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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Mitochondria are double-membrane organelles of the eukaryotes involved in cellular metabolism, signaling, ATP synthesis, and programmed cell death.  Each of these processes requires specific proteins and enzymes that must be correctly sorted to the right mitochondrial subcompartment for the proper functioning of the organelle.
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Mitochondrial unfolded protein response gene CLPP changes mitochondrial dynamics and affects mitochondrial function.

GuiJun Wu1, Qing Xiong1, XiaoJun Wei2

  • 1Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, China.

Peerj
|July 16, 2019
PubMed
Summary

Mitochondrial unfolded protein response gene CLPP improves mitochondrial dynamics and function in islet cells under high glucose and fat conditions. This study reveals CLPP

Keywords:
Caseinolytic peptidase PFissionFusionMitochondrial dynamicsMitochondrial unfolded protein response

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Area of Science:

  • Mitochondrial Biology
  • Cellular Metabolism
  • Diabetes Research

Background:

  • Mitochondrial dynamics and function are critical for islet beta-cell health and are implicated in diabetes.
  • The mitochondrial unfolded protein response (UPRmt) plays a role in cellular stress, but its specific impact on islet mitochondrial dynamics remains unexplored.
  • CLPP, a key UPRmt gene, has not been previously investigated for its role in islet cell mitochondrial dynamics.

Purpose of the Study:

  • To investigate the effects of CLPP on mitochondrial dynamics and function in the Min6 islet beta-cell line under conditions mimicking diabetes (high glucose and high fat).
  • To determine if CLPP influences mitochondrial fission, fusion, ultrastructure, and overall function in response to metabolic stress.

Main Methods:

  • Utilized the mouse islet beta-cell line Min6.
  • Exposed cells to high glucose (HG) and high fat (HF) conditions.
  • Manipulated CLPP expression using siRNA (siCLPP) and control (NC) treatments.
  • Assessed mitochondrial dynamics (fission/fusion), ultrastructure, ATP levels, reactive oxygen species (ROS) production, mitochondrial membrane potential, insulin secretion, and apoptosis.

Main Results:

  • High glucose and high fat conditions increased CLPP mRNA and protein expression in mitochondria.
  • siCLPP treatment led to increased mitochondrial fission, decreased fusion, and damaged mitochondrial ultrastructure.
  • Mitochondrial function was impaired in siCLPP groups, evidenced by decreased ATP, increased ROS, and reduced mitochondrial membrane potential.
  • Insulin secretion decreased and apoptosis rates increased in siCLPP-treated cells.

Conclusions:

  • CLPP plays a protective role against high glucose and high fat-induced mitochondrial dysfunction in islet beta-cells.
  • CLPP alleviates mitochondrial dynamics imbalance and preserves mitochondrial function under metabolic stress.
  • Targeting CLPP may offer a therapeutic strategy for managing diabetes-related mitochondrial dysfunction.