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在具有基质小泡样脂质组成的模型脂质体中,膜介导的磷酸钙沉淀。

Membrane-mediated precipitation of calcium phosphate in model liposomes with matrix vesicle-like lipid composition.

作者信息

Skrtic D, Eanes E D

机构信息

Bone Research Branch Research Associate Program, National Institute of Dental Research, National Institute of Standards and Technology, Gaithersburg, Maryland.

出版信息

Bone Miner. 1992 Feb;16(2):109-19. doi: 10.1016/0169-6009(92)90881-d.

DOI:10.1016/0169-6009(92)90881-d
PMID:1576486
Abstract

The present study examined calcium phosphate precipitation in aqueous suspensions of artificial liposomes which closely resembled matrix vesicles (MV) in membrane lipid composition. At 22 degrees C, the liposomes per se did not initiate precipitation in the suspending medium for up to 120 h when the latter was made supersaturated with respect to hydroxyapatite (2.25 mM Ca2+, 1.5 mM PO4, 240 mosmol, pH 7.4). Likewise, the suspending medium remained stable for up to 72 h when precipitation was induced within the aqueous interiors of the liposomes by encapsulating pH 7.4-buffered 50 mM PO4 solutions in the interior spaces and making the enclosing membranes permeable to external solution Ca2+ ions with the ionophore X-537A. However, extraliposomal precipitation readily occurred under these latter conditions when phosphatidylserine (PS) and sphingomyelin (Sph) were deleted from the MV-like lipid formulation used to prepare the liposomes. These results suggest that lipidic membrane constituents such as PS and Sph may have a controlling influence on MV-mediated calcification in vivo by affecting the release of intravesicularly formed mineral crystals into the extracellular matrix space where they can subsequently grow and proliferate.

摘要

本研究检测了人工脂质体水悬浮液中的磷酸钙沉淀情况,该脂质体在膜脂质组成上与基质小泡(MV)极为相似。在22摄氏度时,当悬浮介质相对于羟基磷灰石处于过饱和状态(2.25 mM钙离子、1.5 mM磷酸根、240毫渗量、pH 7.4)时,脂质体本身在长达120小时内不会在悬浮介质中引发沉淀。同样,当通过在内部空间封装pH 7.4缓冲的50 mM磷酸根溶液并使用离子载体X - 537A使包围膜对外部溶液中的钙离子通透,从而在脂质体水相内部诱导沉淀时,悬浮介质在长达72小时内保持稳定。然而,当从用于制备脂质体的类MV脂质配方中去除磷脂酰丝氨酸(PS)和鞘磷脂(Sph)时,在上述条件下脂质体外沉淀很容易发生。这些结果表明,诸如PS和Sph等脂质膜成分可能通过影响泡内形成的矿物晶体释放到细胞外基质空间(在那里它们随后可以生长和增殖),从而对体内MV介导的钙化产生控制作用。

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