Preconditioning reduces tissue complement gene expression in the rabbit isolated heart.

Szczegóły
Abstrakt

Tytuł:: Preconditioning reduces tissue complement gene expression in the rabbit isolated heart.
Autorzy:: Tanhehco EJ; University of Michigan Medical School, Department of Pharmacology, Ann Arbor, Michigan 48109, USA.
Yasojima K
McGeer PL
Washington RA
Kilgore KS
Homeister JW
Lucchesi BR
Źródło:: The American journal of physiology [Am J Physiol] 1999 Dec; Vol. 277 (6), pp. H2373-80.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: Bethesda, MD : American Physiological Society
Original Publication: Washington [etc.] American Physiological Society.
MeSH Terms:: Gene Expression Regulation*/drug effects
Ischemic Preconditioning*
Transcription, Genetic*/drug effects
Complement System Proteins/*genetics
Myocardium/*metabolism
Potassium Channels/*physiology
Animals ; DNA Primers ; Glyburide/pharmacology ; In Vitro Techniques ; Male ; Myocardial Ischemia ; Myocardial Reperfusion ; Pinacidil/pharmacology ; Potassium Channel Blockers ; RNA, Messenger/genetics ; Rabbits ; Reverse Transcriptase Polymerase Chain Reaction
Molecular Sequence:: GENBANK AF089083; AF108768
Substance Nomenclature:: 0 (DNA Primers)
0 (Potassium Channel Blockers)
0 (Potassium Channels)
0 (RNA, Messenger)
7B0ZZH8P2W (Pinacidil)
9007-36-7 (Complement System Proteins)
SX6K58TVWC (Glyburide)
Entry Date(s):: Date Created: 19991222 Date Completed: 20000119 Latest Revision: 20180829
Update Code:: 20240104
DOI:: 10.1152/ajpheart.1999.277.6.H2373
PMID:: 10600858
: Czasopismo naukowe

Both preconditioning and inhibition of complement activation have been shown to ameliorate myocardial ischemia-reperfusion injury. The recent demonstration that myocardial tissue expresses complement components led us to investigate whether preconditioning affects complement expression in the isolated heart. Hearts from New Zealand White rabbits were exposed to either two rounds of 5 min global ischemia followed by 10 min reperfusion (ischemic preconditioning) or 10 microM of the ATP-dependent K+ (KATP) channel opener pinacidil for 30 min (chemical preconditioning) before induction of 30 min global ischemia followed by 60 min of reperfusion. Both ischemic and chemical preconditioning significantly (P < 0.05) reduced myocardial C1q, C1r, C3, C8, and C9 mRNA levels. Western blot and immunohistochemistry demonstrated a similar reduction in C3 and membrane attack complex protein expression. The K(ATP) channel blocker glyburide (10 microM) reversed the depression of C1q, C1r, C3, C8, and C9 mRNA expression observed in the pinacidil-treated hearts. The results suggest that reduction of local tissue complement production may be one means by which preconditioning protects the ischemic myocardium.

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