Key result
Overexpression of Angptl4 in rat pulmonary microvascular endothelial cells exposed to LPS significantly decreased TNF-α levels (P<0.01) and inhibited LPS-induced increases in cell permeability.
Why the study?
Does Angptl4 overexpression protect rat pulmonary microvascular endothelial cells exposed to LPS?
Population
Rat pulmonary microvascular endothelial cells (RPMVECs) exposed to lipopolysaccharide (LPS)
Comparison
Transfection with Angptl4 expression vector to… vs Empty vector (pcDNA3.1-eGFP) and blank control
Design
Preclinical
Authors
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May attenuate LPS-induced endothelial injury in vitro; hypothesis-generating for acute lung injury therapy.
Does Angptl4 overexpression protect rat pulmonary microvascular endothelial cells exposed to LPS?
p-value: p=<0.01
Overexpression of Angptl4 exerts protective, anti-inflammatory, and anti-angiogenic effects in LPS-exposed rat pulmonary microvascular endothelial cells, suggesting a potential therapeutic target for acute lung injury.
Wang et al. (2013) studied Acute lung injury (LPS-induced). Angptl4 overexpression (pcDNA3.1-eGFP-Angptl4 transfection) vs. Empty vector (pcDNA3.1-eGFP) and blank control was evaluated on Inflammatory cytokine (TNF-α) levels, apoptosis markers, and cell permeability (p=<0.01). Overexpression of Angptl4 in rat pulmonary microvascular endothelial cells exposed to LPS significantly decreased TNF-α levels (P<0.01) and inhibited LPS-induced increases in cell permeability.
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