The Regulation Of β₂ Adrenergic Agonist/antagonist On PPAR-γ2 MRNA Expression Of Human MSCs Osteogenic Differentiation In Vitro

ObjectiveTo investigate the effect ofβ₂ adrenergic agonist/antagonist on theexpression of PPARγ₂mRNA during the process of inducing in vitro humanbone marrow mesenchymal stem cells differentiate toward osteoblast and toexplore the molecular mechanism of sympathetic nerve's effect on bonemetabolism.MethodhMSCs were isolated by means of the adherence screening method fromthe healtby adult volunteer bone marrow. The hMSCs of the second passagewere affirmed by osteogenic induction (OSI) and flow cytometric analysis ofexpressed surface antigens.After osteogenic induced 7 days,the hMSCs weredivided in three groups by randomization: A(β₂ adrenergic agonistgroup),B(β₂ adrenergic antagonist group) and C(normal control group,NC).Aand B group were given Salbutamol(β₂ adrenergic agonist) andICI-118551(β₂ adrenergic antagonist)with 1μmol/L,5μmol/L and 10μmol/Lrespectively.Then 3 days later, the mRNA expression of PPARγ₂ wasmeasured by real-time PCR. Reanlts1. The mRNA expression of PPARγ₂ was detected on hMSCs whenosteogenic induced.2. Salbutamol(β₂ adrenergic agonist) dose-dependently increased the mRNAexpression of PPARγ₂, and the effect was most obvious by 10μmol/L. Onthe contrary, ICI-118551(β₂ adrenergic antagonist) inhibited the mRNAexpression of PPARγ₂.Conclusions1. The mRNA expression of PPARγ₂ was detected on hMSCs of the secondpassage when osteogenic induced.2. During the process of inducing in vitro hMSCs differentiate towardosteoblasts, the mRNA expression of PPARγ₂ can be strengthen byβ₂adrenergic agonist and weaken byβ₂ adrenergic antagonist.It indicates thatβ₂ adrenergic agonist/antagonist may regulate the mRNAexpression of PPARγ₂ during the process of inducing hMSCs differentiatetoward osteoblasts,and then may regulate the bone formation.