Pelargonidin attenuates PDGF-BB-induced aortic smooth muscle cell proliferation and migration by direct inhibition of focal adhesion kinase

Son, Joe Eun; Jeong, Hyein; Kim, Hee Joo; Kim, Yeong A; Lee, Eunjung; Lee, Hyong Joo; Lee, Ki Won

doi:10.1016/j.bcp.2014.02.015

Cited by 24 publications

(23 citation statements)

References 49 publications

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“…Therefore, the activity of AKT signaling after treatment with PDGF-BB with or without formononetin was evaluated in the present study. Treatment with PDGF-BB appeared to enhance the phosphorylated protein level of AKT, indicating that the activity of AKT signaling was upregulated, which is consistent with previous studies (15,33,34). However, treatment with formononetin effectively suppressed PDGF-BB-stimulated upregulation of phospho-AKT protein level in VSMCs, suggesting that formononetin is able to inhibit PDGF-BB-induced activation of AKT signaling in VSMCs.…”

Section: Discussionsupporting

confidence: 81%

Suppressive effect of formononetin on platelet-derived growth factor-BB-stimulated proliferation and migration of vascular smooth muscle cells

Chen

Liu

Cai

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) has been implicated in intimal hyperplasia, atherosclerosis and restenosis following percutaneous coronary intervention. Formononetin, a phytoestrogen extracted from the root of Astragalus membranaceus, has been widely used in Chinese tradition medicine due to its protective effects against certain symptoms of cancer, hypertension, inflammation, hypoxia-induced cytotoxicity and ovariectomy-induced bone loss. However, the effect of formononetin on platelet-derived growth factor (PDGF)-BB-induced proliferation and migration of VSMCs, as well as the underlying molecular mechanism, remains largely unclear. In the present study, treatment with formononetin significantly inhibited PDGF-BB-induced proliferation and migration of human VSMCs. Investigation into the underlying molecular mechanism revealed that the administration of formononetin suppressed PDGF-BB-stimulated switch of VSMCs to a proliferative phenotype. Furthermore, treatment with formononetin inhibited the PDGF-BB-induced upregulation of cell cycle-related proteins, matrix metalloproteinase (MMP2) and MMP9. In addition, the that administration of formononetin inhibited the phosphorylation of AKT induced by PDGF-BB in VSMCs. The present results suggest that formononetin has a suppressive effect on PDGF-BB-stimulated VSMCs proliferation and migration, which may occur partly via the inhibition of AKT signaling pathway. Therefore, formononetin may be useful for the treatment of intimal hyperplasia, atherosclerosis and restenosis.

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Section: Discussionsupporting

confidence: 81%

Suppressive effect of formononetin on platelet-derived growth factor-BB-stimulated proliferation and migration of vascular smooth muscle cells

Chen

Liu

Cai

et al. 2016

Experimental and Therapeutic Medicine

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“…Focal adhesion kinase has been reported to play a role in the proliferation and migration of aortic smooth muscle cells, and the regulation of smooth muscle cell recruitment during blood vessel morphogenesis . Myo1e has previously been reported to induce FAK phosphorylation and FAK kinase activity .…”

Section: Resultsmentioning

confidence: 99%

“…In our study, we demonstrated that miR‐125b targets the 3ʹUTR of Myo1e in VSMCs repressing its expression and affecting subsequent FAK activation. The interaction between Myo1e and FAK and the resulting phosphorylation‐activation of FAK has been shown to be crucial for cell motility, and therefore the transcriptional repression of Myo1e would be expected to inhibit the migratory behaviour of VSMCs.…”

Section: Discussionmentioning

confidence: 99%

“…Heim et al reported that Myo1e binds to the FERM domain of focal adhesion kinase (FAK), activating FAK and inducing Y397 phosphorylation. Previous studies revealed that FAK is involved in the regulation of aortic smooth muscle cell motility and growth, and the regulation of smooth muscle cell recruitment during blood vessel morphogenesis . The potential role of Myo1e and FAK activation in VSMCs in response to MSC‐Exo‐derived signals was also investigated in this study.…”

Section: Introductionmentioning

confidence: 89%

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Exosomes from mesenchymal stem cells expressing miR‐125b inhibit neointimal hyperplasia via myosin IE

Wang

Gao

Yue

et al. 2018

J Cellular Molecular Medi

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Intercellular communication between mesenchymal stem cells (MSCs) and their target cells in the perivascular environment is modulated by exosomes derived from MSCs. However, the potential role of exosome‐mediated microRNA transfer in neointimal hyperplasia remains to be investigated. To evaluate the effects of MSC‐derived exosomes (MSC‐Exo) on neointimal hyperplasia, their effects upon vascular smooth muscle cell (VSMC) growth in vitro and neointimal hyperplasia in vivo were assessed in a model of balloon‐induced vascular injury. Our results showed that MSC‐Exo were internalised by VSMCs and inhibited proliferation and migration in vitro. Further analysis revealed that miR‐125b was enriched in MSC‐Exo, and repressed the expression of myosin 1E (Myo1e) by targeting its 3ʹ untranslated region. Additionally, MSC‐Exo and exosomally transferred miR‐125b repressed Myo1e expression and suppressed VSMC proliferation and migration and neointimal hyperplasia in vivo. In summary, our findings revealed that MSC‐Exo can transfer miR‐125b to VSMCs and inhibit VSMC proliferation and migration in vitro and neointimal hyperplasia in vivo by repressing Myo1e, indicating that miR‐125b may be a therapeutic target in the treatment of vascular diseases.

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“…Taken together with electron microscopic observations and data for growth in honeycombs, proliferative inhibition occurs in parallel with a decrease in the number of focal adhesions, including reduced levels of focal adhesion kinase (FAK). As a high level of phosphorylated FAK promotes proliferative activity [8], the low level of phosphorylated FAK is one of the reasons for proliferative inhibition of VSMCs in honeycombs.…”

Section: Proliferative Inhibition Of Vsmcs Cultured In Honeycombsmentioning

confidence: 99%

Three-Dimensional “Honeycomb” Culture System that Helps to Maintain the Contractile Phenotype of Vascular Smooth Muscle Cells

Ishii¹,

Uchida²

2015

Muscle Cell and Tissue

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Vascular smooth muscle cells (VSMCs) in the normal aorta are described as having a contractile phenotype because they can contract and do not proliferate. VSMCs in pathological conditions such as atherosclerosis and restenosis can proliferate and migrate, but lose their ability to contract, which is referred to as a synthetic phenotype. VSMCs show plasticity by changing their phenotype according to the surrounding environment. When VSMCs are cultured on a plastic plate, which is a normal two-dimensional culture system, they display the synthetic phenotype because they proliferate and migrate without contraction. Recently, we successfully cultured VSMCs that display features similar to the contractile phenotype, using type I collagen three-dimensional matrices, "honeycombs," in the presence of abundant fetal bovine serum albumin. VSMCs cultured in honeycombs stop proliferating and can contract. The honeycomb culture system can maintain VSMCs in the contractile phenotype for a long period of time. In this chapter, we show the method of this new culture system and the characteristics of VSMCs in honeycombs. It is expected that the use of this culture system will generate new information on the characteristics of VSMCs.

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Pelargonidin attenuates PDGF-BB-induced aortic smooth muscle cell proliferation and migration by direct inhibition of focal adhesion kinase

Cited by 24 publications

References 49 publications

Suppressive effect of formononetin on platelet-derived growth factor-BB-stimulated proliferation and migration of vascular smooth muscle cells

Suppressive effect of formononetin on platelet-derived growth factor-BB-stimulated proliferation and migration of vascular smooth muscle cells

Exosomes from mesenchymal stem cells expressing miR‐125b inhibit neointimal hyperplasia via myosin IE

Three-Dimensional “Honeycomb” Culture System that Helps to Maintain the Contractile Phenotype of Vascular Smooth Muscle Cells

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