Inhibition of fas-fas ligand interaction attenuates microvascular hyperpermeability following hemorrhagic shock

Shock

Volumn 39, Issue 2, 2013, Pages 161-167

  Sawant, Devendra A ^a   Tharakan, Binu ^b   Tobin, Richard P ^b   Stagg, Hayden W ^b   Hunter, Felicia A ^a   Newell, M Karen ^b   Smythe, W Roy ^b   Childs, Ed W ^a  

^a MOREHOUSE SCHOOL OF MEDICINE   (United States)

^b TEXAS A M COLLEGE OF MEDICINE   (United States)

Author keywords

adherens junction; apoptosis; Endothelial cells; Fas ligand; Fas receptor; FasFc; vascular permeability

Indexed keywords

CASPASE 3; CELL ANTIBODY; FAS ANTIGEN; FAS LIGAND; FASFC INHIBITOR; REACTIVE OXYGEN METABOLITE; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANTIGEN EXPRESSION; ARTICLE; BLOOD VESSEL PERMEABILITY; CELL JUNCTION; ENZYME ACTIVITY; ENZYME ANALYSIS; FLOW CYTOMETRY; HEMORRHAGIC SHOCK; LUNG ENDOTHELIUM; MALE; MEMBRANE POTENTIAL; MICROVASCULAR HYPERPERMEABILITY; NONHUMAN; PROTEIN INTERACTION; RAT;

ANIMALS; ANTIGENS, CD95; APOPTOSIS; CAPILLARY PERMEABILITY; CASPASE 3; CASPASE INHIBITORS; CELL COMMUNICATION; ENDOTHELIUM, VASCULAR; FAS LIGAND PROTEIN; LUNG; MALE; MICROVESSELS; RATS; RATS, SPRAGUE-DAWLEY; SHOCK, HEMORRHAGIC;

EID: 84872905834     PISSN: 10732322     EISSN: 15400514     Source Type: Journal    
DOI: 10.1097/SHK.0b013e31827bba73     Document Type: Article

References (24)

1. Dewar D, Moore FA, Moore EE, Balogh Z: Postinjury multiple organ failure. Injury 40(9):912-918, 2009.
2. Childs EW, Tharakan B, Hunter FA, Tinsley JH, Cao X: Apoptotic signaling induces hyperpermeability following hemorrhagic shock. Am J Physiol Heart Circ Physiol 292(6):H3179YH3189, 2007.
3. Roumen RM, Hendriks T, van der Ven-Jongekrijg J, Nieuwenhuijzen GA, Sauerwein RW, van der Meer JW, Goris RJ: Cytokine patterns in patients after major vascular surgery, hemorrhagic shock, and severe blunt trauma. Relation with subsequent adult respiratory distress syndrome and multiple organ failure. Ann Surg 218(6):769-776, 1993.
4. Fulda S, Debatin KM: Extrinsic versus intrinsic apoptosis pathways in anti-cancer chemotherapy. Oncogene 25(34):4798-4811, 2006.
5. Suda T, Takahashi T, Golstein P, Nagata S: Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. Cell 75(6):1169-1178, 1993.
6. Nagata S: Apoptosis by death factor. Cell 88(3):355-365, 1997.
7. Kroemer G, Dallaporta B, Resche-Rigon M: The mitochondrial death/life regulator in apoptosis and necrosis. Annu Rev Physiol 60:619-642, 1998.
8. Jeremias I, Kupatt C, Martin-Villalba A, Habazettl H, Schenkel J, Boekstegers P, Debatin KM: Involvement of CD95/Apo1/Fas in cell death after myocardial ischemia. Circulation 102(8):915-920, 2000.
9. Wortinger MA, Foley JW, Larocque P, Witcher DR, Lahn M, Jakubowski JA, Glasebrook A, Song HY: Fas ligandYinduced murine pulmonary inflammation is reduced by a stable decoy receptor 3 analogue. Immunology 110(2): 225-233, 2003.
10. Seitz DH, Palmer A, Niesler U, Braumüller ST, Bauknecht S, Gebhard F, Knöferl MW: Altered expression of Fas receptor on alveolar macrophages and inflammatory effects of soluble Fas ligand following blunt chest trauma. Shock 35(6):610-617, 2011.
11. Sutton TA, Mang HE, Campos SB, Sandoval RM, Yoder MC, Molitoris BA: Injury of the renal microvascular endothelium alters barrier function after ischemia. Am J Physiol Renal Physiol 285(2):F191-F198, 2003.
12. Wanner GA, Mica L, Wanner-Schmid E, Kolb SA, Hentze H, Trentz O, Ertel W: Inhibition of caspase activity prevents CD95-mediated hepatic microvascular perfusion failure and restores Kupffer cell clearance capacity. FASEB J 13(10):1239-1248, 1999.
13. Smyth LA, Brady HJ: cMet and Fas receptor interaction inhibits death-inducing signaling complex formation in endothelial cells. Hypertension 46(1):100-106, 2005.
14. Suzuki M, Aoshiba K, Nagai A: Oxidative stress increases Fas ligand expression in endothelial cells. J Inflamm (Lond) 3:11, 2006.
15. Reap EA, Roof K, Maynor K, Borrero M, Booker J, Cohen PL: Radiation and stress-induced apoptosis: a role for Fas/Fas ligand interactions. Proc Natl Acad Sci 94(11):5750-5755, 1997.
16. Wong M, Ziring D, Korin Y, Desai S, Kim S, Lin J, Gjertson D, Braun J, Reed E, Singh RR: TNFalpha blockade in human diseases: mechanisms and future directions. Clin Immunol 126(2):121-136, 2008.
17. + T cells. Nat Med 4(12):1377-1382, 1998.
18. Childs EW, Tharakan B, Byrge N, Tinsley JH, Hunter FA, Smythe WR: Angiopoietin-1 inhibits intrinsic apoptotic signaling and vascular hyper-permeability following hemorrhagic shock. Am J Physiol Heart Circ Physiol 294(5):H2285-H2295, 2008.
19. Harvey RA, Ferrier DR: Lippincott's Illustrated Reviews: Biochemistry. 5th North American ed. Philadelphia, PA: Lippincott Williams & Wilkins, 75-82, 2010.
20. Saraste M: Oxidative phosphorylation at the fin de siècle. Science 283(5407): 1488-1493, 1999.
21. Childs EW, Tharakan B, Hunter FA, Isong M, Liggins ND: Mitochondrial complex III is involved in proapoptotic BAK-induced microvascular endothe-lial cell hyperpermeability. Shock 29(5):636-641, 2008.
22. Simon HU, Haj-Yehia A, Levi-Schaffer F: Role of reactive oxygen species (ROS) in apoptosis induction. Apoptosis 5(5):415-418, 2000.
23. Steinhusen U, Badock V, Baurer A, Behrens J, Wittman-Liebold B, Dörken B, Bommert K: Apoptosis-induced cleavage of beta-catenin by caspase-3 results in proteolytic fragments with reduced transactivation potential. J Biol Chem 275(21):16345-16353, 2000.
24. Tharakan B, Hellman J, Sawant DA, Tinsley JH, Parrish AR, Hunter FA, Smythe WR, Childs EW: "-catenin dynamics in the regulation of microvascular endothelial cell hyperpermeability. Shock 37(3):306-311, 2012.