Cell membrane fluctuations are regulated by medium macroviscosity: Evidence for a metabolic driving force

Shmuel Tuvia, Ada Almagor, Arkady Bitler, Shlomo Levin, Rafi Korenstein, Saul Yedgar

Research output: Contribution to journalArticlepeer-review

Abstract

Extracellular fluid macroviscosity (EFM), modified by macromolecular cosolvents as occurs in body fluids, has been shown to affect cell membrane protein activities but not isolated proteins. In search for the mechanism of this phenomenon, we examined the effect of EFM on mechanical fluctuations of the cell membrane of human erythrocytes. The macroviscosity of the external medium was varied by adding to it various macromolecules [dextrans (70, 500, and 2,000 kDa), polyethylene glycol (20 kDa), and carboxymethyl-cellulose (100 kDa)], which differ in size, chemical nature, and in their capacity to increase fluid viscosity. The parameters of cell membrane fluctuations (maximal amplitude and half-width of amplitude distribution) were diminished with the elevation of solvent macroviscosity, regardless of the cosolvent used to increase EFM. Because thermally driven membrane fluctuations cannot be damped by elevation of EFM, the existence of a metabolic driving force is suggested. This is supported by the finding that in ATP-depleted red blood cells elevation of EMF did not affect cell membrane fluctuations. This study demonstrates that (i) EFM is a regulator of membrane dynamics, providing a possible mechanism by which EFM affects cell membrane activities; and (ii) cell membrane fluctuations are driven by a metabolic driving force in addition to the thermal one.

Original languageEnglish
Pages (from-to)5045-5049
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume94
Issue number10
DOIs
StatePublished - 13 May 1997

Fingerprint

Dive into the research topics of 'Cell membrane fluctuations are regulated by medium macroviscosity: Evidence for a metabolic driving force'. Together they form a unique fingerprint.

Cite this