Effect of Somatostatin and Octreotide on Proliferation and Vascular Endothelial Growth Factor Secretion from Murine Endothelial Cell Line (HECa10) Culture

Ławnicka, Hanna; Stępień, H; Wyczółkowska, J; Kolago, B; Kunert‐Radek, Jolanta; Komorowski, Jan

doi:10.1006/bbrc.2000.2119

Cited by 50 publications

(40 citation statements)

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“…Stimulation of SSTRs blocks angiogenesis in several model systems (22)(23)(24) and may also have a direct antiproliferative effect on human retinal endothelial cells …”

Section: Diabetes Care 25:2282-2286 2002mentioning

confidence: 99%

“…Furthermore, SSTRs are also expressed in the retina, with SSTR1 and -2 being the most widely expressed (15,18 -21). The production of both somatostatin and its receptors simultaneously suggests an autocrine action in the human retina (18 -20).Stimulation of SSTRs blocks angiogenesis in several model systems (22)(23)(24) and may also have a direct antiproliferative effect on human retinal endothelial cells …”

mentioning

confidence: 99%

“…Stimulation of SSTRs blocks angiogenesis in several model systems (22)(23)(24) and may also have a direct antiproliferative effect on human retinal endothelial cells (12). In addition, it has been demonstrated that somatostatin analogs reduce neovascularization in diabetic retinopathy (5-7,9) and in experimental ischemiainduced retinopathy (25).…”

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confidence: 99%

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Deficit of Somatostatin-Like Immunoreactivity in the Vitreous Fluid of Diabetic Patients

et al. 2002

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OBJECTIVE -To evaluate the vitreous levels of somatostatin-like immunoreactivity (SLI) in patients with proliferative diabetic retinopathy (PDR). RESEARCH DESIGN AND METHODS-A total of 14 diabetic patients with PDR, in whom a vitrectomy was performed, were included in the study. Sixteen nondiabetic patients, with other conditions requiring vitrectomy, served as a control group. Both venous blood and vitreous samples were collected at the time of vitreoretinal surgery. Patients in whom intravitreous hemoglobin was detectable were excluded. In addition, a correction for plasma levels of SLI and intravitreal proteins was performed. SLI was measured by radioimmunoassay and vitreous hemoglobin by spectrophotometry.RESULTS -SLI in the vitreous fluid was significantly lower in diabetic patients than in the control group (68 Ϯ 18.7 vs. 193.6 Ϯ 30.8 pg/ml, P Ͻ 0.01). The vitreous SLI-to-plasma SLI ratio was strikingly higher in nondiabetic subjects than in diabetic patients with PDR (5.3 [1.2-71.1] vs. 0.6 [0.03-4.1], P Ͻ 0.01). After correcting for total vitreous protein concentration, SLI (pg/mg of proteins) remained significantly higher in nondiabetic control subjects than in diabetic patients with , P Ͻ 0.0001). Remarkably, intravitreous levels of SLI were higher than those obtained in plasma in nondiabetic control subjects (193.6 Ϯ 30.8 vs. 43.5 Ϯ 10.7 pg/ml, P Ͻ 0.0001). Finally, a lack of relationship between plasma and vitreous levels of SLI was observed in both diabetic patients with PDR and nondiabetic control subjects.CONCLUSIONS -The significantly higher SLI in the vitreous fluid than in plasma detected in nondiabetic control subjects supports the concept that somatostatin plays a relevant role in retinal homeostasis. In addition, the intravitreous deficit of SLI observed in diabetic patients with PDR suggests that it might contribute to the process of retinal neovascularization. Diabetes Care 25:2282-2286, 2002S omatostatin is a peptide that was originally identified as the hypothalamic factor responsible for inhibition of the release of growth hormone (GH) from the anterior pituitary (1). Subsequent studies have shown that somatostatin has a much broader spectrum of inhibitory actions and that it is much more widely distributed in the body, occurring not only in many regions of the central nervous system but also in many tissues of the digestive tract, including the stomach, intestine, and pancreas (2). Somatostatin-14 and -28 are the two principal bioactive products cleaved from the COOH-terminus of prosomatostatin in different cells and the main circulating forms of somatostatin (2,3). Somatostatin-13, converted from somatostatin-14 by the action of tissue aminopeptidases, is also present in plasma as prosomatostatin, and collectively all of these peptides contribute to the measurement of somatostatin-like immunoreactivity (SLI) (3). Somatostatin mediates its multiple biologic effects via specific plasma membrane receptors that belong to the family of G-protein-coupled receptors having seven transmembrane...

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“…Stimulation of SSTRs blocks angiogenesis in several model systems (22)(23)(24) and may also have a direct antiproliferative effect on human retinal endothelial cells …”

Section: Diabetes Care 25:2282-2286 2002mentioning

confidence: 99%

mentioning

confidence: 99%

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Deficit of Somatostatin-Like Immunoreactivity in the Vitreous Fluid of Diabetic Patients

et al. 2002

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“…[102,103] Four VEGF forms are individuated and examined: VEGF-A, VEGF-B, VEGF-C, and VEGF-D, [104][105][106][107][108] with a different affinity to their three own receptors. [109][110][111][112][113] [ Figure 1] For these reasons, the interest of angiogenesis inhibition was encouraged.…”

Section: Vegf and Its Receptor Inhibitorsmentioning

confidence: 99%

Medical therapy for advanced gastro-entero-pancreatic and bronchopulmonary neuroendocrine tumors

Torniai¹,

Rinaldi²,

Morgese³

et al. 2016

JCMT

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Neuroendocrine tumors (NETs) represent a spectrum of rare neoplasms arising in different organism sites. Depending on the site of onset, they also can be distinguished using lab exams (secreting vs. nonsecreting), clinical symptoms (functioning vs. nonfunctioning), behavioral, morphological characteristics (tumor cells' architectural growth patterns, mitotic and Ki-67 index, presence of necrosis), and grade of cellular differentiation. The aim of this review is to focus on the main signaling pathways targeted by medical treatments of advanced sporadic gastro-entero-pancreatic (GEP) and bronchopulmonary (BP) neuroendocrine neoplasms. The scientific literature regarding treatment of advanced GEP and BP-NETs has been extensively reviewed using MEDLINE and PubMed databases, selecting principal and more recent research articles, clinical trials, and updated guidelines. Somatostatin analogues represent a valid approach to control symptoms in functioning tumors and to inhibit tumor progression in certain categories on the basis of the typical somatostatin receptor expression observed in NETs. The pathogenesis of NETs has been the subject of increased interest in recent years. Many driver mutations pathway genes have been identified as important factors in the carcinogenesis process and, therefore, as potential targets for new anticancer therapies. Activating mutations have been shown in epidermal growth factor receptor, stem cell factor receptor, platelet-derived growth factor receptor, vascular endothelial growth factor, basic-fibroblastic growth factor, transforming growth factor, insulin-like growth factor-1, and their receptors. Effective M-Tor inhibition pathway modulation has led to the approval of drugs in this field such as everolimus. New drugs and several combination regimens with targeted and newer biological agents are being developed and tested in recently conducted and ongoing trials.

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“…On the other hand, we and others have shown that, although somatostatin has no effect on arteries kept under resting tension, it relaxes arteries precontracted with noradrenaline in vitro (11,12). Despite positive effects of somatostatin found in animal models of coronary restenosis, based on the antiproliferative effect of this peptide on both vascular smooth muscle (13) and endothelial cells (14,15), little is known about the effect of somatostatin on vascular responses in endothelium-denuded coronary arteries. The purpose of this work was to determine whether or not somatostatin, in an 'in vitro' model, was able to prevent the vascular alterations, hypercontractibility as well as impairment in endothelium-dependent relaxation, that occur in endotheliumdenuded rabbit coronary arteries.…”

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confidence: 97%

Effect of Somatostatin on Rabbit Isolated Coronary Arteries

Ruiz

Padilla

Tejerina

2002

Japanese Journal of Pharmacology

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ABSTRACT-Somatostatin analogues are capable of inhibiting vascular smooth muscle and endothelial cell proliferation. However, little is known about the effect of somatostatin on vascular responses in endothelium-denuded coronary arteries in vitro. The aim of this work was to determine whether or not somatostatin prevented the contractile response induced by 5-hydroxytryptamine and acetylcholine in endothelium-denuded rabbit coronary arteries. Somatostatin attenuated the contraction produced by 5-hydroxytryptamine in both proximal (PC) and distal coronary (DC) arteries (contraction induced by 10 -4 M 5-hydroxytryptamine was inhibited by 10 -6 M somatostatin by 90.8 ± 11.0% (P<0.001, n = 9) and by 46.2 ± 14.0% (P<0.05, n = 9) in DC and PC, respectively), but concentration-dependently decreased the contraction induced by U46619 (11a-epoxy-methanoprostaglandin F2=) only in PC arteries, suggesting that the response of PC and DC arteries to somatostatin were qualitatively different. Furthermore, we suggest that somatostatin may enhance acetylcholine-induced relaxation by combination of increasing endothelium-dependent relaxation (by a NO-dependent mechanism) and blocking contraction at the muscle level.Keywords: Somatostatin, Coronary artery, Acetylcholine, 5-Hydroxytryptamine, Nitric oxide Vascular diseases as well as surgical interventions such as coronary angioplasty induce endothelial denudation (1, 2) in coronary arteries. Loss of the endothelial layer alters vascular responses to certain agonists; thus 5-hydroxytryptamine and acetylcholine, which induce vasodilatation in normal coronary arteries, might be impaired or even turn into vasoconstriction in endothelium-denuded coronary arteries, leading to coronary spasm (1, 3, 4). In addition, thromboxane A2 released by platelets (5) is another candidate for the mediation of coronary vasospasm (6) since it is found in increasing concentration at the site of coronary arterial stenosis (7).Somatostatin (SRIF) is a neouroendocrine peptide (8) that exerts a wide range of physiological actions. However, the vascular effects of somatostatin are still unclear. A variety of studies have demonstrated species and regional differences in the blood flow responses to somatostatin. Thus, while in the rat superior mesenteric artery, octreotride (a somatostatin analogue) boosts vasoconstriction induced by a -agonists (9), in the vascular bed of cats, somatostatin showed opposite effects (10). On the other hand, we and others have shown that, although somatostatin has no effect on arteries kept under resting tension, it relaxes arteries precontracted with noradrenaline in vitro (11,12). Despite positive effects of somatostatin found in animal models of coronary restenosis, based on the antiproliferative effect of this peptide on both vascular smooth muscle (13) and endothelial cells (14, 15), little is known about the effect of somatostatin on vascular responses in endothelium-denuded coronary arteries. The purpose of this work was to determine whether or not somatostatin, in an 'in ...

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Effect of Somatostatin and Octreotide on Proliferation and Vascular Endothelial Growth Factor Secretion from Murine Endothelial Cell Line (HECa10) Culture

Cited by 50 publications

References 36 publications

Deficit of Somatostatin-Like Immunoreactivity in the Vitreous Fluid of Diabetic Patients

Deficit of Somatostatin-Like Immunoreactivity in the Vitreous Fluid of Diabetic Patients

Medical therapy for advanced gastro-entero-pancreatic and bronchopulmonary neuroendocrine tumors

Effect of Somatostatin on Rabbit Isolated Coronary Arteries

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