Localization of prostaglandin F2α inhibition of lipoprotein use by bovine luteal cells

Localization of prostaglandin F2α inhibition of lipoprotein use by bovine luteal cells
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前列腺素 F2α 对牛黄体细胞脂蛋白利用抑制的定位

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发表时间:
1992
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影响因子:
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通讯作者:
J. Pate
J. Pate
中科院分区:
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文献类型:
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作者:
D. Grusenmeyer;J. Pate

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前列腺素F2 α(PGF 2 α)抑制体外牛黄体细胞产生脂蛋白刺激的孕酮,本研究的目的是定位PGF 2 α的作用部位。用PGF 2 α处理培养的牛黄体细胞7天,然后在氨鲁米特(抑制胆固醇侧链裂解)存在下用脂蛋白或25-羟基胆固醇处理最后48小时。测定PGF 2 α对孕酮产生、细胞胆固醇含量、线粒体胆固醇含量和胆固醇侧链裂解活性的影响。正如预期的那样,PGF 2 α抑制(P <0.05)脂蛋白刺激的孕酮产生。然而,PGF 2 α并不抑制低密度脂蛋白刺激或高密度脂蛋白刺激的细胞胆固醇升高(P <0.05),也不抑制脂蛋白诱导的线粒体胆固醇含量升高(P <0.05)。此外,在PGF 2 α单独存在下,线粒体胆固醇含量增加(P <0.05)。为了确定PGF 2 α诱导的类固醇生成抑制是否发生在侧链裂解反应时或之后,我们用易于扩散的固醇25-羟基胆固醇处理细胞。前列腺素F2 α不抑制25-羟基胆固醇刺激的孕酮产生(P <0.05)。因此,前列腺素F2 α可能在胆固醇转运至线粒体之后但在胆固醇侧链裂解之前的位点发挥其溶黄体作用。
Prostaglandin F2 alpha (PGF2 alpha) inhibits lipoprotein-stimulated progesterone production by bovine luteal cells in vitro and the objective of this study was to localize the site of action of PGF2 alpha. Cultured bovine luteal cells were treated with PGF2 alpha for seven days, and then with either lipoproteins or 25-hydroxycholesterol in the presence of aminoglutethimide (which inhibits cholesterol side-chain cleavage) for the final 48 h. The effects of PGF2 alpha on progesterone production, cellular cholesterol content, mitochondrial cholesterol content and cholesterol side-chain cleavage activity were determined. As expected, PGF2 alpha inhibited (P less than 0.05) lipoprotein-stimulated progesterone production. However, PGF2 alpha did not inhibit low-density lipoprotein-stimulated, or high density lipoprotein-stimulated, increases in cellular cholesterol (P less than 0.05) or inhibit lipoprotein-induced increases in mitochondrial cholesterol content (P less than 0.05). Additionally, cholesterol content of mitochondria increased (P less than 0.05) in the presence of PGF2 alpha alone. To determine if the PGF2 alpha-induced inhibition of steroidogenesis occurred at, or after, the side-chain cleavage reaction, we treated cells with the readily diffusable sterol, 25-hydroxycholesterol. Prostaglandin F2 alpha did not inhibit 25-hydroxycholesterol-stimulated progesterone production (P less than 0.05). Prostaglandin F2 alpha may therefore exert its luteolytic effect at a site after cholesterol transport to the mitochondria but before cholesterol side-chain cleavage.