ArticleArteriosclerosis, thrombosis, and vascular biology2011
Nucleotide-binding oligomerization domain protein 2 deficiency enhances neointimal formation in response to vascular injury.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- NOD1 and NOD2 in inflammatory and infectious diseases.Immunological reviews · 2020Review
- Nucleotide-binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions.The FEBS journal · 2020Article
- Nucleotide-binding oligomerization domain protein 2 attenuates ER stress-induced cell death in vascular smooth muscle cells.BMB reports · 2019Article
- Frontline Science: Targeted expression of a dominant-negative high mobility group A1 transgene improves outcome in sepsis.Journal of leukocyte biology · 2018Article
- NOD2 deficiency exacerbates hypoxia-induced pulmonary hypertension and enhances pulmonary vascular smooth muscle cell proliferation.Oncotarget · 2018Article
- TIPE2 acts as a negative regulator linking NOD2 and inflammatory responses in myocardial ischemia/reperfusion injury.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Elk-3 is a KLF4-regulated gene that modulates the phagocytosis of bacteria by macrophages.Journal of leukocyte biology · 2015Article
- New insights into TRP channels: Interaction with pattern recognition receptors.Channels (Austin, Tex.) · 2014Review
- Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
objectiveNucleotide-binding oligomerization domain protein 2 (NOD2) stimulates diverse inflammatory responses resulting in differential cellular phenotypes. To identify the role of NOD2 in vascular arterial obstructive diseases, we investigated the expression and pathophysiological role of NOD2 in a vascular injury model of neointimal hyperplasia. METHODS AND
resultsWe first analyzed for neointimal hyperplasia following femoral artery injury in NOD2(+/+) and NOD2(-/-) mice. NOD2(-/-) mice showed a 2.86-fold increase in neointimal formation that was mainly composed of smooth muscle (SM) α-actin positive cells. NOD2 was expressed in vascular smooth muscle cells (VSMCs) and NOD2(-/-) VSMCs showed increased cell proliferation in response to mitogenic stimuli, platelet-derived growth factor-BB (PDGF-BB), or fetal bovine serum, compared with NOD2(+/+) VSMCs. Furthermore, NOD2 deficiency markedly promoted VSMCs migration in response to PDGF-BB, and this increased cell migration was attenuated by a phosphatidylinositol 3-kinase inhibitor. However, protein kinase C and c-Jun N-terminal kinase inhibitors exerted negligible effects. Moreover, muramyl dipeptide-stimulated NOD2 prevented PDGF-BB-induced VSMCs migration.
conclusionFunctional NOD2 was found to be expressed in VSMCs, and NOD2 deficiency promoted VSMCs proliferation, migration, and neointimal formation after vascular injury. These results provide evidence for the involvement of NOD2 in vascular homeostasis and tissue injury, serving as a potential molecular target in the modulation of arteriosclerotic vascular disease.
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