Interaction between mitochondrial homeostasis and barrier function in lipopolysaccharide‐induced endothelial cell injury
This 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 m...
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Veröffentlicht in: | International journal of experimental pathology 2023-12, Vol.104 (6), p.272-282 |
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creator | Zhu, Weiwei Liu, Xiaojing Luo, Liqing Huang, Xiao Wang, Xiaozhi |
description | This 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. |
doi_str_mv | 10.1111/iep.12495 |
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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.</description><identifier>ISSN: 0959-9673</identifier><identifier>EISSN: 1365-2613</identifier><identifier>DOI: 10.1111/iep.12495</identifier><language>eng</language><publisher>Chichester: Wiley Subscription Services, Inc</publisher><subject>Adenosine triphosphate ; ATP ; Cell injury ; Endothelial cells ; Heparan sulfate ; Homeostasis ; Lipopolysaccharides ; Membrane potential ; Mitochondria ; Myosin ; Oligomycin ; Phosphorylation ; Reactive oxygen species ; Shedding ; Swelling ; Tight junctions</subject><ispartof>International journal of experimental pathology, 2023-12, Vol.104 (6), p.272-282</ispartof><rights>2023. 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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.</description><subject>Adenosine triphosphate</subject><subject>ATP</subject><subject>Cell injury</subject><subject>Endothelial cells</subject><subject>Heparan sulfate</subject><subject>Homeostasis</subject><subject>Lipopolysaccharides</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Myosin</subject><subject>Oligomycin</subject><subject>Phosphorylation</subject><subject>Reactive oxygen species</subject><subject>Shedding</subject><subject>Swelling</subject><subject>Tight junctions</subject><issn>0959-9673</issn><issn>1365-2613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpdkb1OwzAUhS0EEqUw8AaWWGBI8U_c2COq-KlUiaV75Ng3iqvEDnYiVCYegWfkSUgpE3c4d_nO0ZEOQteULOh09w76BWW5EidoRvlSZGxJ-SmaESVUppYFP0cXKe0IoZzRYoY-1n6AqM3ggscVDO8AHnduCKYJ3kanW9yEDkIadHIJa29xpWN0EHE9-qPNedy6PvSh3SdtTKOjs_D9-eW8HQ1YDN6GoYH2EGagbSfDboz7S3RW6zbB1d-fo-3T43b1km1en9erh01mmBRDZjkoBTkt5FJUlkhjpchrISlXFaGiVkYwEJVQuspzkFIXzHCuFc21FkTwObo9xvYxvI2QhrJz6VBDewhjKpksCi4lmXSObv6huzBGP5WbKEXYFFewibo7UiaGlCLUZR9dp-O-pKQ8jFBOI5S_I_AfQVF9fQ</recordid><startdate>20231201</startdate><enddate>20231201</enddate><creator>Zhu, Weiwei</creator><creator>Liu, Xiaojing</creator><creator>Luo, Liqing</creator><creator>Huang, Xiao</creator><creator>Wang, Xiaozhi</creator><general>Wiley Subscription Services, Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QO</scope><scope>7TK</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-3139-7982</orcidid></search><sort><creationdate>20231201</creationdate><title>Interaction between mitochondrial homeostasis and barrier function in lipopolysaccharide‐induced endothelial cell injury</title><author>Zhu, Weiwei ; Liu, Xiaojing ; Luo, Liqing ; Huang, Xiao ; Wang, Xiaozhi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c285t-d3e99e417865bd08cd854f58139b015f9c52e5b59ab44e88a72c33a914aa5053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adenosine triphosphate</topic><topic>ATP</topic><topic>Cell injury</topic><topic>Endothelial cells</topic><topic>Heparan sulfate</topic><topic>Homeostasis</topic><topic>Lipopolysaccharides</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Myosin</topic><topic>Oligomycin</topic><topic>Phosphorylation</topic><topic>Reactive oxygen species</topic><topic>Shedding</topic><topic>Swelling</topic><topic>Tight junctions</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Weiwei</creatorcontrib><creatorcontrib>Liu, Xiaojing</creatorcontrib><creatorcontrib>Luo, Liqing</creatorcontrib><creatorcontrib>Huang, Xiao</creatorcontrib><creatorcontrib>Wang, Xiaozhi</creatorcontrib><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of experimental pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Weiwei</au><au>Liu, Xiaojing</au><au>Luo, Liqing</au><au>Huang, Xiao</au><au>Wang, Xiaozhi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction between mitochondrial homeostasis and barrier function in lipopolysaccharide‐induced endothelial cell injury</atitle><jtitle>International journal of experimental pathology</jtitle><date>2023-12-01</date><risdate>2023</risdate><volume>104</volume><issue>6</issue><spage>272</spage><epage>282</epage><pages>272-282</pages><issn>0959-9673</issn><eissn>1365-2613</eissn><abstract>This 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.</abstract><cop>Chichester</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1111/iep.12495</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-3139-7982</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adenosine triphosphate ATP Cell injury Endothelial cells Heparan sulfate Homeostasis Lipopolysaccharides Membrane potential Mitochondria Myosin Oligomycin Phosphorylation Reactive oxygen species Shedding Swelling Tight junctions |
title | Interaction between mitochondrial homeostasis and barrier function in lipopolysaccharide‐induced endothelial cell injury |
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