Air Bubble Contact with Endothelial Cells Causes a Calcium-Independent Loss in Mitochondrial Membrane Potential 英文参考文献.docVIP

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Air Bubble Contact with Endothelial Cells Causes a Calcium-Independent Loss in Mitochondrial Membrane Potential 英文参考文献.doc

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Air Bubble Contact with Endothelial Cells Causes a Calcium-Independent Loss in Mitochondrial Membrane Potential 英文参考文献

AirBubbleContactwithEndothelialCellsCauses aCalcium-IndependentLossinMitochondrialMembrane Potential PeterSobolewski1,JudithKandel2,DavidM.Eckmann1,2* 1Department of Anesthesiology and Critical Care, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America, 2Department of Bioengineering, UniversityofPennsylvania,Philadelphia,Pennsylvania,UnitedStatesofAmerica Abstract Objective:Gasmicroembolismremainsaseriousriskassociatedwithsurgicalproceduresanddecompression.Despitethis, thesignalingconsequencesofairbubblesinthevasculaturearepoorlyunderstoodandthereisalackofpharmacological therapiesavailable.Here,weinvestigatethemitochondrialconsequencesofairbubblecontactwithendothelialcells. MethodsandResults:Humanumbilicalveinendothelialcellswereloadedwithanintracellularcalciumindicator(Fluo-4) andeitheramitochondrialcalciumindicator(X-Rhod-1)ormitochondrialmembranepotentialindicator(TMRM).Contact with 50–150mm air bubbles induced concurrent rises in intracellular and mitochondrial calcium, followed by a loss of mitochondrialmembranepotential.Pre-treatingcellswith1mmol/Lrutheniumred,aTRPVfamilycalciumchannelblocker, didnotprotectcellsfromthemitochondrialdepolarization,despiteblockingtheintracellularcalciumresponse.Mitigating the interactions between the air-liquid interface and the endothelial surface layer with 5% BSA or 0.1% Pluronic F-127 prevented the loss of mitochondrial membrane potential. Finally, inhibiting protein kinase C-a (PKCa), with 5mmol/L Go¨6976,protectedcellsfrommitochondrialdepolarization,butdidnotaffecttheintracellularcalciumresponse. Conclusions: Our results indicate that air bubble contact with endothelial cells activates a novel, calcium-independent, PKCa-dependentsignalingpathway,whichresultsinmitochondrialdepolarization.Asaresult,mitochondrialdysfunctionis likely to be a key contributor to the pathophysiology of gas embolism injury. Further, this connection between the endothelialsurfacelayerandendothelialmitochondriamayalsopla