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Paraoxonase-like APMAP maintains endoplasmic reticulum-associated lipid and lipoprotein homeostasis

Blessy Paul1, Holly Merta1, Rupali Ugrankar-Banerjee1

  • 1Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75390.

Biorxiv : the Preprint Server for Biology
|February 8, 2024
PubMed

Insights

The endoplasmic reticulum protein APMAP acts as an antioxidant, crucial for maintaining lipid and lipoprotein homeostasis. Its depletion causes oxidative stress and metabolic dysfunction, highlighting its role in preventing disease.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Diseases

Background:

  • Oxidative stress disrupts lipid homeostasis, contributing to metabolic diseases.
  • Endoplasmic reticulum (ER) generates reactive oxygen species, necessitating antioxidant control.
  • The role of ER-localized antioxidants in lipid and lipoprotein metabolism is understudied.

Purpose of the Study:

  • To characterize the paraoxonase-like APMAP protein.
  • To investigate APMAP's function in ER-localized redox and lipid homeostasis.
  • To determine APMAP's role in lipoprotein maturation.

Main Methods:

  • Multi-organismal profiling (Drosophila, zebrafish, mammalian cells).
  • Analysis of APMAP-depleted cells and organisms.
  • Lipidomics and ApoB-lipoprotein analysis.
  • Rescue experiments with N-acetylcysteine (NAC) and ceramide synthesis inhibitors.

Main Results:

  • APMAP is an ER-localized protein essential for redox and lipid homeostasis.
  • APMAP depletion causes ER stress, lipid droplet accumulation, and perturbed ApoB-lipoprotein metabolism.
  • APMAP loss leads to altered phospholipids and increased ceramides, impacting lipoprotein maturation.
  • APMAP depletion in model organisms disrupts fat and lipoprotein metabolism, with implications for atherosclerosis.

Conclusions:

  • APMAP functions as an ER-localized antioxidant.
  • APMAP is critical for maintaining lipid and lipoprotein homeostasis.
  • Targeting APMAP may offer therapeutic strategies for metabolic diseases.

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