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Published on: September 15, 2017
Cisatracurium attenuates LPS-induced modulation of MMP3 and junctional protein expression in human microvascular
Rana W Kadry1, Mir S Adil1, Andrea Sikora Newsome1
1Clinical and Experimental Therapeutics, University of Georgia, and Charlie Norwood VA Medical Center, Augusta, GA, USA.
Abstract:
Acute respiratory distress syndrome (ARDS) is a life-threatening form of acute lung injury (ALI) associated with hypoxemic lung damage and inflammation. Matrix metalloproteinase protein-3 (MMP3 or Stromelysin-1) is known to promote vascular injury in ALI/ARDS. Cisatracurium, a nicotinic neuromuscular blocker, is used in ARDS patients to decrease mechanical ventilator dyssynchrony, increase oxygenation, and improve mortality. However, the magnitude and the underlying mechanisms of these potential benefits of cisatracurium remains unclear. We investigated the effect of cisatracurium on lipopolysaccharide-induced MMP3 expression in human microvascular endothelial cells. In our results, cisatracurium treatment significantly decreased LPS-induced MMP3 expression and increased expression of cell junction proteins such as vascular endothelial cadherin (VE-cadherin) and claudin-5.
Insights
Cisatracurium, used for acute respiratory distress syndrome (ARDS), reduces matrix metalloproteinase-3 (MMP3) expression and enhances cell junction proteins in lung endothelial cells, potentially improving vascular injury.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Pharmacology
Background:
- Acute respiratory distress syndrome (ARDS) involves lung inflammation and hypoxemic damage.
- Matrix metalloproteinase-3 (MMP3) contributes to vascular injury in ARDS.
- Cisatracurium is used in ARDS patients, but its mechanisms and benefits require clarification.
Purpose of the Study:
- To investigate the effect of cisatracurium on lipopolysaccharide (LPS)-induced MMP3 expression.
- To determine cisatracurium's impact on cell junction protein expression in human microvascular endothelial cells.
Main Methods:
- Human microvascular endothelial cells were treated with LPS to induce MMP3 expression.
- Cisatracurium was administered to assess its effect on MMP3 and cell junction proteins.
- Expression levels of MMP3, VE-cadherin, and claudin-5 were analyzed.
Main Results:
- Cisatracurium significantly decreased LPS-induced MMP3 expression.
- Cisatracurium treatment increased the expression of vascular endothelial cadherin (VE-cadherin).
- Cisatracurium also increased the expression of claudin-5.
Conclusions:
- Cisatracurium may mitigate vascular injury in ARDS by reducing MMP3 expression.
- The drug's ability to enhance cell junction proteins suggests a protective effect on endothelial barrier integrity.
- These findings provide insights into the mechanisms underlying cisatracurium's potential benefits in ARDS management.
