Related Experiment Video

Updated: Aug 16, 2026

Modified Annexin V/Propidium Iodide Apoptosis Assay For Accurate Assessment of Cell Death
07:34

Modified Annexin V/Propidium Iodide Apoptosis Assay For Accurate Assessment of Cell Death

Published on: April 24, 2011

Changes in vimentin in human macrophages during apoptosis induced by oxidised low density lipoprotein

K Müller1, S Dulku, S J Hardwick

  • 1Division of Cellular Molecular Pathology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK. khm20@cam.ac.uk

Atherosclerosis
|May 23, 2001
PubMed

Insights

Oxidized LDL triggers macrophage apoptosis, a key factor in atherosclerosis. Vimentin protein breakdown occurs early in this process, but not via caspase proteolysis.

Area of Science:

  • Cell Biology
  • Cardiovascular Research
  • Immunology

Background:

  • Macrophage apoptosis plays a role in human atherosclerotic lesion development.
  • Oxidized low-density lipoprotein (LDL) is a potential trigger for macrophage death in vivo.

Purpose of the Study:

  • To investigate the morphological and biochemical alterations of the vimentin filament network during human macrophage apoptosis.
  • To determine the specific role of oxidized LDL in inducing macrophage apoptosis and subsequent vimentin changes.

Main Methods:

  • Induction of apoptosis in human macrophages using oxidized LDL.
  • Analysis of vimentin cleavage fragments using gel electrophoresis and Western blotting.
  • Assessment of caspase involvement (caspase-3 and caspase-6) using specific inhibitors.
  • Microscopic examination of vimentin filament morphology during apoptosis.

Main Results:

  • Oxidized LDL, but not native or acetylated LDL, induced macrophage apoptosis.
  • Vimentin was cleaved into specific fragments (48-50, 46, 29, and 26 kDa) during apoptosis.
  • Caspase-6 appeared to mediate the formation of 26 and 46 kDa vimentin fragments, while caspase-3 showed minimal involvement in cleavage despite activation.
  • Vimentin filament breakdown occurred early and was observed in apoptotic bodies, independent of caspase activity.
  • Similar vimentin changes were noted in gliotoxin-induced apoptosis.

Conclusions:

  • Oxidized LDL is a potent inducer of macrophage apoptosis, characterized by specific vimentin cleavage.
  • While caspases, particularly caspase-6, are involved in generating some vimentin fragments, the overall filament breakdown during apoptosis is not solely mediated by caspase proteolysis.
  • These findings highlight the complex mechanisms of vimentin remodeling during programmed cell death in macrophages, relevant to atherosclerosis.

More Related Videos

Experimental Analysis of Apoptotic Thymocyte Engulfment by Macrophages06:47

Experimental Analysis of Apoptotic Thymocyte Engulfment by Macrophages

Published on: May 24, 2019

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Related Concept Videos

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 reduction of the tissue.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...