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, Viktoria; Srivastava, Ashok K.

doi:10.1002/jcb.25260

Cited by 14 publications

(18 citation statements)

References 58 publications

(90 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We have shown earlier that CaM/CaMKII pathway mediates MEK/ERK1/2 activation in response to ET‐1 in VSMC (Bouallegue et al, ). Additionally, we and others have observed that the MEK/ERK1/2 pathway plays a key role in Egr‐1 expression induced by several stimuli (Hasan & Schafer, ; Liu, Yu et al, ; Youreva & Srivastava, ). Therefore, we investigated if the attenuation of Ang‐II‐induced Egr‐1 expression due to STIM‐1 and Orai‐1 silencing in VSMC was associated with a change in ERK1/2 phosphorylation.…”

Section: Resultsmentioning

confidence: 69%

“…Earlier work has demonstrated that MAP kinase signaling plays a key role in inducing Egr‐1 expression in a wide variety of cell types in response to a large number of stimuli (Liu, Yu et al, ; Stefano, Rossler, Griesemer, Hoth, & Thiel, ; Youreva & Srivastava, ). However, our data demonstrating that siRNA‐induced silencing of either STIM‐1 or Orai‐1 resulted in the suppression of ERK1/2 as well as CREB phosphorylation indicated that Ang‐II‐induced SOCE is crucial to induce ERK and CREB phosphorylation in VSMC.…”

Section: Discussionmentioning

confidence: 99%

“…Nuclei were then labelled by staining the coverslips with DAPI (2 μl/1.5 ml H 2 O) before being mounted with a buffer made of 30% Glycerol in PBS. The images were taken using X‐Cite Serie 120, TE2000‐S fluorescence microscope (Youreva & Srivastava, ) .…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

STIM‐1 and ORAI‐1 channel mediate angiotensin‐II‐induced expression of Egr‐1 in vascular smooth muscle cells

Simo‐Cheyou

Tan

Grygorczyk

et al. 2017

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

An upregulation of Egr-1 expression has been reported in models of atherosclerosis and intimal hyperplasia and, various vasoactive peptides and growth promoting stimuli have been shown to induce the expression of Egr-1 in vascular smooth muscle cells (VSMC). Angiotensin-II (Ang-II) is a key vasoactive peptide that has been implicated in the pathogenesis of vascular diseases. Ang-II elevates intracellular Ca through activation of the store-operated calcium entry (SOCE) involving an inositol-3-phosphate receptor (IP3R)-coupled depletion of endoplasmic reticular Ca and a subsequent activation of the stromal interaction molecule 1 (STIM-1)/Orai-1 complex. However, the involvement of IP3R/STIM-1/Orai-1-Ca -dependent signaling in Egr-1 expression in VSMC remains unexplored. Therefore, in the present studies, we have examined the role of Ca signaling in Ang-II-induced Egr-1 expression in VSMC and investigated the contribution of STIM-1 or Orai-1 in mediating this response. 2-aminoethoxydiphenyl borate (2-APB), a dual non-competitive antagonist of IP3R and inhibitor of SOCE, decreased Ang-II-induced Ca release and attenuated Ang-II-induced enhanced expression of Egr-1 protein and mRNA levels. Egr-1 upregulation was also suppressed following blockade of calmodulin and CaMKII. Furthermore, RNA interference-mediated depletion of STIM-1 or Orai-1 attenuated Ang-II-induced Egr-1 expression as well as Ang-II-induced phosphorylation of ERK1/2 and CREB. In addition, siRNA-induced silencing of CREB resulted in a reduction in the expression of Egr-1 stimulated by Ang-II. In summary, our data demonstrate that Ang-II-induced Egr-1 expression is mediated by STIM-1/Orai-1/Ca -dependent signaling pathways in A-10 VSMC.

show abstract

Section: Resultsmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

STIM‐1 and ORAI‐1 channel mediate angiotensin‐II‐induced expression of Egr‐1 in vascular smooth muscle cells

Simo‐Cheyou

Tan

Grygorczyk

et al. 2017

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Therefore, to investigate the specific contribution of IGF-1R and EGFR in IGF-1-induced HDAC5 phosphorylation, we used AG1024 and AG1478, highly specific inhibitors of IGF-1R and EGFR tyrosine kinase (TK) activity, respectively. As depicted in Figure 2a 3.2 | IGF-1-induced HDAC5 phosphorylation is not mediated by mitogen-activated protein kinase-dependent pathways IGF-1 has been shown to mediate its physiological responses through the activation of hypertrophic and growth promoting signaling pathways, including the mitogen-activated protein kinase (MAPK) pathway Youreva & Srivastava, 2016). Therefore, we next investigated whether the MAPK pathway was involved in mediating IGF-1-induced HDAC5 phosphorylation.…”

Section: Resultsmentioning

confidence: 99%

Protein kinase B/AKT mediates insulin‐like growth factor 1‐induced phosphorylation and nuclear export of histone deacetylase 5 via NADPH oxidase 4 activation in vascular smooth muscle cells

Pietruczuk

Jain

Simo‐Cheyou

et al. 2019

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

Insulin‐like growth factor 1 (IGF‐1) mediates the generation of reactive oxygen species (ROS) and the activation of growth promoting signaling pathways. Histone deacetylases (HDACs) regulate gene transcription by deacetylating lysine residues in histone and nonhistone proteins and a heightened HDAC activation, notably of HDAC5, is associated with vascular disorders, such as atherosclerosis. Although the contribution of IGF‐1 in these pathologies is well documented, its role in HDAC phosphorylation and activation remains unexplored. Here, we examined the effect of IGF‐1 on HDAC5 phosphorylation in vascular smooth muscle cells (VSMCs) and identified the signaling pathways involved in controlling HDAC5 phosphorylation and nuclear export. Treatment of A10 VSMCs with IGF‐1 enhanced HDAC5 phosphorylation. Blockade of the IGF‐1 receptor tyrosine kinase (TK) activity with the specific pharmacological inhibitor, AG1024, significantly inhibited IGF‐1‐induced HDAC5 phosphorylation, whereas the epidermal growth factor receptor (EGFR) TK antagonist, AG1478, had no effect. Inhibition of the mitogen‐activated protein kinase pathway with U0126, SP600125, or SB203580, did not affect HDAC5 phosphorylation, whereas two inhibitors of the phosphoinositide 3‐kinase (PI3K)/AKT pathways, wortmannin and SC66, almost completely attenuated IGF‐1‐induced responses as confirmed by immunoblotting of phospho‐HDAC5 and by small interfering RNA (siRNA)‐induced AKT silencing. Moreover, the NAD(P)H oxidase (Nox) inhibitor, diphenyleneiodonium (DPI), and Nox4 siRNA, attenuated IGF‐1‐induced phosphorylation of HDAC5 and AKT. The HDAC5 phosphorylation resulted in its nuclear export, which was reversed by SC66 and DPI. Our results indicate that IGF‐1‐induced phosphorylation and nuclear export of HDAC5 involve Nox4‐dependent ROS generation and PI3K/AKT signaling pathways.

show abstract

“…Besides, IGF plays a crucial role in the homeostasis of the extracellular matrix. Indeed, IGF, by stimulating chondrocytes, may be involved in the regulation of proteoglycan synthesis [53,54]. The presence of proinflammatory cytokines during the period of inflammation that occurs after the damage to the vessel walls can interfere with the balance between synthesis and degradation in IGF.…”

Section: Induction Of Restenosis By Igfmentioning

confidence: 99%

Inflammatory Growth Factors and In-Stent Restenosis: Effect of Cytokines and Growth Factors

Maleknia

Ansari

Haybar

et al. 2020

SN Compr. Clin. Med.

View full text Add to dashboard Cite

Highlights•PDGF is considered as prime culprit among growth factors in the pathogenesis of restenosis.•Inflammatory cytokines can stimulate VSMC migration by recruiting monocytes and releasing growth factors.•VEGF can be used to inhibit restenosis because of its revascularization and re-endothelialization properties. AbstractFollowing stent implantation and vascular injury, restenosis is one of the prominent clinical problems due to the synergism effects of inflammatory cytokines and growth factors. Restenosis development is accompanied by increased proliferation and migration of vascular smooth muscle cells (VSMCs) into the intimal region. The content has been obtained from PubMed database and the Google Scholar search engine through searching English-language articles (1989-2019) using keywords "Vascular injury," "Restenosis," "Growth factors," "Cytokines," and "Smooth muscle cells." After the vascular injury, the secretion of inflammatory factors can stimulate inflammatory cells, which lead to the release of growth factors. This can stimulate the migration of VSMCs and neointimal hyperplasia, and, as a result, lead to restenosis. Inflammatory cytokines, such as transforming growth factor-beta (TGFβ), often stimulate growth factors such as platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF), which can accelerate the restenosis process. Other cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) in the initial inflammation inhibit restenosis by affecting insulin-like growth factor binding proteins (IGFBPs). Considering the synergism effects of inflammatory cytokines and growth factors in the pathogenesis of restenosis, it is expected that these factors can be used as prognostic markers with therapeutic purposes.

show abstract

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

Cited by 14 publications

References 58 publications

STIM‐1 and ORAI‐1 channel mediate angiotensin‐II‐induced expression of Egr‐1 in vascular smooth muscle cells

STIM‐1 and ORAI‐1 channel mediate angiotensin‐II‐induced expression of Egr‐1 in vascular smooth muscle cells

Protein kinase B/AKT mediates insulin‐like growth factor 1‐induced phosphorylation and nuclear export of histone deacetylase 5 via NADPH oxidase 4 activation in vascular smooth muscle cells

Inflammatory Growth Factors and In-Stent Restenosis: Effect of Cytokines and Growth Factors

Contact Info

Product

Resources

About