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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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...
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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...
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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...
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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. 
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Methods for Studying Myofibroblast Apoptotic Pathways.

Yan Zhou1,2,3, David Lagares4,5,6

  • 1Division of Rheumatology, Allergy and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

Methods in Molecular Biology (Clifton, N.J.)
|May 24, 2021
PubMed
Summary
This summary is machine-generated.

Myofibroblasts in fibrosis are primed for apoptosis, contrary to prior belief. BH3 profiling can predict their response to targeted therapies, offering new avenues for treating fibrotic diseases.

Keywords:
Annexin VApoptosisBH3 mimetic drugsBH3 profilingFibrosisMyofibroblasts

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Pathology

Background:

  • Myofibroblast apoptosis evasion drives fibrotic diseases by promoting extracellular matrix deposition.
  • Targeting myofibroblast apoptosis is a promising therapeutic strategy for reversing fibrosis.
  • Fibroblast-to-myofibroblast transdifferentiation increases mitochondrial priming for apoptosis.

Purpose of the Study:

  • To introduce BH3 profiling as a method to measure myofibroblast apoptotic priming.
  • To assess myofibroblast dependencies on pro-survival BCL-2 proteins.
  • To predict myofibroblast response to BH3 mimetic drugs and evaluate extrinsic apoptosis sensitivity.

Main Methods:

  • BH3 profiling to quantify apoptotic priming and anti-apoptotic dependencies in myofibroblasts.
  • Assessment of myofibroblast sensitivity to extrinsic apoptosis using Annexin V staining.
  • Utilizing BH3 profiling to predict responses to targeted pro-survival BCL-2 protein therapies.

Main Results:

  • Stiffness-activated myofibroblasts exhibit significantly increased "mitochondrial priming," indicating a "primed for death" state.
  • This apoptosis-prone phenotype is driven by high pro-apoptotic proteins, counteracted by pro-survival BCL-2 proteins.
  • BH3 profiling effectively measures this priming and predicts drug responses.

Conclusions:

  • Myofibroblasts are not inherently apoptosis-resistant but can be poised for death when survival pathways are blocked.
  • BH3 profiling is a valuable tool for understanding myofibroblast apoptosis regulation and guiding therapeutic strategies.
  • This approach can predict patient response to BH3 mimetic drugs, advancing fibrosis treatment.