# The modulation of the hexosamine biosynthetic pathway impacts the localization of CD36 in macrophages

## TL;DR

This study explores how changes in a biochemical pathway affect the location of a protein called CD36 in macrophages, which could impact atherosclerosis.

## Contribution

The study reveals a novel link between UDP-GlcNAc availability and CD36 localization via Rab-5-mediated trafficking in macrophages.

## Key findings

- Modulating UDP-GlcNAc levels affects CD36 localization in J774 macrophages.
- Rab-5 activity is influenced by UDP-GlcNAc availability, impacting endocytic trafficking.
- Chemical treatments like Thiamet G and Azaserine alter CD36 distribution between plasma membrane and cytoplasm.

## Abstract

CD36 is a type 2 cell surface scavenger receptor expressed in various tissues. In macrophages, CD36 recognizes oxidized low-density lipoprotein (ox-LDL), which promotes the formation of foam cells, the first step toward an atherosclerotic arterial lesion. CD36 possesses a variety of posttranslational modifications, among them N-glycosylation and O-GlcNAc modification. Some of the roles of these modifications on CD36 are known, such as N-linked glycosylation, which provides proper folding and trafficking to the plasma membrane in the human embryonic kidney. This study aimed to determine whether variations in the availability of UDP-GlcNAc could impact Rab-5-mediated endocytic trafficking and, therefore, the cellular localization of CD36. These preliminary results suggest that the availability of the substrate UDP-GlcNAc, modulated in response to treatment with Thiamet G (TMG), OSMI-1 (O-GlcNAcylation enzymes modulators) or Azaserine (HBP modulator), influences the localization of CD36 in J774 macrophages, and the endocytic trafficking as evidenced by the regulatory protein Rab-5, between the plasma membrane and the cytoplasm.