showed positive cytoplasmic reactivity only in the urothelium. BOO caused an increase in TLR 4 and TLR 9 expression. Furthermore, treatment with an alpha-1 adrenergic antagonist had no significant effect on TLR 4 and TLR 9 expression in rats with BOO. BOO caused a significant increase in urine concentration of interleukin 6 (IL-6), while alpha-1 antagonist reduced the urine concentration of IL-6 and the concentration of interleukin 18 (IL-18). Conclusions. The results suggest the participation of TLR 4 and TLR 9 receptors in the induction of inflammation in the bladder, which is the first phase in the development of pathophysiological changes in BOO.

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Section: Discussionmentioning

confidence: 99%

Expression of Toll-Like Receptors in the Animal Model of Bladder Outlet Obstruction

Niemczyk

Fus

Czarzasta

et al. 2020

BioMed Research International

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“…As TLR2 activation via Myd88 leads to the nuclear translocation of NF-κB and the expression of genes related to the inflammatory response. 11,27,28 In summary, we have shown that TLR2 plays a critical role in cisplatin-induced AKI. TLR2-deficient mice exacerbated renal injury in cisplatin-induced AKI, with higher serum Cr and BUN, more severe morphological injury compared with that of wild-type mice.…”

Section: Discussionmentioning

confidence: 81%

“…Potentially, NF‐κB signaling will also be affected in this model system. As TLR2 activation via Myd88 leads to the nuclear translocation of NF‐κB and the expression of genes related to the inflammatory response …”

Section: Discussionmentioning

confidence: 99%

TLR2 protects cisplatin‐induced acute kidney injury associated with autophagy via PI3K/Akt signaling pathway

Shen

Zhang

et al. 2018

J of Cellular Biochemistry

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Toll-like receptors (TLRs), which are essential components of the innate immune response, play an important role in acute kidney injury (AKI). Toll-like receptor 2 (TLR2) is constitutively expressed in tubular epithelial cells of the kidney and participates in cisplatin-induced AKI. The autophagy is a dynamic catabolic process that maintains intracellular homeostasis, which is involved in the pathogenesis of AKI. Recent studies demonstrate that PI3K/Akt signaling pathway regulates autophagy in response to various stimuli. Therefore, we propose that cisplatin might activate TLR2, which subsequently phosphorylates PI3K/Akt, leading to enhanced autophagy of renal tubular epithelial cells and protecting cisplatin-induced AKI. We found that TLR2 expression was significantly increased in the kidney after the cisplatin treatment. TLR2deficient mice exacerbated renal injury in cisplatin-induced AKI, with higher serum creatinine and blood urea nitrogen, more severe morphological injury compared with that of wild-type mice. In vitro, we found that inhibition of TLR2 reduced tubular epithelial cell autophagy after the cisplatin treatment.Mechanistically, TLR2 inhibited autophagy via activating PI3K/Akt signaling pathway in renal tubular epithelial cells after the cisplatin treatment. Take together, these results suggest that TLR2 may protect cisplatin-induced AKI by activating autophagy via PI3K/Akt signaling pathway. K E Y W O R D S acute kidney injury, autophagy, cisplatin, TLR2 J Cell Biochem. 2019;120:4366-4374. wileyonlinelibrary.com/journal/jcb 4366 | F I G U R E 6 Activation of TLR2 signaling using Pam3Cys further increases PI3K and Akt phosphorylation of renal tubular epithelial cells after the cisplatin treatment in vitro. A, Representative Western blots showed PI3K/Akt protein and phosphorylation of PI3K/AKT in vehicle or TLR2 agonist Pam3Cys pretreated renal tubular epithelial cells after the cisplatin (10 μg/ml, 6 hours) or sham treatment in vitro. B, Quantitative analysis of the ratio of phosphorylated Akt/total Akt and the ratio of phosphorylated PI3K/total PI3K. *P < 0.05 versus Vehicle Sham; + P < 0.05 versus Pam3Cys Cisplatin; # P < 0.05 versus Vehicle Cisplatin. n = 4 in each group. TLR2, toll-like receptor 2 SHEN ET AL. | 4373 ORCID Manli Li

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Protective effect of eugenol on hepatic inflammation and oxidative stress induced by cadmium in male rats

Kumar

Siddiqi

Al-Rashood

et al. 2021

Biomedicine & Pharmacotherapy

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Relevance of megalin receptor injury with nuclear factor‐kappa B upregulation in acute kidney injury induced in rats

Cited by 5 publications

References 34 publications

Expression of Toll-Like Receptors in the Animal Model of Bladder Outlet Obstruction

Expression of Toll-Like Receptors in the Animal Model of Bladder Outlet Obstruction

TLR2 protects cisplatin‐induced acute kidney injury associated with autophagy via PI3K/Akt signaling pathway

Protective effect of eugenol on hepatic inflammation and oxidative stress induced by cadmium in male rats

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