Leptin promotes osteoblast differentiation and mineralization of primary cultures of vascular smooth muscle cells by inhibiting glycogen synthase kinase (GSK)-3β

2012 ◽  
Vol 425 (4) ◽  
pp. 924-930 ◽  
Author(s):  
Melec G. Zeadin ◽  
Martin K. Butcher ◽  
Stephen G. Shaughnessy ◽  
Geoff H. Werstuck
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Osteoblast Differentiation ◽  
Glycogen Synthase ◽  
Primary Cultures ◽  
Muscle Cells ◽  
Glycogen Synthase Kinase ◽  
Gsk 3Β

Insulin-like growth-factor-1-induced PKB signaling and Egr-1 expression is inhibited by curcumin in A-10 vascular smooth muscle cells

2013 ◽  
Vol 91 (3) ◽  
pp. 241-247 ◽  
Author(s):  
Viktoria Youreva ◽  
Georgia Kapakos ◽  
Ashok K. Srivastava
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Glycogen Synthase ◽  
Muscle Cells ◽  
Insulin Like Growth Factor ◽  
Dose Dependent Fashion ◽  
Gsk 3Β

Insulin-like growth factor 1 (IGF-1) is a mitogenic factor that stimulates the signaling pathways responsible for inducing hypertrophic and proliferative responses in vascular smooth muscle cells (VSMC). We have previously demonstrated that IGF-1 receptor (IGF-1R) plays a key role in transducing the hypertrophic and proliferative responses of angiotensin II (Ang-II) and endothelin-1 (ET-1). Curcumin, a polyphenolic compound derived from the spice turmeric is known to possess antiproliferative properties and exerts vasculoprotective effects. However, the ability of curcumin to modulate IGF-1-induced signaling responses in VSMC remains to be investigated. In this study, we determined the effect of curcumin on IGF-1-induced phosphorylation of protein kinase B (PKB), glycogen synthase kinase-3β (GSK-3β), and IGF-1R in VSMC. Curcumin inhibited IGF-1-induced phosphorylation of PKB and GSK-3β as well as the IGF-1R β subunit in a dose-dependent fashion. In addition, IGF-1-induced expression of early growth response protein 1 (Egr-1) which plays a pathogenic role in vascular dysfunctions, was also attenuated by curcumin. In conclusion, these results indicate that curcumin is a potent inhibitor of key components of the IGF-1-induced mitogenic and proliferative signaling system in VSMC, and suggest that curcumin-induced attenuation of these signaling components may constitute a potential mechanism for its vasculoprotective effects.

The Potential Effect of Glycogen Synthase Kinase-3β Regulating Myocardin, a Transcription Factor Specific to Vascular Smooth Muscle Cells, on Atherosclerosis

2020 ◽  
Vol 10 (8) ◽  
pp. 1135-1142
Author(s):  
Ying Qin ◽  
Xiaojie Li ◽  
Jianwei Xu ◽  
Xingde Liu ◽  
Yixia Zhou
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Transcriptional Activity ◽  
Glycogen Synthase ◽  
Muscle Cells ◽  
Potential Effect ◽  
Pathological Changes ◽  
Related Factors

Background and Aim: To investigate whether and how inhibition of GSK-3 regulates myocardin activity in the human vascular smooth muscle cells (SMCs), and to explore the action of GSK-3 inhibitor (AR-A014418) on atherosclerosis (AS) in rats. Materials and Methods: The western-blotting and RT-qPCR were conducted to gauging the changes in protein and transcription levels of related factors. Immunoprecipitation was used to discuss the relationship between myocardin and ACTA2. HE staining and red oil staining were performed to demonstrate pathological changes in renal tissue and aorta. Results: AR-A014418 sharply reduced the activity of myocardin and further abated its phosphorylation of serine and threonine and the recruitment of myocardin to ACTA2. Besides, AR-A014418 could alleviate the pathological changes and significantly increase expression levels of ACTA2 in AS rats. Conclusion: GSK-3 may bilaterally regulate the transcriptional activity of myocardin in vascular SMCs. The regulation of GSK-3 on the transcriptional activity of myocardin may be an important mechanism of differentiation and dedifferentiation of vascular smooth muscle and related diseases.

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