Key result
Emphysema patients receiving A1AT therapy had significantly higher plasma angptl4 levels compared to those without therapy (127.1 vs 76.8 ng/ml; p=0.045).
Why the study?
Does α1-antitrypsin (A1AT) upregulate the expression and release of angptl4 in human cells and emphysema patients?
Observational (n=10)
Does α1-antitrypsin (A1AT) upregulate the expression and release of angptl4 in human cells and emphysema patients?
Absolute Event Rate: 127.1% vs 76.8%
p-value: p=0.045
A1AT upregulates the transcription and secretion of the acute-phase protein angptl4, a process mediated by PPARγ.
A1AT therapy was associated with higher angptl4 in emphysema; hypothesis-generating for PPARγ-mediated effects pending prospective trials.
The angiopoietin-like protein 4 (angptl4, also known as peroxisome proliferator-activated receptor [PPAR]γ-induced angiopoietin-related protein) is a multifunctional protein associated with acute-phase response. The mechanisms accounting for the increase in angptl4 expression are largely unknown. This study shows that human α1-antitrypsin (A1AT) upregulates expression and release of angplt4 in human blood adherent mononuclear cells and in primary human lung microvascular endothelial cells in a concentration- and time-dependent manner. Mononuclear cells treated for 1 h with A1AT (from 0.1 to 4 mg/ml) increased mRNA of angptl4 from 2- to 174-fold, respectively, relative to controls. In endothelial cells, the maximal effect on angptl4 expression was achieved at 8 h with 2 mg/ml A1AT (11-fold induction versus controls). In 10 emphysema patients receiving A1AT therapy (Prolastin), plasma angptl4 levels were higher relative to patients without therapy (nanograms per milliliter, mean [95% confidence interval] 127.1 [99.5-154.6] versus 76.8 [54.8-98.8], respectively, p = 0.045) and correlated with A1AT levels. The effect of A1AT on angptl4 expression was significantly diminished in cells pretreated with a specific inhibitor of ERK1/2 activation (UO126), irreversible and selective PPARγ antagonist (GW9662), or genistein, a ligand for PPARγ. GW9662 did not alter the ability of A1AT to induce ERK1/2 phosphorylation, suggesting that PPARγ is a critical mediator in the A1AT-driven angptl4 expression. In contrast, the forced accumulation of HIF-1α, an upregulator of angptl4 expression, enhanced the effect of A1AT. Thus, acute-phase protein A1AT is a physiological regulator of angptl4, another acute-phase protein.
No takes yet. Share an insight, caveat, or question.
Frenzel et al. (2014) conducted an observational in Emphysema (n=10). A1AT therapy (Prolastin) vs. Patients without therapy was evaluated on Plasma angptl4 levels (ng/ml) (p=0.045). Emphysema patients receiving A1AT therapy had significantly higher plasma angptl4 levels compared to those without therapy (127.1 vs 76.8 ng/ml; p=0.045).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: