2011
DOI: 10.1097/aln.0b013e31820a4d5b
|View full text |Cite
|
Sign up to set email alerts
|

Toll-like Receptor 4 Signaling Confers Cardiac Protection against Ischemic Injury via  Inducible Nitric Oxide Synthase- and Soluble Guanylate Cyclase-dependent Mechanisms

Abstract: Background: Prior administration of a small dose of lipopolysaccharide confers a cardiac protection against ischemiareperfusion injury. However, the signaling mechanisms that control the protection are incompletely understood. We tested the hypothesis that Toll-like receptor 4 (TLR4) mediates the ability of lipopolysaccharide to protect against cardiac ischemia-reperfusion injury through distinct intracellular pathways involving myeloid differentiation factor 88 (MyD88), TIR-domain-containing adaptor protein-i… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

6
45
0

Year Published

2011
2011
2024
2024

Publication Types

Select...
9

Relationship

2
7

Authors

Journals

citations
Cited by 40 publications
(51 citation statements)
references
References 53 publications
6
45
0
Order By: Relevance
“…LPS-induced TLR4 activation before myocardial ischemia has been also shown to have cardioprotective effects (Zacharowski et al, 2000). These effects have been primarily attributed to a TLR4-mediated increased production in inducible nitric oxide synthase and nitric 156 oxide with improvements in ventricular function (Wang et al, 2011a).…”
Section: B Toll-like Receptor Signaling Activationmentioning
confidence: 99%
“…LPS-induced TLR4 activation before myocardial ischemia has been also shown to have cardioprotective effects (Zacharowski et al, 2000). These effects have been primarily attributed to a TLR4-mediated increased production in inducible nitric oxide synthase and nitric 156 oxide with improvements in ventricular function (Wang et al, 2011a).…”
Section: B Toll-like Receptor Signaling Activationmentioning
confidence: 99%
“…Ex Vivo Model of Myocardial I/R-The ex vivo model has been described previously (20,24). Briefly, mice were heparinized and euthanized.…”
Section: Methodsmentioning
confidence: 99%
“…As a final method to examine MyD88-dependent versus MyD88-independent signaling in HPAECs we examined downstream induction of MyD88/NFkB-dependent (iNOS) (27,28) and IRF3-dependent (IFN␤ and ISG20) (29,30) genes by RT-PCR. As expected, HMGB1 stimulated the induction of IFN␤ and ISG20 but not iNOS in HPAECs (Fig.…”
Section: Hypoxia-induced Hmgb1 Release Leads To Inhibition Of Hpaec Mmentioning
confidence: 99%