Involvement of insulin-like growth factor 1 receptor transactivation in endothelin-1-induced signaling in vascular smooth muscle cells

Bouallegue, Ali; Vardatsikos, George; Srivastava, Ashok K.

doi:10.1139/y10-030

Cited by 9 publications

(1 citation statement)

References 79 publications

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“…The involvement of growth factors and vasoactive peptides such as endothelin‐1 (ET‐1) and angiotensin‐II (Ang‐II) in these processes has been well documented in the past decades. We have previously shown an involvement of insulin‐like growth factor‐1 receptor (IGF‐1R) transactivation in triggering ET‐1 and Ang‐II‐induced mitogenic and proliferative responses in VSMC [Bouallegue et al, ; Bouallegue et al, ]. Insulin‐like growth factor‐1 (IGF‐1), a potent mitogen and vasoactive factor, is known to induce structural alterations in the vessel wall by its ability to trigger proliferation, migration, hypertrophy, and apoptosis of VSMC [Jackson and Schwartz, ; Bayes‐Genis et al, ; Hsieh et al, ; Higashi et al, ].…”

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Early Growth Response Protein‐1 Expression by Insulin‐Like Growth Factor‐1 Requires ROS‐Dependent Activation of ERK1/2 and PKB Pathways in Vascular Smooth Muscle Cells

Youreva

Srivastava

2015

J of Cellular Biochemistry

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Early growth response protein-1 (Egr-1) is a transcription factor that plays an important role in the regulation of several genes implicated in the pathogenesis of cardiovascular disease (CVD) such as atherosclerosis. Insulin-like growth factor-1 (IGF-1), a potent mitogen, is believed to contribute to the development of CVD through the hyperactivation of mitogenic and growth promoting pathways, including the MAPK and PKB pathways, as well as regulation of multiple transcription factors. Reactive oxygen species (ROS) have been shown to mediate the effects of IGF-1 and are believed to contribute to the pathogenesis of vascular abnormalities. We have previously shown that IGF-1 induces the expression of Egr-1 in vascular smooth muscle cells (VSMC); however, the signaling pathways involved in this process remain unexplored. Therefore, we have investigated the involvement of MAPK, PKB, and ROS in IGF-1-induced Egr-1 expression in VSMC. Treatment of VSMC with IGF-1 enhanced Egr-1 protein levels in a time and dose-dependent fashion and PD98059 and SP600125, two selective inhibitors of ERK1/2 and JNK, respectively, significantly decreased IGF-1-induced increase in Egr-1 expression in these cells. In addition, blockade of PI3-K/PKB pathways by Wortmannin/SC-66 respectively, also attenuated IGF-1-induced Egr-1 protein as well as mRNA expression. Diphenyleneiodonium (DPI), an NAD(P)H oxidase inhibitor, blocked the Egr-1 expression in response to IGF-1. In summary, these data demonstrate that ROS-dependent activation of ERK1/2/JNK, PI3-K/PKB signaling events play a critical role in IGF-1 induced expression of Egr-1 in VSMC.

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Early Growth Response Protein‐1 Expression by Insulin‐Like Growth Factor‐1 Requires ROS‐Dependent Activation of ERK1/2 and PKB Pathways in Vascular Smooth Muscle Cells

Youreva

Srivastava

2015

J of Cellular Biochemistry

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Tumor Tropism of Mesenchymal Stem Cells

Lam

2013

Stem Cell Therapeutics for Cancer

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The Injurious Effects of Hyperinsulinism on Blood Vessels

Wang

Zhang

et al. 2013

Cell Biochem Biophys

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Insulin resistance (IR) is a common feature of hypertension, Type II diabetes, coronary heart disease, Syndrome X, and other vascular diseases. It refers to a state in which a certain concentration of insulin produces less biologic effect than expected in human body. When IR develops, the response of human body to insulin decreases accordingly, thus inducing the compensatory hyper-secretion of insulin and consequently hyperinsulinism. Many clinical and epidemiologic studies have demonstrated that IR and iatrogenic hyperinsulinism induced consequently play an essential role in the pathogenesis of hypertension and atherosclerotic cardiovascular diseases. Therefore, more and more attention should be paid to the mechanism of IR in order to explore more therapeutic basis and prospective for the treatment of atherosclerosis and other cardiovascular diseases. In this review, we provided a general overview on the known molecular mechanisms of IR and summarized the recent findings on the injurious effects of hyperinsulinism in vitro and in vivo, which might be important for researchers and clinicians to better understand the etiology and clinical significance of IR.

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Involvement of insulin-like growth factor 1 receptor transactivation in endothelin-1-induced signaling in vascular smooth muscle cells

Cited by 9 publications

References 79 publications

Early Growth Response Protein‐1 Expression by Insulin‐Like Growth Factor‐1 Requires ROS‐Dependent Activation of ERK1/2 and PKB Pathways in Vascular Smooth Muscle Cells

Early Growth Response Protein‐1 Expression by Insulin‐Like Growth Factor‐1 Requires ROS‐Dependent Activation of ERK1/2 and PKB Pathways in Vascular Smooth Muscle Cells

Tumor Tropism of Mesenchymal Stem Cells

The Injurious Effects of Hyperinsulinism on Blood Vessels

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