Related Experiment Video
Updated: Sep 26, 2026

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
Published on: April 6, 2022
Dual effects of caspase-1, interleukin-1 beta, tumour necrosis factor-alpha and nerve growth factor receptor in
Z Mackiewicz1, M Hukkanen, D Povilenaite
1Institute of Biomedicine/Anatomy, Biomedicum Helsinki, University of Helsinki, Finland.
Objective:
To analyse the expression of factors potentially involved in skeletal muscle degeneration and regeneration in dermatomyositis (DM), systemic sclerosis (SSc), polymyositis (PM), systemic lupus erythematosus (SLE) and non-inflammatory myopathies.
Methods:
Immunohistochemical staining of skeletal muscle biopsies (10 DM, 10 SSc, 10 PM, 10 SLE, 10 non-inflammatory myopathies) for tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), activated caspase-1, pan-macrophage marker CD68, inducible nitric oxide synthase (NOS2) and nerve growth factor receptor (NGFR). TechMate staining robot and biotin-streptavidin protocol were used.
Results:
Expression of TNF-alpha, IL-1 beta, caspase-1 and NOS2 was found in the cytoplasm and sarcolemma of dystrophic skeletal muscle fibres. TNF-alpha and IL-1 beta immunoreactive profiles were faint and few and close to satellite nuclei-containing regenerating muscle fibres both in inflammatory and non-inflammatory myopathies. NGFR expression was found in comparable areas. In non-inflammatory inherited myopathies more nuclei were caspase-1 immunoreactive whereas caspase-1 expression was rarely seen in inflammatory myopathies, implying regeneration of the affected muscle fibres.
Conclusion:
Prominent expression of the proinflammatory factors TNF-alpha, IL-1 beta and NOS2 and caspase-1 is associated with muscle fibre damage, albeit when expressed to a low degree these factors may, like NGFR, contribute to muscle regeneration and healing.
Insights
Pro-inflammatory factors like tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) are linked to muscle damage in myopathies. Low-level expression may aid skeletal muscle regeneration.
Area of Science:
- Muscle biology
- Immunology
- Pathology
Background:
- Myopathies, including inflammatory and non-inflammatory types, involve skeletal muscle degeneration.
- Factors influencing muscle degeneration and regeneration are not fully understood across different myopathies.
Purpose of the Study:
- To analyze the expression of key factors in skeletal muscle degeneration and regeneration.
- To compare these factors across dermatomyositis (DM), systemic sclerosis (SSc), polymyositis (PM), systemic lupus erythematosus (SLE), and non-inflammatory myopathies.
Main Methods:
- Immunohistochemical staining of skeletal muscle biopsies from 50 patients (10 per condition).
- Analysis of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), caspase-1, CD68, inducible nitric oxide synthase (NOS2), and nerve growth factor receptor (NGFR).
- Utilized a TechMate staining robot and biotin-streptavidin protocol.
Main Results:
- TNF-alpha, IL-1 beta, caspase-1, and NOS2 were expressed in dystrophic muscle fibers.
- Low levels of TNF-alpha and IL-1 beta were observed near regenerating fibers in both inflammatory and non-inflammatory myopathies.
- Caspase-1 expression was higher in non-inflammatory myopathies, suggesting a role in regeneration.
Conclusions:
- Prominent expression of TNF-alpha, IL-1 beta, NOS2, and caspase-1 correlates with muscle fiber damage.
- Low-level expression of these factors, along with NGFR, may contribute to muscle regeneration and healing.
Related Concept Videos
Caspases
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Inflammatory Bowel Disease III: Crohn's Disease
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...