Key result
Over-expression of FGL2 in experimental autoimmune myocarditis rats significantly decreased PD-1, deteriorated cardiac function, and increased inflammatory cell infiltrate and cytokines.
Why the study?
Does over-expression of FGL2 deteriorate cardiac function in experimental autoimmune myocarditis rats?
Does over-expression of FGL2 deteriorate cardiac function in experimental autoimmune myocarditis rats?
p-value: p=<0.05
FGL2 over-expression exacerbates cardiac injury and inflammation in autoimmune myocarditis, suggesting it as a potential therapeutic target for immune-induced heart injury.
FGL2 may drive injury in rat autoimmune myocarditis; leaves open its value as a therapeutic target in human disease.
Programmed death-1 (PD-1) plays an important role in protecting against inflammation and myocyte damage in T-cell-mediated myocarditis. To understand whether fibrinogen-like protein-2 (FGL2) can affect the role of the PD-1/PD-L1 pathway in experimental autoimmune myocarditis (EAM), we investigated cardiac function in EAM rats over-expressing FGL2. Over-expression of FGL2 significantly decreased PD-1 and deteriorated cardiac function in rats with autoimmune myocarditis. Histopathology revealed increased inflammatory cell infiltrate in EAM-FGL2 rats compared with the control groups (EAM, EAM-GFP and NC). Notably, transcription factor forkhead box P3 (Foxp3) and retinoic acid-related orphan receptor γt (RORγt) protein and mRNA levels were statistically (P < 0·05) increased in EAM rats. We also found that interferon-γ, interleukin-6, interleukin-17 and brain natriuretic peptide levels were profoundly increased in serum of FGL2 over-expressing EAM rats. Hence, FGL2 plays an important role in the pathogenesis of autoimmune myocarditis that also involves the PD-1/PD-L1 pathway. Our findings may provide novel therapeutic targets for the treatment of immune-induced heart injury.
No takes yet. Share an insight, caveat, or question.
Zheng et al. (2017) studied Experimental autoimmune myocarditis. Over-expression of FGL2 vs. Control groups (EAM, EAM-GFP and NC) was evaluated on Cardiac function, PD-1 levels, inflammatory cell infiltrate, and cytokine levels (p=<0.05). Over-expression of FGL2 in experimental autoimmune myocarditis rats significantly decreased PD-1, deteriorated cardiac function, and increased inflammatory cell infiltrate and cytokines.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: