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Delayed preconditioning in cardiac myocytes with respect to development of a proinflammatory phenotype: role of SOD and NOS.

Abstract：

OBJECTIVE:Both superoxide dismutase (SOD) and nitric oxide synthase (NOS) have been implicated in delayed preconditioning (DP) to ischemia/reperfusion (I/R) in the heart. We used isolated cardiac myocytes to test the hypothesis that SOD and NOS may interact in the development of DP. METHODS:Mouse neonatal cardiac myocytes were challenged with anoxia/reoxygenation (A/R; an in vitro counterpart to I/R) and normoxia/normoxia (N/N) served as the control. Two indices of inflammation were measured: oxidant stress (DHR oxidation) and polymorphonuclear leukocyte (PMN) transendothelial migration (cell culture inserts). The role of SOD was assessed using an antisense approach and the role of NOS was assessed using iNOS and eNOS deficient myocytes. RESULTS:Cardiac myocytes exposed to A/R (1) produced more oxidants (intracellular fluorescence emission from 2.0 +/- 0.1 for N/N to 3.0 +/- 0.3 for A/R; P<0.05) and (2) promoted PMN migration (% migration from 8.4 +/- 0.9 for N/N to 14.1 +/- 1.1 for A/R; P<0.05). DP occurred if the myocytes were pretreated with an A/R challenge 24 h earlier. That is, these A/R-induced responses were significantly reduced (fluorescence emission 1.9 +/- 0.1 and % migration 8.4 +/- 0.7; P<0.05 as compared to A/R with no pretreatment). Myocyte Mn-SOD, but not Cu/Zn-SOD, activity increased 24 h after the initial A/R challenge. A Mn-SOD antisense oligonucleotide prevented the development of DP. DP occurred in iNOS, but not eNOS, deficient myocytes. A/R increased mRNA for eNOS, but not iNOS, in wild-type myocytes. A/R increased Mn-SOD protein in both iNOS and eNOS deficient myocytes. However, Mn-SOD activity increased only in iNOS deficient myocytes. CONCLUSIONS:Collectively, these findings suggest that Mn-SOD and eNOS may act in concert in the development of DP in cardiac myocytes.

journal_name

Cardiovasc Res

journal_title

Cardiovascular research

authors

Rui T,Cepinskas G,Feng Q,Kvietys PR

doi

10.1016/s0008-6363(03)00502-9

subject

Has Abstract

pub_date

2003-10-01 00:00:00

pages

901-11

issue

eissn

0008-6363

issn

1755-3245

pii

S0008636303005029

journal_volume

pub_type

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Delayed preconditioning in cardiac myocytes with respect to development of a proinflammatory phenotype: role of SOD and NOS.