Different effects of neuropeptide Y on proliferation of vascular smooth muscle cells via regulation of Geminin

Jiang, Zhendong; Zhou, Yiding; Chen, Xia; LinYu, Li; Liang, Shi-yu; Lin, Shu; Maoqin, Shu

doi:10.1007/s11010-017-3028-7

Cited by 15 publications

(12 citation statements)

References 26 publications

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“…NPY interacts with receptors on endothelial cells, VSMCs, macrophages, and platelets (Li et al, 2011 ), (Racchi et al, 1997 ; Li et al, 2005 ). Under pathological conditions such as vascular endothelium injury, elevations in sympathetic glial-derived and platelet NPY and its receptors have been shown in mammalian (human and animal) studies (Burnstock, 1976 ; Ghersi et al, 2001 ; Li et al, 2003 ; Legein et al, 2013 ; Zhu et al, 2016 ; Jiang et al, 2017 ).…”

Section: Neuropeptide Y As An Important Mediator Of Cardiovascular DImentioning

confidence: 98%

“…Atherosclerosis is one of the leading cardiovascular diseases, with high global mortality rates. It involves complex molecular and cellular responses comprising of inflammation, proliferation, and matrix modification, following endothelial dysfunction which is a critical atherosclerosis-initiating factor (Jiang et al, 2017 ). Endothelial dysfunction enhances endothelium permeability and promotes leukocyte adhesion, lipid aggregation, macrophage-induced foam cell formation and platelet aggregation.…”

Section: Neuropeptide Y As An Important Mediator Of Cardiovascular DImentioning

confidence: 99%

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The Role of Neuropeptide Y in Cardiovascular Health and Disease

et al. 2018

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Neuropeptide Y (NPY) is an abundant sympathetic co-transmitter, widely found in the central and peripheral nervous systems and with diverse roles in multiple physiological processes. In the cardiovascular system it is found in neurons supplying the vasculature, cardiomyocytes and endocardium, and is involved in physiological processes including vasoconstriction, cardiac remodeling, and angiogenesis. It is increasingly also implicated in cardiovascular disease pathogenesis, including hypertension, atherosclerosis, ischemia/infarction, arrhythmia, and heart failure. This review will focus on the physiological and pathogenic role of NPY in the cardiovascular system. After summarizing the NPY receptors which predominantly mediate cardiovascular actions, along with their signaling pathways, individual disease processes will be considered. A thorough understanding of these roles may allow therapeutic targeting of NPY and its receptors.

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Section: Neuropeptide Y As An Important Mediator Of Cardiovascular DImentioning

confidence: 98%

Section: Neuropeptide Y As An Important Mediator Of Cardiovascular DImentioning

confidence: 99%

The Role of Neuropeptide Y in Cardiovascular Health and Disease

et al. 2018

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“…The NPY system also modulates angiogenic activity. NPY promotes the proliferation and migration of vascular epithelial cells and stimulates the growth of vascular smooth muscle ( 92 ). Administration of the Y2 receptor antagonist BIIE 0246 was found to reduce the capillary density of tumor tissues and serum levels of vascular endothelial growth factor (VEGF) ( 93 ); however, the mechanism is not entirely understood.…”

Section: Neuropeptides Of the Sympathetic Nervous System (Sns)mentioning

confidence: 99%

Neuromodulation of bone: Role of different peptides and their interactions (Review)

Wang

Kang

2020

Mol Med Rep

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Our understanding of the skeletal system has been expanded upon the recognition of several neural pathways that serve important roles in bone metabolism and skeletal homeostasis, as bone tissue is richly innervated. Considerable evidence provided by in vitro, animal and human studies have further elucidated the importance of a host of hormones and local factors, including neurotransmitters, in modulating bone metabolism and osteo-chondrogenic differentiation, both peripherally and centrally. Various cells of the musculoskeletal system not only express receptors for these neurotransmitters, but also influence their endogenous levels in the skeleton. As with a number of physiological systems in nature, a neuronal pathway regulating bone turnover will be neutralized by another pathway exerting an opposite effect. These neuropeptides are also critically involved in articular cartilage homeostasis and pathogenesis of degenerative joint disorders, such as osteoarthritis. In the present Review, data on the role of several neuronal populations in nerve-dependent skeletal metabolism is examined, and the molecular events involved are explored, which may reveal broader relationships between two apparently unrelated organs.

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“…NPY has both potent central and peripheral biological effects, including cardiovascular actions, which participate in the development of cardiovascular diseases. There are also reports indicating that NPY receptor existed in VSMCs, and that stimulation of VSMCs with NPY increased VSMC proliferation and migration (8)(9)(10). In hypertension or atherosclerosis, NPY-mediated migration of VSMCs is augmented (11).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of D3 dopamine receptors on neuropeptide Y-induced migration in vascular smooth muscle cells

Xia

Zhou

Luo

et al. 2017

Molecular Medicine Reports

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Abnormal migration of vascular smooth muscle cells (VSMCs) serves an important role in hypertension, atherosclerosis and restenosis following angioplasty, which is regulated numerous hormonal and humoral factors, including neuropeptide Y (NPY) and dopamine. Dopamine and NPY are both sympathetic neurotransmitters, and a previous study reported that NPY increased VSMC proliferation, while dopamine receptor inhibited it. Therefore, the authors wondered whether or not there is an inhibitory effect of dopamine receptor on NPY‑mediated VSMC migration. The present study demonstrated that stimulation with NPY dose‑dependence (10‑10‑10‑7M, 24 h) increased VSMC migration, the stimulatory effect of NPY was via the Y1 receptor. This is because, in the presence of the Y1 receptor antagonist, BIBP3226 (10‑7 M), the stimulatory effect of NPY on VSMC migration was blocked. Activation of the D3 receptor by PD128907 dose‑dependence (10‑11‑10‑8 M) reduced the stimulatory effect of NPY on VSMC migration. The effect of PD128907 was via the D3 receptor, because the inhibitory effect of PD128907 on NPY‑mediated migration was blocked by the D3 receptor antagonist, U99194. The authors' further study suggested that the inhibitory effect of the D3 receptor was via the PKA signaling pathway, in the presence of the PKA inhibitor, 14‑22 (10‑6 M), the inhibitory effect of PD128907 on VSMC migration was blocked. Moreover, the inhibitory effect of PD128907 was imitated by PKA activator, Sp‑cAMP [S], in the presence of Sp‑cAMP [S], the NPY‑mediated stimulatory effect on VSMC migration was abolished. The present study indicated that activation of the D3 receptor inhibits NPY Y1‑mediated migration on VSMCs, PKA is involved in the signaling pathway.

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Different effects of neuropeptide Y on proliferation of vascular smooth muscle cells via regulation of Geminin

Cited by 15 publications

References 26 publications

The Role of Neuropeptide Y in Cardiovascular Health and Disease

The Role of Neuropeptide Y in Cardiovascular Health and Disease

Neuromodulation of bone: Role of different peptides and their interactions (Review)

Inhibitory effect of D3 dopamine receptors on neuropeptide Y-induced migration in vascular smooth muscle cells

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