CO2 permeability of cell membranes is regulated by membrane cholesterol and protein gas channels

Fabian Itel, Samer Al-Samir, Fredrik Öberg, Mohamed Chami, Manish Kumar, Claudiu T. Supuran, Peter M.T. Deen, Wolfgang Meier, Kristina Hedfalk, Gerolf Gros, Volker Endeward

Research output: Contribution to journalArticlepeer-review

59 Scopus citations

Abstract

Recent observations that some membrane proteins act as gas channels seem surprising in view of the classical concept that membranes generally are highly permeable to gases. Here, we study the gas permeability of membranes for the case of CO2, using a previously established mass spectrometric technique. We first show that biological membranes lacking protein gas channels but containing normal amounts of cholesterol (30-50 mol% of total lipid), e.g., MDCK and tsA201 cells, in fact possess an unexpectedly low CO2 permeability (PCO2) of ∼0.01 cm/s, which is 2 orders of magnitude lower than the PCO2 of pure planar phospholipid bilayers (∼1 cm/s). Phospholipid vesicles enriched with similar amounts of cholesterol also exhibit PCO2 ≈ 0.01 cm/s, identifying cholesterol as the major determinant of membrane PCO2. This is confirmed by the demonstration that MDCK cells depleted of or enriched with membrane cholesterol show dramatic increases or decreases in PCO2, respectively. We demonstrate, furthermore, that reconstitution of human AQP-1 into cholesterol-containing vesicles, as well as expression of human AQP-1 in MDCK cells, leads to drastic increases in PCO2, indicating that gas channels are of high functional significance for gas transfer across membranes of low intrinsic gas permeability.

Original languageEnglish (US)
Pages (from-to)5182-5191
Number of pages10
JournalFASEB Journal
Volume26
Issue number12
DOIs
StatePublished - Dec 1 2012

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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