The role of phospholipase A2 in multiple Sclerosis: A systematic review and meta-analysis
Autor: | Austin Trotter, Emily J. Anstadt, Jorge Cervantes, Robert B. Clark, KoKo Aung, Frank C. Nichols, Alok Dwivedi |
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Rok vydání: | 2019 |
Předmět: |
Encephalomyelitis
Autoimmune Experimental Multiple Sclerosis Phospholipase A2 Inhibitors Encephalomyelitis Inflammation Phospholipase medicine.disease_cause Pathogenesis 03 medical and health sciences 0302 clinical medicine Phospholipase A2 medicine Animals Humans 030212 general & internal medicine biology business.industry Multiple sclerosis Experimental autoimmune encephalomyelitis General Medicine medicine.disease Phospholipases A2 Neurology Immunology biology.protein lipids (amino acids peptides and proteins) Neurology (clinical) medicine.symptom business 030217 neurology & neurosurgery Oxidative stress |
Zdroj: | Multiple Sclerosis and Related Disorders. 27:206-213 |
ISSN: | 2211-0348 |
DOI: | 10.1016/j.msard.2018.10.115 |
Popis: | Phospholipases A2 (PLA2) are a diverse group of enzymes that cleave the fatty acids of membrane phospholipids. They play critical roles in pathogenesis of neurodegenerative diseases such as multiple sclerosis by enhancing oxidative stress and initiating inflammation. The levels of PLA2 activity in MS patients compared to controls and role of inhibiting PLA2 activity on severity scores in different experimental models are not comprehensively assessed in the light of varying evidence from published studies. The objective of this systematic review is to determine the association between PLA2 activity and multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). We performed a systematic review of six studies that assessed PLA2 activity in MS patients compared to controls and nine studies that assessed PLA2 activity in EAE. sPLA2 nor Lp-PLA2 activity were not increased in MS compared to controls in five of those six studies. A difference in sPLA2 activity was only found in a study that measured the enzyme activity in urine. However, inhibiting cPLA2 or sPLA2 led to lower clinical severity or no signs of EAE in mice, and a lower incidence of EAE lesions compared to animals without cPLA2 inhibition. These findings indicate that PLA2 appears to play a role in the pathogenesis of EAE. |
Databáze: | OpenAIRE |
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