Free radicals upregulate complement expression in rabbit isolated heart. Am J Physiol Heart Circ Physiol 2000 Jul;279(1):H195-201
Date
07/19/2000Pubmed ID
10899056DOI
10.1152/ajpheart.2000.279.1.H195Scopus ID
2-s2.0-0033861321 (requires institutional sign-in at Scopus site) 28 CitationsAbstract
Both free radicals and complement activation can injure tissue. Our study determined whether free radicals alter complement production by the myocardium. Isolated hearts from New Zealand White rabbits were perfused on a Langendorff apparatus and exposed to xanthine (X; 100 microM) plus xanthine oxidase (XO; 8 mU/ml) (X/XO). The free radical-generating system significantly (P < 0.05) increased C1q and also increased C1r, C3, C8, and C9 transcription compared with controls. Immunohistological examination revealed augmented membrane attack complex deposition on X/XO-treated tissue. X/XO-treated hearts also exhibited significant (P < 0.05) increases in coronary perfusion pressure and left ventricular end-diastolic pressure and a decrease in left-ventricular developed pressure. N-(2-mercaptopropionyl)-glycine (3 mM), in conjunction with the superoxide dismutase mimetic SC-52608 (100 microM), significantly (P < 0.05) reduced the upregulation of C1q, C1r, C3, C8, and C9 mRNA expression elicited by X/XO. The antioxidants also ameliorated the deterioration in function caused by X/XO. Local complement activation may represent a mechanism by which free radicals mediate tissue injury.
Author List
Tanhehco EJ, Yasojima K, McGeer PL, Washington RA, Lucchesi BRAuthor
Elaine J. Tanhehco MD, PhD Assistant Professor in the Radiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsComplement C1q
Complement C3
Complement C8
Complement C9
Complement System Proteins
Free Radicals
Gene Expression Regulation
Heart
In Vitro Techniques
Male
Myocardium
Rabbits
Receptors, Complement
Transcription, Genetic
Xanthine
Xanthine Oxidase
