ACELL December 46/6
نویسندگان
چکیده
Kyriakides, Constantinos, William Austen, Jr., Yong Wang, Joanne Favuzza, Lester Kobzik, Francis D. Moore, Jr., and Herbert B. Hechtman. Skeletal muscle reperfusion injury is mediated by neutrophils and the complement membrane attack complex. Am. J. Physiol. 277 (Cell Physiol. 46): C1263–C1268, 1999.—The relative inflammatory roles of neutrophils, selectins, and terminal complement components are investigated in this study of skeletal muscle reperfusion injury. Mice underwent 2 h of hindlimb ischemia followed by 3 h of reperfusion. The role of neutrophils was defined by immunodepletion, which reduced injury by 38%, as did anti-selectin therapy with recombinant soluble P-selectin glycoprotein ligand-immunoglobulin (Ig) fusion protein. Injury in C5-deficient and soluble complement receptor type 1-treated wild-type mice was 48% less than that of untreated wild-type animals. Injury was restored in C5-deficient mice reconstituted with wild-type serum, indicating the effector role of C5–9. Neutropenic C5-deficient animals showed additive reduction in injuries (71%), which was lower than C5-deficient neutrophil-replete mice, indicating neutrophil activity without C5a. Hindlimb histological injury was worse in ischemic wild-type and C5-deficient animals reconstituted with wild-type serum. In conclusion, the membrane attack complex and neutrophils act additively to mediate skeletal muscle reperfusion injury. Neutrophil activity is independent of C5a but is dependent on selectin-mediated adhesion.
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ACELL September 46/3
Dodd, J. S., J. A. Raleigh, and T. S. Gross. Osteocyte hypoxia: a novel mechanotransduction pathway. Am. J. Physiol. 277 (Cell Physiol. 46): C598–C602, 1999.—Bone is a unique tissue in which to examine mechanotransduction due to its essential role in weight bearing. Within bone, the osteocyte is an ideal cellular mechanotransducer candidate. Because osteocytes reside distant from the blood supp...
متن کاملACELL September 46/3
Zeiske, Wolfgang, Ilse Smets, Marcel Ameloot, Paul Steels, and Willy Van Driessche. Intracellular pH shifts in cultured kidney (A6) cells: effects on apical Na1 transport. Am. J. Physiol. 277 (Cell Physiol. 46): C469–C479, 1999.—We report, for the epithelial Na1 channel (ENaC) in A6 cells, the modulation by cell pH (pHc) of the transepithelial Na1 current (INa), the current through the individu...
متن کاملACELL October 46/4
NABENDU S. CHATTERJEE,1 CHANDIRA K. KUMAR,1 ALVARO ORTIZ,1 STANLEY A. RUBIN,2 AND HAMID M. SAID1 1Medical Research Service, Veterans Affairs Medical Center, Long Beach 90822, and Department of Medicine and Physiology/Biophysics, University of California School of Medicine, Irvine 92697; and 2Veterans Affairs West Los Angeles, Los Angeles 90073, and Department of Medicine, University of Californ...
متن کاملACELL August 46/2
JOHN M. PARK,1 ROSALYN M. ADAM,1 CRAIG A. PETERS,1 PAUL D. GUTHRIE,1 ZIJIE SUN,2 MICHAEL KLAGSBRUN,3 AND MICHAEL R. FREEMAN3 1Urologic Laboratory, Department of Urology, 3Laboratory for Surgical Research, Children’s Hospital, and Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115; and 2Departments of Surgery and Genetics, Stanford University School of Medicine, Stanford,...
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