Coenzyme Q10 suppresses apoptosis of mouse pancreatic β-cell line MIN6

Keisuke Sumi1, Tsuyoshi Okura1, Youhei Fujioka1

  • 11Division of Endocrinology and Metabolism, Molecular Medicine and Therapeutics, Faculty of Medicine, Tottori University, 36-1 Nishi-chou, Yonago, Tottori 683-8504 Japan.

Abstract

Insights

Coenzyme Q10 (CoQ10) protects pancreatic beta cells from apoptosis induced by mitochondrial stress. This study details how CoQ10 preserves cell viability and inhibits key apoptotic pathways in mitochondrial diabetes research.

Area of Science:

  • Mitochondrial biology
  • Cellular apoptosis
  • Endocrinology

Background:

  • Mitochondrial diabetes involves beta-cell apoptosis due to mitochondrial stress, impacting insulin secretion.
  • Coenzyme Q10 (CoQ10) is suggested to have therapeutic benefits for mitochondrial diabetes.
  • Previous work indicated CoQ10 protects against mitochondrial stress in beta cells, but mechanisms were unclear.

Purpose of the Study:

  • To investigate the protective effects of CoQ10 on pancreatic beta cells against apoptosis.
  • To elucidate the detailed apoptotic cascade inhibited by CoQ10 in mitochondrial stress models.

Main Methods:

  • MIN6 mouse pancreatic beta cells were treated with staurosporine (STS) to induce apoptosis, with or without CoQ10.
  • Apoptosis was assessed using WST-8 assays, annexin-V staining, western blotting, and DNA degradation analysis.

Main Results:

  • CoQ10 significantly increased cell viability (76%) compared to STS treatment alone (47%).
  • CoQ10 inhibited phosphatidylserine externalization, a key marker of early apoptosis.
  • CoQ10 prevented mitochondrial cytochrome c release and caspase-3 activation, crucial steps in the apoptotic cascade.

Conclusions:

  • Coenzyme Q10 demonstrates significant anti-apoptotic effects on pancreatic beta cells.
  • CoQ10 protects beta cells from STS-induced apoptosis by inhibiting key molecular events in the apoptotic cascade.

Related Concept Videos

Cofactors and Coenzymes01:27

Cofactors and Coenzymes

Enzymes require additional components for proper function. There are two such classes of molecules: cofactors and coenzymes. Cofactors are metallic ions and coenzymes are non-protein organic molecules. Both of these types of helper molecule can be tightly bound to the enzyme or bound only when the substrate binds.
87.6K
Cofactors and Coenzymes01:24

Cofactors and Coenzymes

Enzymes are proteins made of amino acids. The functional group of each constituent amino acid catalyzes a wide variety of chemical reactions via ionic interactions or acid-base reactions. However, amino acids cannot catalyze oxidation-reduction and group transfer reactions and need to be aided by non-protein components called cofactors. Cofactors are also referred to as the chemical teeth of an enzyme.
Cofactors can be metallic ions or organic molecules called coenzymes. These types of helper...
12.8K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
15.2K
Role of Reduced Coenzymes NADH and FADH₂01:29

Role of Reduced Coenzymes NADH and FADH₂

The energy released from the breakdown of the chemical bonds within nutrients can be stored either through the reduction of electron carriers or in the bonds of adenosine triphosphate (ATP). In living systems, a small class of compounds functions as mobile electron carriers, molecules that bind to and shuttle high-energy electrons between compounds in pathways. The principal electron carriers that will be considered originate from the B vitamin group and are derivatives of nucleotides; they are...
16.9K
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
710
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.6K