The effect of ferulic acid ethyl ester on leptin-induced proliferation and migration of aortic smooth muscle cells

Tsai, Yao‐Chou; Lee, Yen-Mei; Hsu, Chih-Hsiung; Leu, Sy-Ying; Chiang, Hung-Che; Yen, Mao‐Hsiung; Cheng, Pao-Yun

doi:10.1038/emm.2015.56

Cited by 19 publications

(18 citation statements)

References 52 publications

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“…Cells were treated with leptin (1–100 ng/ml; R&D Systems, Inc., Minneapolis, MN, USA) for 72 hrs and/or pre‐treated with genistein (1, 5 μM; Sigma‐Aldrich, St Louis, MO, USA) for 1 hr, and the relative cell numbers were assessed using the MTS‐based CellTiter 96 ® AQueous One Solution kit (Promega, Madison, WI, USA), according to the manufacturer's directions .…”

Section: Methodsmentioning

confidence: 99%

“…The proliferation of cells was also measured by DNA synthesis using a bromodeoxyuridine (BrdU) proliferation assay kit (Cell Signaling Technology, Danvers, MA, USA), according to the manufacturer's directions, as described previously .…”

Section: Methodsmentioning

confidence: 99%

“…Cell migration assay was performed with the Transwell ® Permeable Support Culture Plate System (Corning Inc., Corning, NY, USA) as described previously .…”

Section: Methodsmentioning

confidence: 99%

“…For the measurement of MMP‐2 activity of culture media, gelatin zymography was conducted. Briefly, culture media were subject to electrophoresis on a Novex 10% gelatin zymogram gel (Invitrogen, Life Technologies, Carlsbad, CA, USA) as described previously .…”

Section: Methodsmentioning

confidence: 99%

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Genistein suppresses leptin‐induced proliferation and migration of vascular smooth muscle cells and neointima formation

Tsai

Leu

Peng

et al. 2016

J Cellular Molecular Medi

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Obesity is a strong risk factor for the development of cardiovascular diseases and is associated with a marked increase in circulating leptin concentration. Leptin is a peptide hormone mainly produced by adipose tissue and is regulated by energy level, hormones and various inflammatory mediators. Genistein is an isoflavone that exhibits diverse health‐promoting effects. Here, we investigated whether genistein suppressed the atherogenic effect induced by leptin. The A10 cells were treated with leptin and/or genistein, and then the cell proliferation and migration were analysed. The reactive oxygen species (ROS) and proteins levels were also measured, such as p44/42MAPK, cell cycle‐related protein (cyclin D1 and p21) and matrix metalloproteinase‐2 (MMP‐2). Immunohistochemistry and morphometric analysis were used for the neointima formation in a rat carotid artery injury model. Genistein (5 μM) significantly inhibited both the proliferation and migration of leptin (10 ng/ml)‐stimulated A10 cells. In accordance with these finding, genistein decreased the leptin‐stimulated ROS production and phosphorylation of the p44/42MAPK signal transduction pathway. Meanwhile, genistein reversed the leptin‐induced expression of cyclin D1, and cyclin‐dependent kinase inhibitor, p21. Genistein attenuated leptin‐induced A10 cell migration by inhibiting MMP‐2 activity. Furthermore, the leptin (0.25 mg/kg)‐augmented neointima formation in a rat carotid artery injury model was attenuated in the genistein (5 mg/kg body weight)‐treated group when compared with the balloon injury plus leptin group. Genistein was capable of suppressing the atherogenic effects of leptin in vitro and in vivo, and may be a promising candidate drug in the clinical setting.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…Cell migration assay was performed with the Transwell ® Permeable Support Culture Plate System (Corning Inc., Corning, NY, USA) as described previously .…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Genistein suppresses leptin‐induced proliferation and migration of vascular smooth muscle cells and neointima formation

Tsai

Leu

Peng

et al. 2016

J Cellular Molecular Medi

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“…p27 blocks the G1-S transition in the cell cycle, and is a negative regulator of the protein kinases, cyclin/CDK ( 5 ). The interaction of the two factors regulates cell proliferation and apoptosis ( 6 ). The activity of extracellular signal-regulated kinase 1/2 (ERK1/2), a major mitogenic signaling pathway, has been shown to be significantly enhanced in a variety of animal models of pulmonary arterial hypertension ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Exogenous spermine inhibits the proliferation of human pulmonary artery smooth muscle cells caused by chemically-induced hypoxia via the suppression of the ERK1/2- and PI3K/AKT-associated pathways

Wei

Wang

et al. 2015

International Journal of Molecular Medicine

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Pulmonary vascular remodeling is a significant pathological feature of hypoxia-induced pulmonary hypertension (HPH), while pulmonary artery smooth muscle cell (PASMC) proliferation plays a leading role in pulmonary vascular remodeling. Spermine (Sp), a polyamine, plays a critical role in periodic cell proliferation and apoptosis. The present study was conducted to observe the association between hypoxia-induced PASMC proliferation and polyamine metabolism, and to explore the effects of exogenous Sp on PASMC poliferation and the related mechanisms. In the present study, PASMCs were cultured with cobalt chloride (CoCl2) to establish a hypoxia model, and Sp at various final concentrations (0.1, 1, 10 and 100 µM) was added to the medium of PASMCs 40 min prior to the induction of hypoxia. Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, cell counting kit-8 assay and 5-bromo-2′-deoxyuridine (BrdU) incorporation assay. Cell cycle progression was determined by flow cytometry, and the protein expression levels of spermidine/spermine N1-acetyltransferase (SSAT; the key enzyme in the terminal degradation of polyamine), ornithine decar boxylase (ODC; the key enzyme of polyamine biosynthesis), cyclin D1 and p27 were measured by western blot analysis. The results revealed that the proliferation of the PASMCs cultured with CoCl2 at 50 µM for 24 h markedly increased. The expression of ODC was decreased and the expression of SSAT was increased in the cells under hypoxic conditions. Exogenous Sp at concentrations of 1 and 10 µM significantly inhibited hypoxia induced PASMC proliferation, leading to cell cycle arrest at the G1/G0 phase. In addition, Sp decreased cyclin D1 expression, increased p27 expression, and suppressed the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT); however, the above-metioned parameters were not markedly affected by Sp at concentrations of 0.1 or 100 µM. These results suggest that hypoxia disrupts polyamine metabolism, and Sp at concentrations of 1 and 10 µM inhibits the increase in human PASMC proliferation caused by chemically-induced hypoxia via the suppression of the ERK1/2- and PI3K/AKT-associated pathways. This study thus offer new insight into the prevention and treatment of HPH.

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Leptin promotes proliferation of neonatal mouse stem/progenitor spermatogonia

Yersal

Köse

Horzum

et al. 2020

J Assist Reprod Genet

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Purpose To keep and increase spermatogonial stem cell number (SSC) is the only available option for pediatric cancer survivors to maintain fertility. Leptin is secreted by the epididymal white adipose tissue and has receptors on stem/progenitor spermatogonia. The purpose of this study is to demonstrate dose-and time-dependent proliferative effect of leptin on stem/progenitor spermatogonia cultures from prepubertal mice testes. Methods CD90.2 (+) stem/progenitor spermatogonia were isolated from the C57BL/6 mouse testis on postnatal day 6 and placed in culture. The proliferative effect of leptin supplementation was assessed by colony formation (diameter and number), WST proliferation assays, and xCELLigence real-time cell analysis (RTCA) on days 3, 5, and 7 of culture. Expressions of p-ERK1/2, p-STAT3, total STAT3, and p-SHP2 levels were determined by western blot analysis. Results Leptin supplementation of 100 ng/ml increased the diameter (p = 0.001) and number (p = 0.01) of colonies in stem/ progenitor spermatogonial cultures and caused higher proliferation by WST-1 (p = 0.009) compared with the control on day 7. The EC50 was calculated as 114 ng/ml for leptin by RTCA. Proliferative dose of leptin induced increased expression of p-ERK1/ 2 (p = 0.009) and p-STAT3 (p = 0.023) on stem/progenitor spermatogonia when compared with the untreated group. ConclusionThe results indicated that leptin supplementation exhibited a dose-and time-dependent proliferative effect on stem/ progenitor spermatogonia that was associated with increased expression of ERK1/2 and STAT3 pathways while maintaining their undifferentiated state. This output presents a new agent that may help to expand the stem/progenitor spermatogonia pool from the neonatal testis in order to autotransplant after cancer treatment.

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The effect of ferulic acid ethyl ester on leptin-induced proliferation and migration of aortic smooth muscle cells

Cited by 19 publications

References 52 publications

Genistein suppresses leptin‐induced proliferation and migration of vascular smooth muscle cells and neointima formation

Genistein suppresses leptin‐induced proliferation and migration of vascular smooth muscle cells and neointima formation

Exogenous spermine inhibits the proliferation of human pulmonary artery smooth muscle cells caused by chemically-induced hypoxia via the suppression of the ERK1/2- and PI3K/AKT-associated pathways

Leptin promotes proliferation of neonatal mouse stem/progenitor spermatogonia

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