Nod1 and Nod2 Are Expressed in Human and Murine Renal Tubular Epithelial Cells and Participate in Renal Ischemia Reperfusion Injury

Shigeoka, Alana A.; Kambo, Amanpreet; Mathison, John C.; King, Andrew J.; Hall, Wesley F.; Correia, Jean da Silva; Ulevitch, Richard J.; McKay, Dianne B.

doi:10.4049/jimmunol.0903065

Cited by 90 publications

(90 citation statements)

References 61 publications

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“…While these data have to be further investigated, they elicit the question concerning the role of Nod2 in other cell types than monocytes/macrophages, dendritic and epithelial cells. Indeed, Nod2 has been shown to be expressed in neutrophils [93], preadipocytes [94], osteoblasts [95], renal tubular epithelial cells [96],. .…”

Section: Discussionmentioning

confidence: 99%

The protein Nod2: An innate receptor more complex than previously assumed

Lecat

Piette

Legrand-Poels

2010

Biochemical Pharmacology

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Please check your proof carefully and mark all corrections at the appropriate place in the proof (e.g., by using on-screen annotation in the PDF file) or compile them in a separate list.For correction or revision of any artwork, please consult http://www.elsevier.com/artworkinstructions.Any queries or remarks that have arisen during the processing of your manuscript are listed below and highlighted by flags in the proof. Click on the 'Q' link to go to the location in the proof. Location inQuery / Remark: click on the Q link to go article Please insert your reply or correction at the corresponding line in the proof Q1If there are fewer than seven authors, please supply all their names; if there are seven or more authors, please supply the first six authors' names, followed by 'et al.'Thank you for your assistance. Graphical AbstractBiochemical Pharmacology xxx (2010) xxx-xxx pp: xxx-xxx The protein Nod2: An innate receptor more complex than previously assumed

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Section: Discussionmentioning

confidence: 99%

The protein Nod2: An innate receptor more complex than previously assumed

Lecat

Piette

Legrand-Poels

2010

Biochemical Pharmacology

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“…Heterozygous mice were intercrossed to generate homozygous Apoe 2/2 mice bearing combinations of Nod1 +/+ and Nod1 2/2 mice. The genotype for Apoe or Nod1 was confirmed using primers and conditions described in the The Jackson Laboratory Web site or the previous report (17), respectively. All mice were fed a normal chow diet and housed in a specific pathogen-free environment throughout the experiment.…”

Section: Methodsmentioning

confidence: 99%

Activation of an Innate Immune Receptor, Nod1, Accelerates Atherogenesis in Apoe−/− Mice

Kanno

Nishio

Tanaka

et al. 2015

The Journal of Immunology

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Atherosclerosis is essentially a vascular inflammatory process in the presence of an excess amount of lipid. We have recently reported that oral administration of a nucleotide-binding oligomerization domain (Nod)-1 ligand, FK565, induced vascular inflammation in vivo. No studies, however, have proven the association between Nod1 and atherosclerosis in vivo. To investigate a potential role of NOD1 in atherogenesis, we orally administered FK565 to apolipoprotein E knockout (Apoe−/−) mice for 4 wk intermittently and performed quantification of atherosclerotic lesions in aortic roots and aortas, immunohistochemical analyses, and microarray-based gene expression profiling of aortic roots. FK565 administration accelerated the development of atherosclerosis in Apoe−/− mice, and the effect was dependent on Nod1 in non–bone marrow origin cells by bone marrow transplantation experiments. Immunohistochemical studies revealed the increases in the accumulation of macrophages and CD3 T cells within the plaques in aortic roots. Gene expression analyses of aortic roots demonstrated a marked upregulation of the Ccl5 gene during early stage of atherogenesis, and the treatment with Ccl5 antagonist significantly inhibited the acceleration of atherosclerosis in FK565-administered Apoe−/− mice. Additionally, as compared with Apoe−/− mice, Apoe and Nod1 double-knockout mice showed reduced development of atherosclerotic lesions from the early stage as well as their delayed progression and a significant reduction in Ccl5 mRNA levels at 9 wk of age. Data in the present study show that the Nod1 signaling pathway in non–bone marrow-derived cells contributes to the development of atherosclerosis.

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“…Experimental studies have suggested that innate pattern recognition receptors may prime tissue and organ damage during ischemic states (Shigeoka et al, 2007(Shigeoka et al, , 2010Haneklaus et al, 2013). Testicular torsion is characterized by tissue damage and represents a urological emergency (Ringdahl and Teague, 2006), which, when misdiagnosed and inappropriately treated, can lead to male infertility (Antonuccio et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

NLRP3 Inflammasome Involvement in the Organ Damage and Impaired Spermatogenesis Induced by Testicular Ischemia and Reperfusion in Mice

Minutoli

Antonuccio

Irrera

et al. 2015

J Pharmacol Exp Ther

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We investigated the role of the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome during testis ischemia and reperfusion injury (TI/R) in wild-type (WT) and NLRP3 knock-out (KO) mice. WT and KO mice underwent 1 hour testicular ischemia followed by 4 hours and 1 and 7 days of reperfusion or a sham TI/R. Furthermore, two groups of WT mice were treated at the beginning of reperfusion and up to 7 days with two inflammasome inhibitors, BAY 11-7082 (20 mg/kg i.p.) or Brilliant Blue G (45.5 mg/kg i.p.), or vehicle. Animals were killed with a pentobarbital sodium overdose at 4 hours and 1 and 7 days, and bilateral orchidectomies were performed. Biochemical and morphologic studies were carried out in all groups. TI/R in WT mice significantly increased caspase-1 and interleukin (IL)-1b mRNA after 4 hours and IL-18 mRNA at 1 day of reperfusion (P # 0.05). There was also a significant increase in caspase-3 and terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine nick-end labeling-positive cells, marked histologic damage, and altered spermatogenesis in WT mice in both testes after 1 and 7 days of reperfusion. KO TI/R mice, WT TI/R BAY 11-7082, and Brilliant Blue G treated mice showed a significant reduced IL-1b and IL-18 mRNA expression, blunted caspase-1 and -3 expression, minor histologic damages, low terminal deoxynucleotidyl transferase-mediated digoxigenindeoxyuridine nick-end labeling activity, and preserved spermatogenesis. These data suggest that the activation of NLRP3 plays a key role in TI/R, and its inhibition might represent a therapeutic target for the management of patients with unilateral testicular torsion.

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Nod1 and Nod2 Are Expressed in Human and Murine Renal Tubular Epithelial Cells and Participate in Renal Ischemia Reperfusion Injury

Cited by 90 publications

References 61 publications

The protein Nod2: An innate receptor more complex than previously assumed

The protein Nod2: An innate receptor more complex than previously assumed

Activation of an Innate Immune Receptor, Nod1, Accelerates Atherogenesis in Apoe−/− Mice

NLRP3 Inflammasome Involvement in the Organ Damage and Impaired Spermatogenesis Induced by Testicular Ischemia and Reperfusion in Mice

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