Immunoreactive neuropeptide Y (NPY) in plasma and platelets of rat and mouse strains and human volunteers

Myers, Adam K.; Duarte, Armida P. Torres; Zukowska‐Grojec, Zofia

doi:10.1016/0167-0115(93)90391-k

Cited by 21 publications

(17 citation statements)

References 14 publications

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“…Similar to NPY, chronic stress increased plasma NPY-ir levels not only in plasma but also in the platelet fraction; interestingly, angioplasty alone was already a powerful stimulus for activating NPY release from the sympathetic nerves (elevated plasma levels) and platelets (changes in PRP). Although the relevance of these findings to humans, who reportedly do not express platelet NPY, 37 remains unknown, similar association between elevated platelet NPY and propensity for neointima formation has been observed recently by us in several murine strains (Abe et al, unpublished observations, 2005). The notion that expression/induction of platelet NPY is a critical mediator of stress-accelerated atherosclerosis is currently being investigated.…”

Section: Discussionmentioning

confidence: 70%

Chronic Stress Induces Rapid Occlusion of Angioplasty-Injured Rat Carotid Artery by Activating Neuropeptide Y and Its Y1 Receptors

Jönsson‐Rylander

Abe

et al. 2005

ATVB

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Objective-We reported previously that neuropeptide Y (NPY) induces an atherosclerotic-like lesion that is significantly reduced by NPY-Y1 and NPY-Y5 receptor (R) inhibitors. Because antagonists also inhibit neointima induced by angioplasty alone, we now test whether stress-induced endogenous NPY release mimic these changes. Methods and Results-Rats were nonstressed or stressed (4°C water; 2 hours per day for 14 days) starting immediately before and continuing after carotid artery angioplasty. Stress acutely and chronically increased blood pressure and doubled plasma NPY levels. After 14 days, angioplasty-induced neointima was markedly greater in stressed (than nonstressed) rats, in which most of the vessels became occluded with an atherosclerotic-like lesion containing macrophages, lipids, thrombus, and microvessels that was similar but more inflammatory than the injury in the NPY-treated vessels. Fourteen days after angioplasty combined with stress or NPY, Y1R and Y5R (mRNA and protein) became upregulated in areas of neointima, microvessels, and macrophages in injured carotid arteries. Stress-and NPY-induced changes were completely prevented by a selective Y1R antagonist (0.02 mol/kg per minute for 14 days), whereas neointima induced by angioplasty alone was reduced by 60%. Conclusions-Because of sympathetic NPY release, stress may be a less-than-appreciated risk factor for restenosis/atherosclerosis, and Y1R antagonists a potential therapy for these conditions. (Arterioscler Thromb Vasc

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Section: Discussionmentioning

confidence: 70%

Chronic Stress Induces Rapid Occlusion of Angioplasty-Injured Rat Carotid Artery by Activating Neuropeptide Y and Its Y1 Receptors

Jönsson‐Rylander

Abe

et al. 2005

ATVB

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“…NPY, a relatively new substance discovered in human platelets [14], is a linear peptide containing 36 amino acid residues [15] closely related to peptide YY and pancreatic polypeptide (PP). NPY has a wide distribution in the organism and besides in platelets it exists in heart, brain, spleen, peripheral noradrenergic neurones innervating lymphoid tissues, adrenal medulla and bone marrow.…”

Section: Introductionmentioning

confidence: 99%

Expression of platelet P-selectin and detection of soluble P-selectin, NPY and RANTES in patients with inflammatory bowel disease

Fägerstam¹,

Whiss²,

Ström

et al. 2000

Inflamm res.

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Patients with IBD in remission have higher basal platelet surface P-selectin expression. An exaggerated platelet activity with increased expression of platelet P-selectin and release of inflammatory mediators such as RANTES, which is chemotactic and induce chemokine production, could have a reinforcing and aggravating influence on the inflammatory response and increase the susceptibility to IBD. In addition IL-8 has a down-regulating effect on platelet surface P-selectin expression and 5ASA medication seems to lower plasma RANTES. If 5ASA is responsible for lowering the concentration of RANTES this could be one of the beneficial outcomes of 5ASA medication.

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“…In support for this observation, those strains of mice which respond to vascular injury with increased neointimal growth [45] also have genetic expression of NPY in megakaryocytes and platelets while those strains that respond with minimal remodeling, do not [46]. Whether or not this is merely a rodent phenomenon is not certain, as healthy humans do not appear to express NPY in platelets [46]. If NPY is inducible in human platelets, for instance during stress or disease states, targeting NPY production in platelets could prove to be a viable option for treatment.…”

Section: Neointimal Hyperplasia and Athero-sclerosismentioning

confidence: 56%

“…Russell Ross and colleagues hypothesized that platelet activation is an early, yet crucial factor in atherosclerosis progression [37][38][39][40], and since, this has been well documented in numerous studies [41][42][43][44]. In support for this observation, those strains of mice which respond to vascular injury with increased neointimal growth [45] also have genetic expression of NPY in megakaryocytes and platelets while those strains that respond with minimal remodeling, do not [46]. Whether or not this is merely a rodent phenomenon is not certain, as healthy humans do not appear to express NPY in platelets [46].…”

Section: Neointimal Hyperplasia and Athero-sclerosismentioning

confidence: 62%

NPY and NPY Receptors in Vascular Remodeling

Abe¹,

Tilan²,

Żukowska

2007

CTMC

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Neuropeptide Y (NPY) is a sympathetic neurotransmitter that acts on multiple receptors (Y1-Y6) and exerts a variety of cardiovascular effects. Originally known as a vasoconstrictor acting on Y1 receptors, NPY is also a potent angiogenic factor as well as a powerful stimulator of vascular smooth muscle proliferation and atherogenesis in vitro and in vivo. These two types of vascular remodeling are predominantly mediated by Y2/Y5 and Y1 receptors respectively, but evidence suggests that all receptors are activated in both conditions. A strategy to inhibit neointima formation and atherosclerotic lesions without impairing ischemic angiogenesis and collateral vessel formation has been a major challenge to overcome. Studies in rodents show that Y1 receptor antagonist inhibits angioplasty-induced atherosclerotic-like vascular remodeling, without affecting ischemic revascularization. Conversely, Y2 receptor activation appears to be sufficient to stimulate angiogenesis in various animal models. Thus, the use of selective receptor agonists to promote angiogenesis through the Y2 receptor while antagonizing the pro-atherosclerotic and pro-stenotic effects with Y1 receptor-selective antagonists may help to successfully treat vascular remodeling in cardiovascular diseases.

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Immunoreactive neuropeptide Y (NPY) in plasma and platelets of rat and mouse strains and human volunteers

Cited by 21 publications

References 14 publications

Chronic Stress Induces Rapid Occlusion of Angioplasty-Injured Rat Carotid Artery by Activating Neuropeptide Y and Its Y1 Receptors

Chronic Stress Induces Rapid Occlusion of Angioplasty-Injured Rat Carotid Artery by Activating Neuropeptide Y and Its Y1 Receptors

Expression of platelet P-selectin and detection of soluble P-selectin, NPY and RANTES in patients with inflammatory bowel disease

NPY and NPY Receptors in Vascular Remodeling

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