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Transglutaminase 2 and neuroinflammation
Riccardo Ientile1, Monica Currò, Daniela Caccamo
1Department of Biomedical Sciences and Morphological and Functional Imaging, University of Messina, AOU Policlinico "G. Martino", Via C. Valeria, Messina, Italy, ientile@unime.it.
Amino Acids
|November 16, 2014
Summary
Transglutaminase 2 (TG2) plays a key role in neuroinflammation by sustaining the activation of NF-κB, a crucial inflammation regulator. This TG2/NF-κB pathway is implicated in neurodegenerative diseases like Alzheimer's and Parkinson's.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Neuroinflammation is central to neurodegenerative diseases, often involving protein aggregates.
- Transglutaminases, particularly transglutaminase 2 (TG2), catalyze protein crosslinking and are implicated in inflammation.
- Astrocytes and microglia are key inflammatory cells in the central nervous system.
Purpose of the Study:
- To review the role of TG2 in neuroinflammation.
- To examine TG2 expression and activity in response to inflammatory stimuli in glial and monocyte models.
- To explore the link between TG2 and the NF-κB pathway in neuroinflammation.
Main Methods:
- Review of existing literature on TG2, NF-κB, and neuroinflammation.
- Analysis of studies showing increased TG2 expression and activity in glial and monocyte cell models.
- Examination of evidence for TG2/NF-κB co-localization and pathway activation.
Main Results:
- TG2 expression and activity increase in astroglial, microglial, and monocyte cells under inflammatory conditions.
- Over-expressed TG2 sustains the activation of the transcription factor NF-κB.
- The TG2/NF-κB pathway is potentially involved in Alzheimer's, Parkinson's, multiple sclerosis, and ALS.
Conclusions:
- TG2 is upregulated by inflammatory stimuli in key CNS immune cells.
- TG2 contributes to sustained NF-κB activation, a central inflammatory mechanism.
- The TG2/NF-κB pathway is a potential therapeutic target for neurodegenerative diseases involving neuroinflammation.
