2010Immunological JournalRequires access

Effects of arotinoid ethylester on the proliferation,apoptosis and TGF-β1 secretion of mouse glomerular mesangial cells

Rupeng Wang

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Abstract

This study aimed to investigate and evaluate the effects of arotinoid ethylester(AE) on proliferation,apoptosis,and TGF-β1 secretion of mouse glomerular mesangial cells(GMC).We treated mice glomerular mesangial cells with AE or atRA at different concentrations.Then the cell proliferation and apoptosis of mouse glomerular mesangial cells were assessed respectively by MTT assay and Annexin V/PI doubled-labeled flow cytometry.ELISA was used to detect the content of TGF-β1 in supernatant fluid.Compared with normal group,the GMC proliferation of AE group was inhibited significantly(P0.05) in a dose dependent manner when the concentration of AE is between 10~(-8) mol/L to 10~(-5) mol/L.Compared with atRA,AE can get the same inhibition effect at lower concentration. AE also could induce apoptosis of GMC:the apoptosis rates of GMC in normal group and AE groups(10~(-7) mol/L,10~(-5) mol/L ) were(1.13±0.36)%,(9.52±0.99)%,and(27.23±2.88)%,respectively;AE could decrease the expression of TGF-β1 in supernatant fluid of GMC significantly(P0.05).The results mean that AE could inhibit cell proliferation and induce cell apoptosis in mouse glomerular mesangial cells,and the effect of inhibiting proliferation maybe related with the decrease of TGF-β1.

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What this paper is about

This study aimed to investigate and evaluate the effects of arotinoid ethylester(AE) on proliferation,apoptosis,and TGF-β1 secretion of mouse glomerular mesangial cells(GMC).We treated mice glomerular mesangial cells with AE or atRA at different concentrations.Then the cell proliferation and apoptosis of mouse glomerular mesangial cells were assessed respectively by MTT assay and Annexin V/PI doubled-labeled flow cytometry.ELISA was used to detect the content of TGF-β1 in supernatant fluid.Compared with normal group,the GMC proliferation of AE group was inhibited significantly(P0.05) in a dose dependent manner when the concentration of AE is between 10~(-8) mol/L to 10~(-5) mol/L.Compared with atRA,AE can get the same inhibition effect at lower concentration. AE also could induce apoptosis of GMC:the apoptosis rates of GMC in normal group and AE groups(10~(-7) mol/L,10~(-5) mol/L ) were(1.13±0.36)%,(9.52±0.99)%,and(27.23±2.88)%,respectively;AE could decrease the expression of TGF-β1 in supernatant fluid of GMC significantly(P0.05).The results mean that AE could inhibit cell proliferation and induce cell apoptosis in mouse glomerular mesangial cells,and the effect of inhibiting proliferation maybe related with the decrease of TGF-β1.

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Available abstract

This study aimed to investigate and evaluate the effects of arotinoid ethylester(AE) on proliferation,apoptosis,and TGF-β1 secretion of mouse glomerular mesangial cells(GMC).We treated mice glomerular mesangial cells with AE or atRA at different concentrations.Then the cell proliferation and apoptosis of mouse glomerular mesangial cells were assessed respectively by MTT assay and Annexin V/PI doubled-labeled flow cytometry.ELISA was used to detect the content of TGF-β1 in supernatant fluid.Compared with normal group,the GMC proliferation of AE group was inhibited significantly(P0.05) in a dose dependent manner when the concentration of AE is between 10~(-8) mol/L to 10~(-5) mol/L.Compared with atRA,AE can get the same inhibition effect at lower concentration. AE also could induce apoptosis of GMC:the apoptosis rates of GMC in normal group and AE groups(10~(-7) mol/L,10~(-5) mol/L ) were(1.13±0.36)%,(9.52±0.99)%,and(27.23±2.88)%,respectively;AE could decrease the expression of TGF-β1 in supernatant fluid of GMC significantly(P0.05).The results mean that AE could inhibit cell proliferation and induce cell apoptosis in mouse glomerular mesangial cells,and the effect of inhibiting proliferation maybe related with the decrease of TGF-β1.

Key concepts: Apoptosis, Mesangial cell, Annexin, Flow cytometry, Cell growth, Transforming growth factor, Internal medicine, Endocrinology

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