Related Experiment Video
Updated: Aug 14, 2026
06:36
An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices
Published on: February 5, 2015
Oxides and apoptosis in inflammatory myopathies
1Department of Neurology, Universitätsklinikum Benjamin Franklin, Free University Berlin, D-12200 Berlin, Germany.
Microscopy Research and Technique
|December 19, 2001
Summary
Reactive oxygen intermediates and nitric oxide are abundant in inflammatory myopathies but their pathogenic role is unclear. Cell-protective effects and Bcl-2 upregulation suggest caution with antioxidant therapies.
Area of Science:
- Muscle Inflammation
- Autoimmune Diseases
- Cellular Pathology
Background:
- Reactive oxygen intermediates (ROI) and nitric oxide (NO) are elevated in polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM).
- The precise role of ROI and NO in the pathogenesis of these autoimmune muscle diseases remains undetermined.
- Unlike demyelinating neuropathies, evidence for oxide-induced apoptosis in inflammatory myopathies is lacking.
Purpose of the Study:
- To investigate the role of reactive oxygen intermediates and nitric oxide in the pathogenesis of inflammatory myopathies.
- To explore the potential protective effects of nitric oxide at low concentrations.
- To identify mechanisms of apoptosis resistance in affected cells.
Main Methods:
- Analysis of reactive oxygen intermediate and nitric oxide production in inflammatory myopathies.
- Assessment of apoptosis in myocytes and inflammatory cells.
- Evaluation of anti-apoptotic protein expression, such as Bcl-2.
Main Results:
- No clear evidence for oxide-induced apoptosis in myocytes or inflammatory cells in PM, DM, and IBM.
- Low concentrations of nitric oxide may exert cell-protective effects.
- Upregulation of anti-apoptotic proteins like Bcl-2 appears to be a key survival mechanism.
Conclusions:
- The pathogenic role of reactive oxygen intermediates and nitric oxide in inflammatory myopathies requires further elucidation.
- Antioxidative and anti-apoptotic therapies should be used cautiously until the specific roles of oxides and apoptosis are resolved in individual cases.
- Bcl-2 upregulation is a significant factor in protecting myocytes and inflammatory cells from apoptosis.
More Related Videos
09:18Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
12:23Flow Cytometry Analysis of Immune Cell Subsets within the Murine Spleen, Bone Marrow, Lymph Nodes and Synovial Tissue in an Osteoarthritis Model
Published on: April 24, 2020
Related Concept Videos
01:30Apoptosis
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.
01:24Caspases
Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
01:17The 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...
01:31The 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...
01:17Phagocytosis 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.
Normal cells contain receptors that prevent them from being recognized by phagocytes.
01:16Necrosis
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...