Affordable Access

Publisher Website

Phosphatidylcholine and cholesterol inhibit phosphatidate-mediated calcium traversal of liposomal bilayers

Authors
Journal
Biochimica et Biophysica Acta (BBA) - Biomembranes
0005-2736
Publisher
Elsevier
Publication Date
Volume
857
Issue
2
Identifiers
DOI: 10.1016/0005-2736(86)90357-3
Keywords
  • Phosphatidic Acid
  • Phosphatidylcholine
  • Cholesterol
  • Hydrogen Belt
  • Ca2+Transport
  • Phospholipid Bilayer
Disciplines
  • Biology

Abstract

Abstract Rates of phosphatidic acid- (PA-) mediated Ca 2+-traversal are maximal in ‘passive bilayers’ void of lipid CO and OH groups: dietherphosphatidylcholine (diether-PC) or OH-blocked cholesterol liposomes. Phosphatidylcholine (PC) as bilayer matrix causes 99% inhibition, while 45 mol% cholesterol in passive bilayers inhibits by about 70%. Possibly, the absence of CO and OH groups causes a dehydration of the ‘hydrogen belts’, i.e., the membrane strata occupied by hydrogen bond acceptors (CO of phospholipids) and donors (OH of cholesterol, sphingosine) and thereby facilitates the formation of dehydrated Ca(PA) 2, the ionophoric vehicle; or (our preferred explanation) PC engages in a (non-ionophoric) Ca(PA - PC) complex and thus reduces the concentration of the ionophore, while cholesterol competes with Ca 2+ for the CO groups of phosphatidic acid by hydrogen-bonding. The Ca 2+-traversal rates realized in bilayers with modified hydrogen belts lend support to the speculation that a Ca(PA) 2 ferry may be of physiological importance, e.g., in membranes (such as myelin) containing much ether phospholipid (plasmalogen); and that Ca 2+-membrane association and traversal may be controlled by the composition of the hydrogen belts.

There are no comments yet on this publication. Be the first to share your thoughts.