Related Experiment Video

Updated: Jun 10, 2026

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy
10:45

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy

Published on: July 20, 2012

Mitochondrial remodeling following fission inhibition by 15d-PGJ2 involves molecular changes in mitochondrial fusion

Rekha Kar1, Nandita Mishra, Prajjal K Singha

  • 1Department of Pathology, UT Health Science Center at San Antonio, San Antonio, TX 78229, USA.

Biochemical and Biophysical Research Communications
|August 4, 2010
PubMed

Insights

15 deoxy Delta(12,14) prostaglandin J2 (15d-PGJ2) initially promotes mitochondrial fusion but prolonged exposure causes mitochondrial swelling and dysfunction. This involves OPA1 degradation and Mfn1/Mfn2 downregulation, highlighting complex mitochondrial remodeling.

Area of Science:

  • Cell Biology
  • Mitochondrial Dynamics
  • Biochemistry

Background:

  • Mitochondrial fusion and fission are critical for cellular function.
  • 15 deoxy Delta(12,14) prostaglandin J2 (15d-PGJ2) was previously shown to inactivate Drp1 and induce mitochondrial fusion.

Purpose of the Study:

  • To investigate the long-term effects of 15d-PGJ2 on mitochondrial morphology and dynamics.
  • To elucidate the molecular mechanisms underlying 15d-PGJ2-induced mitochondrial remodeling.

Main Methods:

  • Cell culture and prolonged incubation with 15d-PGJ2.
  • Analysis of mitochondrial fusion and fission proteins (Mfn1, Mfn2, OPA1, Drp1).
  • Assessment of protein degradation and ubiquitination.
  • Treatment with thiol antioxidants.

Main Results:

  • Prolonged 15d-PGJ2 exposure led to mitochondrial swelling and cristae disorganization.
  • Initial fusion required Mfn1, Mfn2, and OPA1, but later stages involved OPA1 degradation and ubiquitination, alongside Mfn1/Mfn2 downregulation.
  • Drp1 inhibition mimicked these effects, causing loss of fusion proteins.
  • Thiol antioxidants prevented OPA1 loss and ubiquitination, mitigating mitochondrial elongation.

Conclusions:

  • 15d-PGJ2 induces complex, biphasic changes in mitochondrial dynamics.
  • Mitochondrial dysfunction arises from dysregulation of fusion/fission proteins and post-translational modifications.
  • Thiol antioxidants may protect against 15d-PGJ2-induced mitochondrial damage.

More Related Videos

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells06:14

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells

Published on: November 14, 2025

Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs08:15

Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs

Published on: August 15, 2025

Related Concept Videos

Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial precursors...
Mitochondrial Protein Sorting01:39

Mitochondrial Protein Sorting

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.
Most of these mitochondrial proteins are encoded by the nucleus and imported to the mitochondria as unfolded or loosely folded precursors. Mitochondrial precursors...
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...