Department of Physiology and Biophysics, Weill Cornell Medical College of Cornell University, New York, New York, USA.
J Phys Chem B. 2010 Sep 23;114(37):12046-57. doi: 10.1021/jp106373r.
The ligands of certain G-protein coupled receptors (GPCRs) are membrane soluble and reach their target from the lipid bilayer. Lipid composition and dynamics will therefore modulate the activity of these receptors, but specific roles of lipid components, including the ubiquitous cholesterol (Chol), are not clear. We have probed the organization and dynamics of such a lipid-bilayer-penetrating ligand, the endogenous ligand for the κ-opioid receptor (KOR) dynorphin A (1-17) (DynA), using molecular dynamics (MD) simulations of DynA in cholesterol-depleted and cholesterol-enriched model membranes. DynA is found to penetrate deep inside fluid dimyristoylphosphatidylcholine (DMPC) bilayers, and resides with its N-terminal helix at ∼6 Å away from the bilayer midplane, in a tilted orientation, at an ∼50° angle with respect to the membrane normal. In contrast, DynA inside DMPC/Chol membranes with 20% cholesterol (DMPC/Chol) is situated with its helical segment ∼5 A higher, i.e., closer to the lipid/water interface and in a relatively vertical orientation. The DMPC membrane shows greater thinning around the insertion and permits a stronger influx of water inside the hydrocarbon core than the DMPC/Chol membranes. Relating these results to data about key GPCR residues that have been implicated in interactions with membrane-inserting GPCR ligands, we conclude that the position of DynA in DMPC/Chol, but not in pure DMPC, correlates with generally proposed GPCR ligand entry pathways. Our predictions provide a possible mechanistic explanation as to why DynA binding to KOR, and the subsequent activation of the receptor, is facilitated in cholesterol-enriched environments. A quantitative description of DynA-induced membrane deformations is obtained with a continuum theory of membrane deformations (CTMD) that is based on hydrophobic matching. Comparison with the MD data reveals the significance of the lipid tail packing energy contribution in the DMPC/Chol mixtures in predicting equilibrium membrane shape around DynA. On this basis, specific corrections are introduced to this energy term within the CTMD framework, thereby extending the applicability of the CTMD framework to lipid raft mixtures and their interactions with GPCR proteins and their ligands.
某些 G 蛋白偶联受体 (GPCR) 的配体是膜溶性的,它们从脂质双层中到达靶标。因此,脂质组成和动力学将调节这些受体的活性,但包括普遍存在的胆固醇 (Chol) 在内的脂质成分的特定作用尚不清楚。我们使用耗尽和富含胆固醇的模型膜中的分子动力学 (MD) 模拟研究了这种穿透脂质双层的配体,即 κ-阿片受体 (KOR) 的内源性配体 κ-阿片肽 A (1-17)(DynA) 的组织和动力学。发现 DynA 可以穿透富含二肉豆蔻酰磷脂酰胆碱 (DMPC) 的双层 (DMPC) 双层的内部,并且其 N 端螺旋位于距双层中间平面约 6 Å 的位置,以相对于膜法线约 50°的倾斜角度存在。相比之下,在含有 20%胆固醇的 DMPC/Chol 膜(DMPC/Chol)中的 DynA 位于其螺旋段约 5 A 处更高的位置,即更靠近脂质/水界面并且处于相对垂直的位置。DMPC 膜在插入周围显示出更大的变薄,并且允许更多的水流入烃核内部,而不是 DMPC/Chol 膜。将这些结果与有关涉及与插入膜的 GPCR 配体相互作用的关键 GPCR 残基的数据相关联,我们得出结论,DynA 在 DMPC/Chol 中的位置,但不在纯 DMPC 中,与普遍提出的 GPCR 配体进入途径相关。我们的预测提供了一种可能的机制解释,即为什么 DynA 与 KOR 结合以及随后受体的激活在富含胆固醇的环境中更容易发生。使用基于疏水性匹配的膜变形连续体理论 (CTMD) 获得 DynA 诱导的膜变形的定量描述。与 MD 数据的比较揭示了在预测 DynA 周围的平衡膜形状时,DMPC/Chol 混合物中脂质尾部堆积能贡献的重要性。在此基础上,在 CTMD 框架内引入了该能量项的特定校正,从而将 CTMD 框架的适用性扩展到脂质筏混合物及其与 GPCR 蛋白及其配体的相互作用。