Galectin-1 Induces Reversible Phosphatidylserine Exposure at the Plasma Membrane
Galectin-1 Induces Reversible Phosphatidylserine Exposure at the Plasma Membrane
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DOI：
10.1091/mbc.e08-07-0786
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发表时间：
2009-03-01
影响因子：
3.3
通讯作者：
Cummings, Richard D.
中科院分区：
文献类型：
--
作者：
Stowell, Sean R.;Karmakar, Sougata;Cummings, Richard D.
正常情况下，细胞通过诱导凋亡和吞噬清除进行生理更新，部分原因是暴露于细胞表面磷脂酰丝氨酸（PS）。相反，中性粒细胞似乎具有与凋亡无关的清除机制。在这里，我们表明半乳糖凝集素-1 （Gal-1）诱导PS暴露独立于线粒体电位、半胱天冬酶激活或细胞死亡的改变。此外，Gal-1诱导的PS暴露在Gal-1去除后恢复，而不改变细胞活力。gal -1诱导的PS暴露是独特的微结构域限制，但暴露于PS的细胞不会表现出明显的膜形态改变，也不会表现出典型的凋亡细胞中所见的泡形成。长期暴露于Gal-1会延长PS暴露时间，但不会改变细胞周期进程或细胞生长。这些结果表明，gal -1诱导的PS暴露和随后的活细胞吞噬清除代表了细胞更新的新范式。
Cells normally undergo physiological turnover through the induction of apoptosis and phagocytic removal, partly through exposure of cell surface phosphatidylserine (PS). In contrast, neutrophils appear to possess apoptosis-independent mechanisms of removal. Here we show that Galectin-1 (Gal-1) induces PS exposure independent of alterations in mitochondrial potential, caspase activation, or cell death. Furthermore, Gal-1-induced PS exposure reverts after Gal-1 removal without altering cell viability. Gal-1-induced PS exposure is uniquely microdomain restricted, yet cells exposing PS do not display evident alterations in membrane morphology nor do they exhibit bleb formation, typically seen in apoptotic cells. Long-term exposure to Gal-1 prolongs PS exposure with no alteration in cell cycle progression or cell growth. These results demonstrate that Gal-1-induced PS exposure and subsequent phagocytic removal of living cells represents a new paradigm in cellular turnover.