Carter Rhonda L, Grisanti Laurel A, Yu Justine E, Repas Ashley A, Woodall Meryl, Ibetti Jessica, Koch Walter J, Jacobson Marlene A, Tilley Douglas G
Center for Translational Medicine (R.L.C., L.A.G., J.E.Y., A.A.R., M.W., J.I., W.J.K. and D.G.T.) and Department of Pharmacology (W.J.K. and D.G.T.), Temple University School of Medicine, and Moulder Center for Drug Discovery Research and Temple University School of Pharmacy (M.A.J.), Philadelphia, PA 19140, USA.
Pharmacol Res Perspect. 2014 Feb;2(1). doi: 10.1002/prp2.24.
Label-free systems for the agnostic assessment of cellular responses to receptor stimulation have been shown to provide a sensitive method to dissect receptor signaling. β-adenergic receptors (βAR) are important regulators of normal and pathologic cardiac function and are expressed in cardiomyocytes as well as cardiac fibroblasts, where relatively fewer studies have explored their signaling responses. Using label-free whole cell dynamic mass redistribution (DMR) assays we investigated the response patterns to stimulation of endogenous βAR in primary neonatal rat cardiac fibroblasts (NRCF). Catecholamine stimulation of the cells induced a negative DMR deflection resulting in a concentration-dependent pharmacological response that was competitively blocked by βAR blockade and non-competitively blocked by irreversible uncoupling of Gs proteins. Pharmacological profiling of subtype-selective βAR agonists and antagonists revealed a dominant role of β2AR in mediating the DMR responses, consistent with the relative expression levels of β2AR and β1AR in NRCF. Additionally, βAR-mediated cAMP generation was assessed via a fluorescence biosensor, revealing similar kinetics between DMR responses and cAMP generation. As such, βAR-dependent DMR responses were enhanced via inhibition of cAMP degradation, as well as dynamin-mediated receptor internalization. Finally, we assessed G protein-independent βAR signaling through epidermal growth factor receptor (EGFR). While inhibition of EGFR reduced the DMR response to βAR stimulation, our results demonstrate that G protein-dependent signaling produces a majority of the biological response to βAR stimulation in NRCF. Altogether, measurement of DMR responses in primary cardiac fibroblasts provides a sensitive readout for investigating endogenous βAR signaling via both G protein-dependent and -independent pathways.
已证明用于对细胞对受体刺激的反应进行无偏评估的无标记系统可提供一种剖析受体信号传导的灵敏方法。β-肾上腺素能受体(βAR)是正常和病理性心脏功能的重要调节因子,在心肌细胞以及心脏成纤维细胞中均有表达,而在心脏成纤维细胞中对其信号反应的研究相对较少。我们使用无标记全细胞动态质量重分布(DMR)测定法,研究了原代新生大鼠心脏成纤维细胞(NRCF)中内源性βAR受刺激后的反应模式。儿茶酚胺刺激细胞会引起DMR负向偏转,从而产生浓度依赖性的药理学反应,该反应可被βAR阻断剂竞争性阻断,并被Gs蛋白的不可逆解偶联非竞争性阻断。亚型选择性βAR激动剂和拮抗剂的药理学分析表明,β2AR在介导DMR反应中起主导作用,这与NRCF中β2AR和β1AR的相对表达水平一致。此外,通过荧光生物传感器评估了βAR介导的cAMP生成,结果显示DMR反应和cAMP生成之间具有相似的动力学。因此,通过抑制cAMP降解以及发动蛋白介导的受体内化,βAR依赖性DMR反应得到增强。最后,我们通过表皮生长因子受体(EGFR)评估了G蛋白非依赖性βAR信号传导。虽然抑制EGFR会降低对βAR刺激的DMR反应,但我们的结果表明,G蛋白依赖性信号传导在NRCF中对βAR刺激产生了大部分生物学反应。总之,原代心脏成纤维细胞中DMR反应的测量为研究内源性βAR通过G蛋白依赖性和非依赖性途径的信号传导提供了灵敏的读数。