Amyloid β-protein stimulates trafficking of cholesterol and caveolin-1 from the plasma membrane to the Golgi complex in mouse primary astrocytes

U. Igbavboa, G. Y. Sun, G. A. Weisman, Yan He, W. G. Wood

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

The Golgi complex plays a key role in cholesterol trafficking in cells. Our earlier study demonstrated amyloid β-protein (Aβ) alters cholesterol distribution and abundance in the Golgi complex of astrocytes. We now test the hypothesis that the Aβ-induced increase in Golgi complex cholesterol is due to retrograde movement of the cholesterol carrier protein caveolin-1 from the cell plasma membrane to the Golgi complex in astrocytes. Results with mouse primary astrocytes indicated that Aβ1-42-induced increase in cholesterol and caveolin abundance in the Golgi complex was accompanied by a reduction in cholesterol and caveolin levels in the plasma membrane. Transfected rat astrocytes (DITNC1) with siRNA directed at caveolin-1 mRNA inhibited the Aβ1-42-induced redistribution of both cholesterol and caveolin from the plasma membrane to the Golgi complex. In astrocytes not treated with Aβ1-42, suppression of caveolin-1 expression also significantly reduced cholesterol abundance in the Golgi complex, further demonstrating the role for caveolin in retrograde transport of cholesterol from the plasma membrane to the Golgi complex. Perturbation of this process by Aβ1-42 could have consequences on membrane structure and cellular functions requiring optimal levels of cholesterol.

Original languageEnglish (US)
Pages (from-to)328-338
Number of pages11
JournalNeuroscience
Volume162
Issue number2
DOIs
StatePublished - Aug 18 2009

Bibliographical note

Funding Information:
This work was supported by NIH grants AG-23524, AG-18357 and the Department of Veterans Affairs.

Keywords

  • Alzheimer's disease
  • Golgi complex
  • amyloid β-protein
  • astrocytes
  • caveolin
  • cholesterol

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