Abstract

This study aims to evaluate the effect of peroxisome proliferator-activated receptor (PPAR) γ gene inhibition on the adipogenic differentiation of rabbit bone marrow mesenchymal stem cells (BMSCs). Primary BMSCs were isolated from rabbit bone marrow, cultured, and the markers of BMSCs on cell’s surface were analyzed using flow cytometry. The experiment involved five groups, namely, control: untreated BMSCs; model: BMSCs treated with ethanol; empty siRNA: BMSCs treated with ethanol + empty siRNA; PPARγ: BMSCs treated with ethanol + PPARγ siRNA; and PPARγ inhibitor: BMSCs treated with ethanol + T0070907. RT-PCR and Western blotting were used to detect changes in the expression level of PPARγ, PETALA2 (AP2), lipoprotein lipase (LPL), fatty acid transport protein (FATP) 1, and fatty acid transporter (FAT). Adipocyte count and triacylglycerol content of the model and the empty siRNA groups were considerably greater than the control group ( P < 0.01 ). After the inhibition with PPARγ or T0070907, adipocyte count and triacylglycerol content of the PPARγ and T0070907 groups were significantly reduced ( P < 0.01 ), with no statistically significantly difference than the control group ( P > 0.05 ). The expression levels of PPARγ gene and protein in the model and empty siRNA groups were ominously enhanced than the control group ( P < 0.01 ), and after inhibition with PPARγ or T0070907, the PPARγ gene or protein expression level of PPARγ and T0070907 groups significantly reduced ( P < 0.01 ), with no statistically significance difference compared to the control group ( P > 0.05 ). The expression levels of Ap2, LPL, FATP1, and FAT genes in the model and empty siRNA groups were considerably greater compared to the control group ( P < 0.01 ). Inhibition with PPARγ or T0070907 in the PPARγ and T0070907 groups, respectively, lead to significantly reduced expression levels of adipogenic genes ( P < 0.01 ), with no statistically significance difference compared to the control ( P > 0.05 ). Inhibition of PPARγ gene downregulates the differentiation of BMSCs into adipocytes, indicating its putative role in the expression of adipogenic genes.

Highlights

  • Academic Editor: M Pallikonda Rajasekaran is study aims to evaluate the effect of peroxisome proliferator-activated receptor (PPAR) c gene inhibition on the adipogenic differentiation of rabbit bone marrow mesenchymal stem cells (BMSCs)

  • After the inhibition with PPARc or T0070907, adipocyte count and triacylglycerol content of the PPARc and T0070907 groups were significantly reduced (P < 0.01), with no statistically significantly difference than the control group (P > 0.05). e expression levels of PPARc gene and protein in the model and empty siRNA groups were ominously enhanced than the control group (P < 0.01), and after inhibition with PPARc or T0070907, the PPARc gene or protein expression level of PPARc and T0070907 groups significantly reduced (P < 0.01), with no statistically significance difference compared to the control group (P > 0.05). e expression levels of Ap2, lipoprotein lipase (LPL), FATP1, and fatty acid transporter (FAT) genes in the model and empty siRNA groups were considerably greater compared to the control group (P < 0.01)

  • Inhibition of PPARc gene downregulates the differentiation of BMSCs into adipocytes, indicating its putative role in the expression of adipogenic genes

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Summary

Introduction

Academic Editor: M Pallikonda Rajasekaran is study aims to evaluate the effect of peroxisome proliferator-activated receptor (PPAR) c gene inhibition on the adipogenic differentiation of rabbit bone marrow mesenchymal stem cells (BMSCs). E expression levels of Ap2, LPL, FATP1, and FAT genes in the model and empty siRNA groups were considerably greater compared to the control group (P < 0.01). Differentiation of bone marrow mesenchymal stem cells (BMSCs) into osteoblasts is significantly reduced, but their differentiation into adipocytes is greatly increased [5, 6]. Alcohol promotes the expression of adipogenic genes and induces the differentiation of pluripotent stromal stem cells into adipocytes in BMSCs at a certain stage of osteogenesis [11]. PPARc inhibitor: BMSCs were treated with 0.09 mol/L ethanol + T0070907 (Cayman Chemical, MI, USA)

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