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Cyclosporine A–protection against microvascular hyperpermeability is calcineurin independent

Abstract Background Mitochondria-mediated apoptotic signaling contributes to microvascular hyperpermeability. We hypothesized that cyclosporine A (CsA), which protects mitochondrial transition pores, would attenuate hyperpermeability independent of its calcineurin inhibitory property. Methods Hyperp...

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Published in:The American journal of surgery 2010-04, Vol.199 (4), p.542-548
Main Authors: Childs, Ed W., M.D, Tharakan, Binu, Ph.D, Nurudeen, Suliat, B.S, Delmas, Thomas L., B.S, Hellman, Joseph, B.S, Christie, Tasheika, B.S, Hunter, Felicia A., B.S, Smythe, W. Roy, M.D
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cited_by cdi_FETCH-LOGICAL-c560t-dd8ea67807a8e3c569733b88ba28de3437ef1e471b6ca2257372674066ca53393
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container_start_page 542
container_title The American journal of surgery
container_volume 199
creator Childs, Ed W., M.D
Tharakan, Binu, Ph.D
Nurudeen, Suliat, B.S
Delmas, Thomas L., B.S
Hellman, Joseph, B.S
Christie, Tasheika, B.S
Hunter, Felicia A., B.S
Smythe, W. Roy, M.D
description Abstract Background Mitochondria-mediated apoptotic signaling contributes to microvascular hyperpermeability. We hypothesized that cyclosporine A (CsA), which protects mitochondrial transition pores, would attenuate hyperpermeability independent of its calcineurin inhibitory property. Methods Hyperpermeability was induced in microvascular endothelial cell monolayers using proapoptotic BAK or active caspase-3 after CsA or a specific calcineurin inhibitor, calcineurin autoinhibitory peptide (CIP), treatment. Permeability was measured based on fluorescein isothiocyanate–albumin flux across the monolayers. Mitochondrial transmembrane potential (MTP) was determined using 5,5′,6,6′-tetrachoro-1,1′,3,3′-tetraethylbenzimidazolyl carbocyanine iodide. Mitochondrial release of cytochrome c was measured using an enzyme-linked immunosorbent assay and caspase-3 activity fluorometrically. Results CsA-attenuated (10 nmol/L) but not CIP-attenuated (100 μmol/L) BAK induced hyperpermeability ( P < .05), CsA- but not CIP-attenuated BAK induced a decrease in MTP and an increase in cytochrome c levels and caspase-3 activity ( P < .05). CsA and CIP were ineffective against caspase-3–induced hyperpermeability. Conclusions CsA attenuated hyperpermeability by protecting MTP, thus preventing mitochondria-mediated apoptotic signaling. The protective effect of CsA is independent of calcineurin inhibition.
doi_str_mv 10.1016/j.amjsurg.2009.11.002
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Roy, M.D</creator><creatorcontrib>Childs, Ed W., M.D ; Tharakan, Binu, Ph.D ; Nurudeen, Suliat, B.S ; Delmas, Thomas L., B.S ; Hellman, Joseph, B.S ; Christie, Tasheika, B.S ; Hunter, Felicia A., B.S ; Smythe, W. Roy, M.D</creatorcontrib><description>Abstract Background Mitochondria-mediated apoptotic signaling contributes to microvascular hyperpermeability. We hypothesized that cyclosporine A (CsA), which protects mitochondrial transition pores, would attenuate hyperpermeability independent of its calcineurin inhibitory property. Methods Hyperpermeability was induced in microvascular endothelial cell monolayers using proapoptotic BAK or active caspase-3 after CsA or a specific calcineurin inhibitor, calcineurin autoinhibitory peptide (CIP), treatment. Permeability was measured based on fluorescein isothiocyanate–albumin flux across the monolayers. Mitochondrial transmembrane potential (MTP) was determined using 5,5′,6,6′-tetrachoro-1,1′,3,3′-tetraethylbenzimidazolyl carbocyanine iodide. Mitochondrial release of cytochrome c was measured using an enzyme-linked immunosorbent assay and caspase-3 activity fluorometrically. Results CsA-attenuated (10 nmol/L) but not CIP-attenuated (100 μmol/L) BAK induced hyperpermeability ( P &lt; .05), CsA- but not CIP-attenuated BAK induced a decrease in MTP and an increase in cytochrome c levels and caspase-3 activity ( P &lt; .05). CsA and CIP were ineffective against caspase-3–induced hyperpermeability. Conclusions CsA attenuated hyperpermeability by protecting MTP, thus preventing mitochondria-mediated apoptotic signaling. The protective effect of CsA is independent of calcineurin inhibition.</description><identifier>ISSN: 0002-9610</identifier><identifier>EISSN: 1879-1883</identifier><identifier>DOI: 10.1016/j.amjsurg.2009.11.002</identifier><identifier>PMID: 20359571</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Albumin ; Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins ; Attenuation ; BAK protein ; Calcineurin ; Calcineurin - metabolism ; Capillary Permeability - drug effects ; Carrier Proteins - metabolism ; Caspase ; Caspase Inhibitors ; Caspase-3 ; Cell death ; Cyclosporine - pharmacology ; Cyclosporins ; Cytochrome ; Cytochrome c ; Cytochromes c - metabolism ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Enzyme-linked immunosorbent assay ; Fluorescein ; Fluorescein isothiocyanate ; Iodides ; Ischemia ; Kinases ; Laboratories ; Lung - blood supply ; Membrane potential ; Microcirculation ; Microvasculature ; Mitochondria ; Mitochondria - metabolism ; Monolayers ; Peptides ; Permeability ; Phenols ; Proteins ; Rats ; Rodents ; Signal Transduction - drug effects ; Studies ; Surgery ; Vascular permeability ; “Intrinsic” apoptotic cascade</subject><ispartof>The American journal of surgery, 2010-04, Vol.199 (4), p.542-548</ispartof><rights>Elsevier Inc.</rights><rights>2010 Elsevier Inc.</rights><rights>Copyright 2010 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Apr 1, 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-dd8ea67807a8e3c569733b88ba28de3437ef1e471b6ca2257372674066ca53393</citedby><cites>FETCH-LOGICAL-c560t-dd8ea67807a8e3c569733b88ba28de3437ef1e471b6ca2257372674066ca53393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20359571$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Childs, Ed W., M.D</creatorcontrib><creatorcontrib>Tharakan, Binu, Ph.D</creatorcontrib><creatorcontrib>Nurudeen, Suliat, B.S</creatorcontrib><creatorcontrib>Delmas, Thomas L., B.S</creatorcontrib><creatorcontrib>Hellman, Joseph, B.S</creatorcontrib><creatorcontrib>Christie, Tasheika, B.S</creatorcontrib><creatorcontrib>Hunter, Felicia A., B.S</creatorcontrib><creatorcontrib>Smythe, W. Roy, M.D</creatorcontrib><title>Cyclosporine A–protection against microvascular hyperpermeability is calcineurin independent</title><title>The American journal of surgery</title><addtitle>Am J Surg</addtitle><description>Abstract Background Mitochondria-mediated apoptotic signaling contributes to microvascular hyperpermeability. We hypothesized that cyclosporine A (CsA), which protects mitochondrial transition pores, would attenuate hyperpermeability independent of its calcineurin inhibitory property. Methods Hyperpermeability was induced in microvascular endothelial cell monolayers using proapoptotic BAK or active caspase-3 after CsA or a specific calcineurin inhibitor, calcineurin autoinhibitory peptide (CIP), treatment. Permeability was measured based on fluorescein isothiocyanate–albumin flux across the monolayers. Mitochondrial transmembrane potential (MTP) was determined using 5,5′,6,6′-tetrachoro-1,1′,3,3′-tetraethylbenzimidazolyl carbocyanine iodide. Mitochondrial release of cytochrome c was measured using an enzyme-linked immunosorbent assay and caspase-3 activity fluorometrically. Results CsA-attenuated (10 nmol/L) but not CIP-attenuated (100 μmol/L) BAK induced hyperpermeability ( P &lt; .05), CsA- but not CIP-attenuated BAK induced a decrease in MTP and an increase in cytochrome c levels and caspase-3 activity ( P &lt; .05). CsA and CIP were ineffective against caspase-3–induced hyperpermeability. Conclusions CsA attenuated hyperpermeability by protecting MTP, thus preventing mitochondria-mediated apoptotic signaling. The protective effect of CsA is independent of calcineurin inhibition.</description><subject>Albumin</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins</subject><subject>Attenuation</subject><subject>BAK protein</subject><subject>Calcineurin</subject><subject>Calcineurin - metabolism</subject><subject>Capillary Permeability - drug effects</subject><subject>Carrier Proteins - metabolism</subject><subject>Caspase</subject><subject>Caspase Inhibitors</subject><subject>Caspase-3</subject><subject>Cell death</subject><subject>Cyclosporine - pharmacology</subject><subject>Cyclosporins</subject><subject>Cytochrome</subject><subject>Cytochrome c</subject><subject>Cytochromes c - metabolism</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fluorescein</subject><subject>Fluorescein isothiocyanate</subject><subject>Iodides</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lung - blood supply</subject><subject>Membrane potential</subject><subject>Microcirculation</subject><subject>Microvasculature</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Monolayers</subject><subject>Peptides</subject><subject>Permeability</subject><subject>Phenols</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Studies</subject><subject>Surgery</subject><subject>Vascular permeability</subject><subject>“Intrinsic” apoptotic cascade</subject><issn>0002-9610</issn><issn>1879-1883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqFks9u1DAQxi0EotvCI4AicegpYWwnsXMBVSsKSJU4FK5YjjNbHPIPO6mUW9-BN-RJOqtdqNQLkmVrRp8_z_w8jL3ikHHg5ds2s30bl3CTCYAq4zwDEE_YhmtVpVxr-ZRtgFJpVXI4YacxthRynsvn7ESALKpC8Q37vl1dN8ZpDH7A5OLP3e8pjDO62Y9DYm-sH-Kc9N6F8dZGt3Q2JD_WCQOtHm3tOz-viY-Js50jh4VsEj80OCFtw_yCPdvZLuLL43nGvl1--Lr9lF59-fh5e3GVuqKEOW0ajbZUGpTVKClXKSlrrWsrdIMylwp3HHPF69JZIQollShVDiWFhZSVPGPnB1-q_teCcTa9jw67zg44LtGQnc5LLSUp3zxStuMSBirO8EoUFQgCRqrioKLGYwy4M1PwvQ2r4WD2_E1rjvzNnr_h3BBsuvf66L7UPTb_bv0FToL3BwESjVuPwUTncXDY-EDUTTP6_z7x7pGD6_zg6QN-4orxoRsThQFzvR-C_QxABaBKAHkPDwOv8A</recordid><startdate>20100401</startdate><enddate>20100401</enddate><creator>Childs, Ed W., M.D</creator><creator>Tharakan, Binu, Ph.D</creator><creator>Nurudeen, Suliat, B.S</creator><creator>Delmas, Thomas L., B.S</creator><creator>Hellman, Joseph, B.S</creator><creator>Christie, Tasheika, B.S</creator><creator>Hunter, Felicia A., B.S</creator><creator>Smythe, W. 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Roy, M.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclosporine A–protection against microvascular hyperpermeability is calcineurin independent</atitle><jtitle>The American journal of surgery</jtitle><addtitle>Am J Surg</addtitle><date>2010-04-01</date><risdate>2010</risdate><volume>199</volume><issue>4</issue><spage>542</spage><epage>548</epage><pages>542-548</pages><issn>0002-9610</issn><eissn>1879-1883</eissn><abstract>Abstract Background Mitochondria-mediated apoptotic signaling contributes to microvascular hyperpermeability. We hypothesized that cyclosporine A (CsA), which protects mitochondrial transition pores, would attenuate hyperpermeability independent of its calcineurin inhibitory property. Methods Hyperpermeability was induced in microvascular endothelial cell monolayers using proapoptotic BAK or active caspase-3 after CsA or a specific calcineurin inhibitor, calcineurin autoinhibitory peptide (CIP), treatment. Permeability was measured based on fluorescein isothiocyanate–albumin flux across the monolayers. Mitochondrial transmembrane potential (MTP) was determined using 5,5′,6,6′-tetrachoro-1,1′,3,3′-tetraethylbenzimidazolyl carbocyanine iodide. Mitochondrial release of cytochrome c was measured using an enzyme-linked immunosorbent assay and caspase-3 activity fluorometrically. Results CsA-attenuated (10 nmol/L) but not CIP-attenuated (100 μmol/L) BAK induced hyperpermeability ( P &lt; .05), CsA- but not CIP-attenuated BAK induced a decrease in MTP and an increase in cytochrome c levels and caspase-3 activity ( P &lt; .05). CsA and CIP were ineffective against caspase-3–induced hyperpermeability. Conclusions CsA attenuated hyperpermeability by protecting MTP, thus preventing mitochondria-mediated apoptotic signaling. The protective effect of CsA is independent of calcineurin inhibition.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>20359571</pmid><doi>10.1016/j.amjsurg.2009.11.002</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Albumin
Animals
Apoptosis
Apoptosis - drug effects
Apoptosis Regulatory Proteins
Attenuation
BAK protein
Calcineurin
Calcineurin - metabolism
Capillary Permeability - drug effects
Carrier Proteins - metabolism
Caspase
Caspase Inhibitors
Caspase-3
Cell death
Cyclosporine - pharmacology
Cyclosporins
Cytochrome
Cytochrome c
Cytochromes c - metabolism
Endothelium, Vascular - cytology
Endothelium, Vascular - drug effects
Enzyme-linked immunosorbent assay
Fluorescein
Fluorescein isothiocyanate
Iodides
Ischemia
Kinases
Laboratories
Lung - blood supply
Membrane potential
Microcirculation
Microvasculature
Mitochondria
Mitochondria - metabolism
Monolayers
Peptides
Permeability
Phenols
Proteins
Rats
Rodents
Signal Transduction - drug effects
Studies
Surgery
Vascular permeability
“Intrinsic” apoptotic cascade
title Cyclosporine A–protection against microvascular hyperpermeability is calcineurin independent
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