Cytidine monophosphate-dependent synthesis of phosphatidylglycerol in permeabilized type II pneumonocytes.

Cytidine monophosphate-dependent synthesis of phosphatidylglycerol in permeabilized type II pneumonocytes.
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透化 II 型肺细胞中磷脂酰甘油的胞苷单磷酸依赖性合成。

DOI:
10.1042/bj2320539
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发表时间:
1985
期刊:
The Biochemical journal
影响因子:
--
通讯作者:
Tesan,M
Tesan,M
中科院分区:
--
文献类型:
--
作者:
Bleasdale,JE;Thakur,NR;Rader,GR;Tesan,M

文献摘要

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先前的研究结果支持这样的观点:在 II 型肺细胞中,CMP 参与肺表面活性物质磷脂酰胆碱和磷脂酰甘油的合成整合。在本研究中,直接改变大鼠 II 型肺细胞中 CMP 的量,并检查了磷脂酰甘油合成的变化。通过用无 Ca2+ 培养基处理,使 II 型肺细胞对 CMP 具有渗透性,然后通过测量放射性标记前体 [14C]甘油 3-磷酸的掺入来评估磷脂酰甘油合成,该前体不能被抵抗渗透的细胞有效利用。 CMP 极大地刺激[14C]甘油3-磷酸掺入磷脂酰甘油(但不掺入其他脂质)(约0.1 mM 的半最大刺激)。 CMP 刺激[14C]甘油3-磷酸并入磷脂酰基部分和磷脂酰甘油的头基中。 CMP 还刺激[14C]棕榈酸酯掺入磷脂酰甘油中。胎儿大鼠血清中的肌醇浓度 (0.2-2.0 mM) 抑制 CMP 依赖性[14C]甘油 3-磷酸掺入磷脂酰甘油,并促进 CMP 依赖性掺入磷脂酰肌醇。这些数据,当外推到胎儿 II 型肺细胞时,与这样的观点是一致的,即胎儿肺合成表面活性剂磷脂酰甘油的发育增加是由细胞内 CMP 的增加和肌醇可用性的下降所促进的,而先前发现这与该发育时期有关。
Results of previous investigations support the proposition that, in type II pneumonocytes, CMP is involved in integration of the synthesis of phosphatidylcholine and phosphatidylglycerol for lung surfactant. In the present investigation, the amount of CMP in rat type II pneumonocytes was altered directly and resultant changes in the synthesis of phosphatidylglycerol were examined. Type II pneumonocytes were made permeable to CMP by treatment with Ca2+-free medium, and phosphatidylglycerol synthesis was then assessed by measurement of the incorporation of a radiolabelled precursor, [14C]glycerol 3-phosphate, that was not effectively utilized by cells that resisted permeabilization. Incorporation of [14C]glycerol 3-phosphate into phosphatidylglycerol (but not into other lipids) was stimulated greatly by CMP (half-maximal stimulation at approx. 0.1 mM). CMP stimulated the incorporation of [14C]glycerol 3-phosphate into both the phosphatidyl moiety and the head group of phosphatidylglycerol. Incorporation of [14C]palmitate into phosphatidylglycerol was also stimulated by CMP. myo-Inositol, at concentrations found in foetal-rat serum (0.2-2.0 mM), inhibited CMP-dependent incorporation of [14C]glycerol 3-phosphate into phosphatidylglycerol and promoted, instead, CMP-dependent incorporation into phosphatidylinositol. These data, when extrapolated to foetal type II pneumonocytes, are consistent with the view that the developmental increase in the synthesis of phosphatidylglycerol for surfactant by foetal lungs is promoted by the increase in intracellular CMP and the declining availability of myo-inositol that were found previously to be associated with this period of development.