Campus Units
Chemistry, Ames Laboratory
Document Type
Article
Publication Version
Accepted Manuscript
Publication Date
1-2018
Journal or Book Title
European Biophysics Journal
Volume
47
Issue
1
First Page
39
Last Page
48
DOI
10.1007/s00249-017-1227-5
Abstract
Membrane diffusion is one of the key mechanisms in the cellular function of receptors. The signaling of receptors for advanced glycation end-products (RAGE) has been extensively studied in the context of several pathological conditions, however, very little is known about RAGE diffusion. To fill this gap, RAGE lateral diffusion is probed in native, cholesterol-depleted, and cytoskeleton-altered cellular conditions. In native GM07373 cellular conditions, RAGE has a 90% mobile fraction and an average diffusion coefficient of 0.3 μm2/s. When depolymerization of the actin cytoskeleton is inhibited with the small molecule jasplakinolide (Jsp), the RAGE mobile fraction and diffusion coefficient decrease by 22 and 37%, respectively. In contrast, depolymerizing the filamentous actin cytoskeleton using the small molecule cytochalasin D (CD) does not alter the RAGE diffusion properties. There is a 70 and 50% decrease in phosphorylation of extracellular signal-regulated kinase (p-ERK) when the actin cytoskeleton is disrupted by CD or Jsp, respectively, in RAGE-expressing GM07373 cells. Disrupting the actin cytoskeleton in GM07373 cells that do not express detectable amounts of RAGE results in no change in p-ERK. Cholesterol depletion results in no statistically significant change in the diffusion properties of RAGE or p-ERK. This work presents a strong link between the actin cytoskeleton and RAGE diffusion and downstream signaling, and serves to further our understanding of the factors influencing RAGE lateral diffusion.
Copyright Owner
Springer Nature
Copyright Date
2017
Language
en
File Format
application/pdf
Recommended Citation
Syed, Aleem; Zhu, Qiaochu; and Smith, Emily A., "Lateral diffusion and signaling of receptor for advanced glycation end-products (RAGE): a receptor involved in chronic inflammation" (2018). Chemistry Publications. 1227.
https://lib.dr.iastate.edu/chem_pubs/1227
Included in
Analytical Chemistry Commons, Biological Phenomena, Cell Phenomena, and Immunity Commons, Biophysics Commons, Cell Biology Commons
Comments
This is a post-peer-review, pre-copyedit version of an article published in European Biophysics Journal. The final authenticated version is available online at: http://dx.doi.org/10.1007/s00249-017-1227-5. Posted with permission.