Receptors for insulin and insulin-like growth factor in cultured arterial smooth muscle cells depend on their growth state

Pfeifle, Beate; Ditschuneit, H.

doi:10.1677/joe.0.0960251

Cited by 24 publications

(8 citation statements)

References 11 publications

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“…Third, among the various growth factors involved in atherosclerotic plaque development, IGFs play a relevant role. Type I IGF receptors are present on smooth muscle cells [29], inflammatory cells [30], and arterial endothelial cells [31] within the atherosclerotic lesion. Macrophage accumulation is an early event in atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Insulin-Like Growth Factor-1 as a Prognostic Marker in Patients with Acute Ischemic Stroke

Tang

et al. 2014

PLoS ONE

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ObjectiveInsulin-like growth factor-1 (IGF-1) has been associated with cardiovascular risk factors and atherosclerosis. The aim of the present study was to evaluate the prognostic value of IGF-1 levels in patients with acute ischemic stroke (AIS).MethodsAll patients with first-ever AIS from August 1, 2012 to August 31, 2013 were recruited to participate in the study. Clinical data were collected. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to serum IGF-1 levels. For the assessment of functional outcome at 90 days Modified Rankin Scale (mRS) was used. On admission, serum IGF-1 levels were determined by chemiluminescence immunoassay. The influence of IGF-1 levels on functional outcome and death was assessed by multivariate logistic regression analysis.ResultsPatients with an unfavorable outcomes and non-survivors had significantly decreased serum IGF-1 levels on admission (P<0.0001 for both). IGF-1 was an independent prognostic marker of functional outcome and death [odds ratio 0.89 (0.84–0.93) and 0.90 (0.84–0.95), respectively, P<0.0001 for both, adjusted for age, NIHSS score and other predictors] in patients with ischemic stroke. Serum IGF-1 levels ≤130 ng/mL was as an value indicator for unfavorable functional outcome (OR 3.31, 95% CI:1.87–5.62; P<0.0001), after adjusting for other significant confounders.ConclusionsWe reported a significant association between low serum IGF-1 levels and unfavorable functional outcome and death.

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Section: Discussionmentioning

confidence: 99%

Insulin-Like Growth Factor-1 as a Prognostic Marker in Patients with Acute Ischemic Stroke

Tang

et al. 2014

PLoS ONE

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“…The potency of insulin to displace 1251I-IGF is 1,000-2,000 times less than IGF itselfas studied in rat cultured VSMC (28,29). Therefore, control studies were performed using 2.5 ng/ml IGF-I and IGF-II, a concentration that does not significantly cross-react with other receptors (29,30), but is approximately equivalent to the displacement of IGFs from their receptors by 100 mU/ml insulin. (Fig.…”

Section: Methodsmentioning

confidence: 99%

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

Saito¹,

Hori²,

Fittingoff³

et al. 1993

J. Clin. Invest.

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Insulin has been shown to attenuate pressor-induced vascular contraction, but the mechanism for this vasodilatory action is unknown. This study examines the effect of insulin on angiotensin II (ANG II)-induced increments in cytosolic calcium in cultured rat vascular smooth muscle cells (VSMC). 20-min incubations with insulin (10 ,U/ml to 100 mU/ml) did not alter basal intracellular calcium concentration (ICa2I,), but inhibited the response to 100 nM ANGII in a dose-dependent manner (ANG II alone, 721±54 vs. ANG II + 100 mU/ml insulin, 315±35 nM, P < 0.01). A similar effect of insulin on ANGII action was observed in calcium poor buffer. Moreover, insulin did not effect calcium influx. ANG II receptor density and affinity were not affected by 24-h incubation with insulin. To further clarify the mechanisms of these observations, we measured ANG II-induced production of inositol 1,4,5-triphosphate (IP3), and IP3-releasable 45Ca. Insulin treatment did not alter ANG Il-stimulated IP3 production. However, IP3-stimulated release of45Ca in digitonin permeabilized cells was significantly reduced after 5-min incubations with 100 mU/ml insulin. Thapsigargin induced release of calcium stores was also blocked by insulin. Thus, insulin attenuates ANG 11-stimulated ICa2"I, primarily by altering IP3-releasable calcium stores. Insulin effects on ANG II-induced ICa2`Ii were mimicked by preincubation of VSMC with either sodium nitroprusside or 8-bromo-cGMP. As elevations in cGMP in vascular tissue lower ICa2I1j, it is possible that insulin affects IP3 release of calcium by a cGMP-dependent mechanism that would contribute to its vasodilatory effects. (J. Clin. Invest. 1993. 92:1161-1167

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“…Among the various growth factors involved in atherosclerotic plaque development, IGFs play a relevant role ( Figure 2). The different cell types of atherosclerosis secrete IGFs, and type I IGF receptors are present on smooth muscle cells, 23 inflammatory cells, 24 and arterial endothelial cells 25 within the atherosclerotic lesion.…”

Section: Atherosclerosismentioning

confidence: 99%

The Insulin-Like Growth Factor Axis

Bayés‐Genís

Conover

Schwartz

2000

Circulation Research

374

154

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Insulin-like growth factors I and II (IGF-I and -II) and their regulatory proteins are secreted by cells of the cardiovascular system. They are growth promoters for arterial cells and mediators of cardiovascular disease. IGFs are bound to IGF binding proteins (IGFBPs), which modulate IGF ligand-receptor interaction and consequently to IGF action. IGFBPs are in turn posttranslationally modulated by specific proteases. This dynamic balance (IGFs, IGFBPs, and IGFBP proteases) constitutes the IGF axis and ultimately determines the extent of IGF-dependent cellular effects. Dysregulated actions of this axis influence coronary atherosclerosis through effects on vascular smooth muscle cell growth, migration, and extracellular matrix synthesis in the atherosclerotic plaque. IGF-I promotes macrophage chemotaxis, excess LDL cholesterol uptake, and release of proinflammatory cytokines. Endothelial cells also receive the effects of IGFs stimulating their migration and organization forming capillary networks. Neointimal hyperplasia of restenosis after coronary artery injury is also modulated by the IGF axis. IGFs stimulate vascular smooth muscle cell proliferation and migration to form the neointima and upregulate tropoelastin synthesis after disruption of the elastic layer. Understanding IGF axis regulation establishes a scientific basis for strategies directed to limit or reverse plaque growth and vulnerability in atherosclerosis and in the neointimal hyperplasia of restenosis.

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Receptors for insulin and insulin-like growth factor in cultured arterial smooth muscle cells depend on their growth state

Cited by 24 publications

References 11 publications

Insulin-Like Growth Factor-1 as a Prognostic Marker in Patients with Acute Ischemic Stroke

Insulin-Like Growth Factor-1 as a Prognostic Marker in Patients with Acute Ischemic Stroke

Insulin attenuates agonist-mediated calcium mobilization in cultured rat vascular smooth muscle cells.

The Insulin-Like Growth Factor Axis

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