scholarly journals Anti-Inflammatory Role of Cilostazol in Vascular Smooth Muscle Cells In vitro and In vivo

2010 ◽  
Vol 17 (5) ◽  
pp. 503-509 ◽  
Author(s):  
Chie Aoki ◽  
Yoshiyuki Hattori ◽  
Atsuko Tomizawa ◽  
Teruo Jojima ◽  
Kikuo Kasai
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Anti Inflammatory

scholarly journals 738 Role of non-coding RNA uc.194 and uc.443+A in the intrastent restenosis

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Fabiola Boccuto ◽  
Laura Tammè ◽  
Claudio Iaconetti ◽  
Jolanda Sabatino ◽  
Alberto Polimeni ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Antisense Oligonucleotides ◽  
Muscle Cells ◽  
Stent Restenosis

Abstract Aims Vascular smooth muscle cells (VSMCs) play a key role in the vessel wall, being active partaker in vascular remodelling and influencing multiple pathophysiological phenomena, such as progression of atherosclerosis, in-stent restenosis and vascular reactivity. Recently antisense oligonucleotides have shown promising results as a therapeutic option. The aim of this study was to analyse the expression profile and function of T-UCRs in vascular smooth muscle cells (VSMCs)—both in vitro and in vivo—and to evaluate the effects of their inhibition by the use of specific antisense oligonucleotides. Methods After obtaining cell cultures of vascular smooth muscle cells, we modified their phenotype varying growth conditions. A microarray and qRT-PCR expression profile analysis and a cell cycle analysis with cell proliferation/apoptosis/migration assay were performed. In vivo studies were performed on rat carotids after cell damage and administration of specific antisense oligonucleotides. Results There were significant differences in the expression of T-UCRs in VSMCs with a proliferating and quiescent phenotype. In particular, 5 T-UCRs were found to be upregulated in VSMCs. These types of cells were subsequently transfected with specific antisense oligonucleotides obtaining a reduction in their proliferative activity in particular with the inhibition of the T-UCRs uc.194 and uc.443 + A. MiR-10A and miR-34b-5p were identified with complementary sequences respectively to uc.194 and uc.443 + A. The increase of these miRs following the inhibition of the T-UCRs were closely related to the inhibition of the proliferative signals of VSMCs. Similarly, the same results were obtained in vivo. Conclusions The expression levels of non-coding RNAs uc.194 and uc. 443 + A increase in proliferating smooth muscle cells in vitro and in the vascular wall following damage, suggesting an important role of these molecules in the phenomenon of intra-stent restenosis. Through the inhibition of uc.194 and uc.443 + A using an antisense strategy, we demonstrated a reduction in cell proliferation and migration processes and, consequently, in the formation of neointima. A possible relationship was also highlighted between the aforementioned non-coding RNAs and some micro-RNAs (miR-10A and miR-34b-5p), negative regulators of the proliferative phenotype of VSMCs. The inhibition of the analysed T-UCRs would allow the maintenance of the contractile phenotype thanks to the activity of the miRs analysed in this study. Our results might pave the way for the identification of new therapeutic targets in order to prevent and reduce the incidence of intra-stent restenosis.

scholarly journals Induction of cyclooxygenase-2 in rat vascular smooth muscle cells in vitro and in vivo.

1994 ◽  
Vol 269 (11) ◽  
pp. 8504-8509
Author(s):  
K.A. Pritchard ◽  
M.K. O'Banion ◽  
J.M. Miano ◽  
N. Vlasic ◽  
U.G. Bhatia ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cyclooxygenase 2

Angiotensin II modulates frizzled-2 receptor expression in rat vascular smooth muscle cells

2005 ◽  
Vol 108 (6) ◽  
pp. 523-530 ◽  
Author(s):  
Giovanna CASTOLDI ◽  
Serena REDAELLI ◽  
Willy M. M. van de GREEF ◽  
Cira R. T. di GIOIA ◽  
Giuseppe BUSCA ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ang Ii ◽  
Aortic Smooth Muscle

Ang II (angiotensin II) has multiple effects on vascular smooth muscle cells through the modulation of different classes of genes. Using the mRNA differential-display method to investigate gene expression in rat aortic smooth muscle cells in culture in response to 3 h of Ang II stimulation, we observed that Ang II down-regulated the expression of a member of the family of transmembrane receptors for Wnt proteins that was identified as Fzd2 [Fzd (frizzled)-2 receptor]. Fzds are a class of highly conserved genes playing a fundamental role in the developmental processes. In vitro, time course experiments demonstrated that Ang II induced a significant increase (P<0.05) in Fzd2 expression after 30 min, whereas it caused a significant decrease (P<0.05) in Fzd2 expression at 3 h. A similar rapid up-regulation after Ang II stimulation for 30 min was evident for TGFβ1 (transforming growth factor β1; P<0.05). To investigate whether Ang II also modulated Fzd2 expression in vivo, exogenous Ang II was administered to Sprague–Dawley rats (200 ng·kg−1 of body weight·min−1; subcutaneously) for 1 and 4 weeks. Control rats received normal saline. After treatment, systolic blood pressure was significantly higher (P<0.01), whereas plasma renin activity was suppressed (P<0.01) in Ang II- compared with the saline-treated rats. Ang II administration for 1 week did not modify Fzd2 expression in aorta of Ang II-treated rats, whereas Ang II administration for 4 weeks increased Fzd2 mRNA expression (P<0.05) in the tunica media of the aorta, resulting in a positive immunostaining for fibronectin at this time point. In conclusion, our data demonstrate that Ang II modulates Fzd2 expression in aortic smooth muscle cells both in vitro and in vivo.

scholarly journals SIRT1 and FOXO Mediate Contractile Differentiation of Vascular Smooth Muscle Cells under Cyclic Stretch

2015 ◽  
Vol 37 (5) ◽  
pp. 1817-1829 ◽  
Author(s):  
Kai Huang ◽  
Zhi-Qiang Yan ◽  
Dan Zhao ◽  
Si-Guo Chen ◽  
Li-Zhi Gao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mechanical Stretch ◽  
Cyclic Stretch ◽  
Underlying Mechanisms

Background/Aims: Physiological mechanical stretch in vivo helps to maintain the quiescent contractile differentiation of vascular smooth muscle cells (VSMCs), but the underlying mechanisms are still unclear. Here, we investigated the effects of SIRT1 in VSMC differentiation in response to mechanical cyclic stretch. Methods and Results: Rat VSMCs were subjected to 10%-1.25Hz-cyclic stretch in vitro using a FX-4000T system. The data indicated that the expression of contractile markers, including α-actin, calponin and SM22α, was significantly enhanced in VSMCs that were subjected to cyclic stretch compared to the static controls. The expression of SIRT1 and FOXO3a was increased by the stretch, but the expression of FOXO4 was decreased. Decreasing SIRT1 by siRNA transfection attenuated the stretch-induced expression of contractile VSMC markers and FOXO3a. Furthermore, increasing SIRT1 by either treatment with activator resveratrol or transfection with a plasmid to induce overexpression increased the expression of FOXO3a and contractile markers, and decreased the expression of FOXO4 in VSMCs. Similar trends were observed in VSMCs of SIRT1 (+/-) knockout mice. The overexpression of FOXO3a promoted the expression of contractile markers in VSMCs, while the overexpression of FOXO4 demonstrated the opposite effect. Conclusion: Our results indicated that physiological cyclic stretch promotes the contractile differentiation of VSMCs via the SIRT1/FOXO pathways and thus contributes to maintaining vascular homeostasis.

Calpain counteracts mechanosensitive apoptosis of vascular smooth muscle cells in vitro and in vivo

2007 ◽  
Vol 22 (2) ◽  
pp. 579-589 ◽  
Author(s):  
Daniel G. Sedding ◽  
Matthias Homann ◽  
Ulrike Seay ◽  
Harald Tillmanns ◽  
Klaus T. Preissner ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

scholarly journals Kv1.3 blockade inhibits proliferation of vascular smooth muscle cells in vitro and intimal hyperplasia in vivo

2020 ◽  
Vol 224 ◽  
pp. 40-54 ◽  
Author(s):  
Joaquim Bobi ◽  
Manel Garabito ◽  
NÚria Solanes ◽  
Pilar Cidad ◽  
Víctor Ramos-Pérez ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Intimal Hyperplasia ◽  
Muscle Cells
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