Skip to main content
  • Poster presentation
  • Open access
  • Published:

Lipopolysaccharide induces mitochondrial dysfunction in rat cardiac microvascular endothelial cells


Endothelial injury and dysfunction are key patho-physiological processes in sepsis. The aim of the study was to evaluatethe effects of bacterial lipopolysaccharide (LPS) on cellular respiration of rat primary cardiac microvascular endothelial cells (CMEC).


CMEC were isolated from adult (250 to 300 g) male Wistar rats and cultured. Cells were exposed to LPS (1 μg/ml) for 4, 8, 16 hours and cellular respiration was measured by high-resolution respirometry (Oxygraph-2k; Oroboros Instruments, Innsbruck, Austria). Activation of caspase-3 protein as an early apoptotic event was examined by western blot analysis. Electron microscopy was performed to reveal any alterations in mitochondrial morphology.


After 4 and 8 hours of LPS incubation (1 μg/ml) no significant changes in CMEC mitochondrial respiration was observed. However, cells treated with LPS for 16 hours exhibited a significant reduction in the maximal complex I-dependent (control: 146 ± 45 pmol/(second*million cells) vs. LPS: 127 ± 38 pmol/(second*million cells)) and IV-dependent (control:148 ± 89 pmol/(second*million cells) vs. LPS: 108 ± 80 pmol/(second*million cells)) mitochondrial respiration (n = 16) (Figure 1). Relatively little, if any, processing of procaspase-3 to active caspase-3 was detected in untreated cells or in cells treated with LPS (1 μg/ml, 16 hours of incubation) (data not shown), and electron microscopy examination revealed no major alterations in cellular and mitochondrial ultrastucture under LPS treatment (Figure 2). Statistical analysis for cellular respiration was performed using a paired t test.

Figure 1
figure 1

Cardiac microvascular endothelial cells' oxygen consumption.

Figure 2
figure 2

CMEC cells under control and LPS treatment conditions.


The data suggest that prolonged exposure to LPS impairs CMEC complex I-dependent and IV-dependent respiration slightly but significantly, without apparent signs of apoptosis or mitochondrial ultrastructural damage.

Author information

Authors and Affiliations


Rights and permissions

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article

Vuda, M., Chiusa, M., Jakob, S. et al. Lipopolysaccharide induces mitochondrial dysfunction in rat cardiac microvascular endothelial cells. Crit Care 15 (Suppl 1), P245 (2011).

Download citation

  • Published:

  • DOI: