Affiliation:
1. Department of Intensive Care Unit Binzhou Medical University Hospital Binzhou China
2. Department of Hematology Binzhou Medical University Hospital Binzhou China
Abstract
AbstractThis study aimed to investigate the effects of mitochondrial homeostasis on lipopolysaccharide (LPS)‐induced endothelial cell barrier function and the mechanisms that underlie these effects. Cells were treated with LPS or oligomycin (mitochondrial adenosine triphosphate synthase inhibitor) and the mitochondrial morphology, mitochondrial reactive oxygen species (mtROS), and mitochondrial membrane potential (ΔΨm) were evaluated. Moreover, the shedding of glycocalyx‐heparan sulphate (HS), the levels of HS‐specific degrading enzyme heparanase (HPA), and the expression of occludin and zonula occludens (ZO‐1) of Tight Junctions (TJ)s, which are mediated by myosin light chain phosphorylation (p‐MLC), were assessed. Examining the changes in mitochondrial homeostasis showed that adding heparinase III, which is an exogenous HPA, can destroy the integrity of glycocalyx. LPS simultaneously increased mitochondrial swelling, mtROS, and ΔΨm. Without oligomycin effects, HS, HPA levels, and p‐MLC were found to be elevated, and the destruction of occludin and ZO‐1 increased. Heparinase III not only damaged the glycocalyx by increasing HS shedding but also increased mitochondrial swelling and mtROS and decreased ΔΨm. Mitochondrial homeostasis is involved in LPS‐induced endothelial cell barrier dysfunction by aggravating HPA and p‐MLC levels. In turn, the integrated glycocalyx protects mitochondrial homeostasis.
Funder
National Natural Science Foundation of China
Natural Science Foundation of Shandong Province
Taishan Scholar Project of Shandong Province
Subject
Cell Biology,Molecular Biology,Pathology and Forensic Medicine
Cited by
1 articles.
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