Induction and localization of NOD2 protein in human endothelial cells

Oh, Hyun-Mee; Lee, Hyunju; Seo, Geom-Seog; Choi, Eun‐Young; Kweon, Seok-Hyun; Chun, Churl Hong; Han, Weon‐Cheol; Lee, Kang‐Min; Lee, Myeung Su; Choi, Suck-Chei; Jun, Chang‐Duk

doi:10.1016/j.cellimm.2005.09.006

Cited by 47 publications

(39 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our study concurs with these observations: in response to the invading microbes, NOD2 loss of function in mice stimulates TLR2 signaling by up-regulation of TRAF6 and JNK3, leading to the production of NF-κB and resulting in the overexpression of serum cytokines, which play an important role in alveolar bone resorption in periodontitis and atherosclerosis. The elevated levels of cytokines further substantiate the role of NOD2 in modulating the P. gingivalis effects in this murine periodontitis model and atherosclerosis, especially knowing that NOD2 is expressed in gingival, pulp and periodontal fibroblasts, oral epithelial cells, and vascular endothelial cells (20,(22)(23)(24)(25). Surprisingly, IL-10, an antiinflammatory and antiatherogenic cytokine produced by macrophages, Th1, and B cells, was also significantly elevated in NOD2-deficent mice.…”

Section: Discussionmentioning

confidence: 79%

See 1 more Smart Citation

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Yuan¹,

Zelkha²,

Burkatovskaya³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Significance Apolipoprotein E −/− (ApoE −/− ) mice deficient in nucleotide binding oligomerization domain-containing protein 2 (NOD2) and subjected to an oral gavage of Porphyromonas gingivalis developed elevated serum inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis. Stimulation of NOD2 by Muramyl DiPeptide (MDP) in ApoE −/− mice reduced P. gingivalis -induced inflammatory cytokines, cholesterol, alveolar bone loss, and atherosclerosis by reducing the expression of inhibitor of NF-κB kinase-β, NF-κB, JNK mRNA, and TNF-α protein levels. A reduction in body weight gain was observed in ApoE −/− mice fed a high-fat diet (HFD) and injected with MDP compared to ApoE −/− mice fed a HFD but saline injected. MDP activation of NOD2 should be considered in the treatment of inflammatory processes affecting atherosclerosis, bone loss, and possibly, weight gain.

show abstract

Section: Discussionmentioning

confidence: 79%

“…NOD2 expression and unique functions have also been described in other cell types, including adipocytes, gingival, pulp and periodontal fibroblasts, oral epithelial cells, and vascular endothelial cells (20)(21)(22)(23)(24)(25). However, the precise role of NOD2 in chronic inflammatory diseases remains unclear.…”

Section: Apoementioning

confidence: 99%

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Yuan¹,

Zelkha²,

Burkatovskaya³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…In addition, it has been observed that a synergistic effect of lipopeptide Pam 3 CS(K) 4 and MDP in wild-type mice is absent in mouse macrophages deficient in NOD2. Also, down regulation of NOD2 in vascular endothelial cells by interfering RNA reduced synergistic effects (31). Thus, these studies indicate that the NOD proteins are involved in the apparently synergistic effect of muropeptides with LPS.…”

Section: Discussionmentioning

confidence: 74%

Modification of the Structure of Peptidoglycan Is a Strategy To Avoid Detection by Nucleotide-Binding Oligomerization Domain Protein 1

2007

View full text Add to dashboard Cite

Nucleotide-binding oligomerization domain (NOD) protein 1 (NOD1) and NOD2 are pathogen recognition receptors that sense breakdown products of peptidoglycan (PGN) (muropeptides). It is shown that a number of these muropeptides can induce tumor necrosis factor alpha (TNF-␣) gene expression without significant TNF-␣ translation. This translation block is lifted when the muropeptides are coincubated with lipopolysaccharide (LPS), thereby accounting for an apparently synergistic effect of the muropeptides with LPS on TNF-␣ protein production. The compounds that induced synergistic effects were also able to activate NF-B in a NOD1-or NOD2-dependent manner, implicating these proteins in synergistic TNF-␣ secretion. It was found that a diaminopimelic acid (DAP)-containing muramyl tetrapeptide could activate NF-B in a NOD1-dependent manner, demonstrating that an exposed DAP is not essential for NOD1 sensing. The activity was lost when the ␣-carboxylic acid of iso-glutamic acid was modified as an amide. However, agonists of NOD2, such as muramyl dipeptide and lysine-containing muramyl tripeptides, were not affected by amidation of the ␣-carboxylic acid of iso-glutamic acid. Many pathogens modify the ␣-carboxylic acid of iso-glutamic acid of PGN, and thus it appears this is a strategy to avoid recognition by the host innate immune system. This type of immune evasion is in particular relevant for NOD1.The ability to rapidly recognize microbial components and respond by initiating an acute inflammatory response is a crucial first line of defense against a microbial challenge. Overactivation of this inflammatory response can, however, lead to the clinical symptoms of septic shock and results in 100,000 deaths annually in the United States (33, 34). It has been estimated that 1% of hospitalized patients and 20 to 30% of patients in intensive care units develop sepsis. The advent of new antimicrobial resistance patterns, the increasing use of chemotherapeutic agents, and the emergence of diseases characterized by immunosuppression have caused the incidence of septic shock to increase dramatically.Lipopolysaccharide (LPS), peptidoglycan (PGN), and lipoteichoic acid are three principal bacterial cell wall components implicated in inducing the clinical manifestations of septic shock (47). These components exert their biological effects by stimulating the host's monocytes and macrophages to produce proinflammatory mediators, such as tumor necrosis factor alpha (TNF-␣), interleukin-1 (IL-1), and IL-6. These mediators in turn elicit a variety of inflammatory responses in the host.LPS, a vital component of the outer leaflet of the gramnegative bacterial outer membrane, comprises three structural units: an outer polysaccharide component, a core oligosaccharide region, and the innermost portion, lipid A (5, 32). The lipid A region is largely responsible for the proinflammatory activity of LPS and generally consists of a hexa-acylated bis-1,4Ј-phosphorylated glucosamine disaccharide. The results of recent studies indicate that the lipid ...

show abstract

“…gcNOD1 0 1 2 2 2 2 2 2 2 2 zfNOD1 0 1 2 2 2 2 2 2 2 2 hNOD1 0 1 2 2 2 2 2 2 2 2 gcNOD2 0 1 2 2 2 2 2 2 2 zfNOD2 0 1 2 2 2 2 2 2 2 hNOD2 0 1 2 2 2 2 2 2 2 mesodiaminopimelic-acid-containing peptidoglycan, which is found in most Gram-negative, but not Gram-positive bacteria [11]. In mammals, the bacterial component, LPS, has been shown to influence NOD1 and NOD2 mRNA expression in immune, epithelial and endothelial cells [23][24][25]. We further assessed the influence of LPS on the expression of gcNOD1 and gcNOD2 and found that the induced expression patterns of gcNOD1 were similar with that of gcNOD2 in all four tissues analyzed.…”

Section: Tablementioning

confidence: 99%

Molecular characterization and expression analysis of nuclear oligomerization domain proteins NOD1 and NOD2 in grass carp Ctenopharyngodon idella

Chen

Chang

et al. 2010

Fish & Shellfish Immunology

View full text Add to dashboard Cite

Induction and localization of NOD2 protein in human endothelial cells

Cited by 47 publications

References 34 publications

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss

Modification of the Structure of Peptidoglycan Is a Strategy To Avoid Detection by Nucleotide-Binding Oligomerization Domain Protein 1

Molecular characterization and expression analysis of nuclear oligomerization domain proteins NOD1 and NOD2 in grass carp Ctenopharyngodon idella

Contact Info

Product

Resources

About