Differential expression of neuropeptide Y Y1 receptors during pulpal inflammation

Rethnam, Sivakami; Raju, Bina; Fristad, Inge; Berggreen, Ellen; Heyeraas, Karin J.

doi:10.1111/j.1365-2591.2010.01704.x

Cited by 12 publications

(6 citation statements)

References 31 publications

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“…Neuropeptide‐Y1R is a multifunctional receptor with previously reported effects such as vasoconstriction, vascular permeability, nociception, and immune modulation (25, 26, 57, 58). Our results substantiate previous studies indicating that NPY‐Y1R is a major modulator of immune/inflammatory responses (59, 60). Effective migration of innate immune cells depends on cytoskeleton remodeling (61), and recent studies demonstrated that MAPK phosphorylation activates this remodeling (62).…”

Section: Discussionsupporting

confidence: 92%

Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T _h 2 polarization

et al. 2014

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Neuropeptide Y (NPY), a major autonomic nervous system and stress mediator, is emerging as an important regulator of inflammation, implicated in autoimmunity, asthma, atherosclerosis, and cancer. Yet the role of NPY in regulating phenotype and functions of dendritic cells (DCs), the professional antigen-presenting cells, remains undefined. Here we investigated whether NPY could induce DCs to migrate, mature, and polarize naive T lymphocytes. We found that NPY induced a dose-dependent migration of human monocyte-derived immature DCs through the engagement of NPY Y1 receptor and the activation of ERK and p38 mitogen-activated protein kinases. NPY promoted DC adhesion to endothelial cells and transendothelial migration. It failed to induce phenotypic DC maturation, whereas it conferred a T helper 2 (Th2) polarizing profile to DCs through the up-regulation of interleukin (IL)-6 and IL-10 production. Thus, during an immune/inflammatory response NPY may exert proinflammatory effects through the recruitment of immature DCs, but it may exert antiinflammatory effects by promoting a Th2 polarization. Locally, at inflammatory sites, cell recruitment could be amplified in conditions of intense acute, chronic, or cold stress. Thus, altered or amplified signaling through the NPY-NPY-Y1 receptor-DC axis may have implications for the development of inflammatory conditions.-Buttari, B., Profumo, E., Domenici, G., Tagliani, A., Ippoliti, F., Bonini, S., Businaro, R., Elenkov, I., Riganò, R. Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a Th2 polarization.

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Section: Discussionsupporting

confidence: 92%

Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T _h 2 polarization

et al. 2014

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“…Y1R has also been reported to be involved in many physiological activities, such as mitogenic activity, macrophage migration, and pulpal development ( 17 , 21 , 22 ). In bone tissue, Y1R is highly expressed in BMSCs, osteoblast, osteocyte, monocyte/macrophage, and osteoclast ( 2 ), prompting it to play a regulatory role in the local area.…”

Section: Neuropeptide Y and Its Receptorsmentioning

confidence: 99%

The Role of NPY in the Regulation of Bone Metabolism

Chen

Zhang

2022

Front. Endocrinol.

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Bone diseases are the leading causes of disability and severely compromised quality of life. Neuropeptide Y (NPY) is a multifunctional neuropeptide that participates in various physiological and pathological processes and exists in both the nerve system and bone tissue. In bone tissue, it actively participates in bone metabolism and disease progression through its receptors. Previous studies have focused on the opposite effects of NPY on bone formation and resorption through paracrine modes. In this review, we present a brief overview of the progress made in this research field in recent times in order to provide reference for further understanding the regulatory mechanism of bone physiology and pathological metabolism.

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“…In line, enrichment for Biological Process revealed "leukocyte mediated immunity", "neutrophil mediated immunity" and "neutrophil activation". Together, these analysis are indicative of ongoing activation and neutrophil degranulation, and supportive of the observed subclinical pulpal inflammation 9 , enhanced emigration of neutrophils into the inflamed pulp 10,11 and increased numbers of degranulated neutrophils in periodontitis patients 14 . It is thus likely that "neutrophil degranulation" is a confounding element of the salivary protein signature of MIH patients, reflecting ongoing inflammation.…”

Section: Discussionmentioning

confidence: 57%

Saliva proteomic patterns in patients with molar incisor hypomineralization

Bekes

Mitulović

Meißner³

et al. 2020

Sci Rep

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Molar incisor hypomineralization (MiH) is an endemic pediatric disease with an unclear pathogenesis. considering that saliva controls enamel remineralization and that MiH is associated with higher saliva flow rate, we hypothesized that the protein composition of saliva is linked to disease. To test this, we enrolled 5 children aged 6-14 years with MIH showing at least one hypersensitive molar and 5 cariesfree children without hypomineralization. Saliva samples were subjected to proteomic analysis followed by protein classification in to biological pathways. Among 618 salivary proteins identified with high confidence, 88 proteins were identified exclusively in MIH patients and 16 proteins in healthy controls only. Biological pathway analysis classified these 88 patient-only proteins to neutrophil-mediated adaptive immunity, the activation of the classical pathway of complement activation, extracellular matrix degradation, heme scavenging as well as glutathione-and drug metabolism. The 16 controlsonly proteins were associated with adaptive immunity related to platelet degranulation and the lysosome. This report suggests that the proteaneous composition of saliva is affected in MIH patients, reflecting a catabolic environment which is linked to inflammation. The term molar incisor hypomineralization (MIH) was coined in 2001 and defines a qualitative enamel defect affecting one or more first permanent molars with or without the involvement of permanent incisors 1. The global prevalence of MIH exceeds one-tenth of children, ranging from 0.5% to 40.2% and differing between countries 2. Demarcated hypomineralized enamel lesions are caused by the process of amelogenesis being altered or interrupted 3. Compared to normal teeth, affected enamel is characterized by a reduction in mineral quantity and quality, increased porosity and reduced hardness 4. The clinical management of MIH is challenging because of rapid wear, progressing enamel loss, increased susceptibility to caries, loss of fillings, and severe hypersensitivity 5. Although MIH is a pandemic pediatric disease, the etiology remains unknown 6. Several hypotheses are proposed, including childhood illness, genetic influences 7,8 , and a putative individual threshold of susceptibility 3. Thus, there is an increasing demand to better understand the cause and consequence(s) of MIH at the cellular and molecular level. Chronic subclinical pulpal inflammation is a consequence of increased enamel porosity and reduced hardness in MIH 9. Pulpitis is characterized by enhanced neutrophil emigration into the pulp tissue 10,11 and biomarkers can be identified in gingival crevicular fluid 12. Moreover, in periodontitis patients, neutrophils constantly migrate through the oral epithelia into the saliva 13 , with increasing numbers exhibiting apoptosis and augmented levels of degranulation markers 14. Further, saliva of MIH patients reportedly displays altered physicochemical properties such as altered flow rates, viscosity, pH and acid buffering capacity 15. Thus, it is conceivabl...

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Differential expression of neuropeptide Y Y1 receptors during pulpal inflammation

Abstract: This study gives evidence that Y1R is a modulator of pulpal inflammation.

Cited by 12 publications

References 31 publications

Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T _h 2 polarization

Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T _h 2 polarization

The Role of NPY in the Regulation of Bone Metabolism

Saliva proteomic patterns in patients with molar incisor hypomineralization

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Differential expression of neuropeptide Y Y1 receptors during pulpal inflammation

Abstract: This study gives evidence that Y1R is a modulator of pulpal inflammation.

Cited by 12 publications

References 31 publications

Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T h 2 polarization

Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T h 2 polarization

The Role of NPY in the Regulation of Bone Metabolism

Saliva proteomic patterns in patients with molar incisor hypomineralization

Contact Info

Product

Resources

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Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T _h 2 polarization

Neuropeptide Y induces potent migration of human immature dendritic cells and promotes a T _h 2 polarization