Myocardial gene reprogramming associated with a cardiac  cross-resistant state induced by LPS preconditioning

Meng, Xianzhong; Brown, James M.; Ao, Lihua; Rowland, Robert T.; Nordeen, Steven K.; Banerjee, Anirban; Harken, Alden H.

doi:10.1152/ajpcell.1998.275.2.c475

Cited by 39 publications

(18 citation statements)

References 32 publications

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“…7B). A similar LPS-induced cardiac cross-resistance to ischemia has been reported previously (23) and had shown that LPS preconditioning induces cardiac resistance to subsequent ischemia. Our findings suggested a similar LPS preconditioning of mouse lung-specific Mig-6 expression in response to MV.…”

Section: Discussionsupporting

confidence: 83%

Bioinformatic identification of novel early stress response genes in rodent models of lung injury

Fan¹,

Grigoryev²,

Taylor³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

100

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Acute lung injury is a complex illness with a high mortality rate (>30%) and often requires the use of mechanical ventilatory support for respiratory failure. Mechanical ventilation can lead to clinical deterioration due to augmented lung injury in certain patients, suggesting the potential existence of genetic susceptibility to mechanical stretch (6, 48), the nature of which remains unclear. To identify genes affected by ventilator-induced lung injury (VILI), we utilized a bioinformatic-intense candidate gene approach and examined gene expression profiles from rodent VILI models (mouse and rat) using the oligonucleotide microarray platform. To increase statistical power of gene expression analysis, 2,769 mouse/rat orthologous genes identified on RG_U34A and MG_U74Av2 arrays were simultaneously analyzed by significance analysis of microarrays (SAM). This combined ortholog/SAM approach identified 41 up- and 7 downregulated VILI-related candidate genes, results validated by comparable expression levels obtained by either real-time or relative RT-PCR for 15 randomly selected genes. K-mean clustering of 48 VILI-related genes clustered several well-known VILI-associated genes (IL-6, plasminogen activator inhibitor type 1, CCL-2, cyclooxygenase-2) with a number of stress-related genes (Myc, Cyr61, Socs3). The only unannotated member of this cluster (n = 14) was RIKEN_1300002F13 EST, an ortholog of the stress-related Gene33/Mig-6 gene. The further evaluation of this candidate strongly suggested its involvement in development of VILI. We speculate that the ortholog-SAM approach is a useful, time- and resource-efficient tool for identification of candidate genes in a variety of complex disease models such as VILI.

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Section: Discussionsupporting

confidence: 83%

Bioinformatic identification of novel early stress response genes in rodent models of lung injury

Fan¹,

Grigoryev²,

Taylor³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

100

View full text Add to dashboard Cite

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“…Since it was previously shown that endothelial cells (EC) express PPARs (31), accumulating interests were focused on the anti-inflammatory effects of PPAR agonists on the vascular tissue. In addition, it was revealed that the activation of PPAR-␥ with its agonists effectively attenuates inflammatory processes in a number of organs such as heart (32)(33)(34)(35), kidney (36,37), lung (38), and intestine (15, 39) against ischemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator-Activated Receptor-γ Ligand, 15-Deoxy-Δ12,14-Prostaglandin J2, Reduces Neutrophil Migration via a Nitric Oxide Pathway

Napimoga

Vieira

Dal-Secco³

et al. 2008

The Journal of Immunology

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Ligands for peroxisome proliferator-activated receptor γ (PPAR-γ), such as 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) have been implicated as a new class of anti-inflammatory compounds with possible clinical applications. Based on this concept, this investigation was designed to determine the effect of 15d-PGJ2-mediated activation of PPAR-γ ligand on neutrophil migration after an inflammatory stimulus and clarify the underlying molecular mechanisms using a mouse model of peritonitis. Our results demonstrated that 15d-PGJ2 administration decreases leukocyte rolling and adhesion to the inflammated mesenteric tissues by a mechanism dependent on NO. Specifically, pharmacological inhibitors of NO synthase remarkably abrogated the 15d-PGJ2-mediated suppression of neutrophil migration to the inflammatory site. Moreover, inducible NOS−/− mice were not susceptible to 15d-PGJ2-mediated suppression of neutrophil migration to the inflammatory sites when compared with their wild type. In addition, 15d-PGJ2-mediated suppression of neutrophil migration appeared to be independent of the production of cytokines and chemokines, since their production were not significantly affected in the carrageenan-injected peritoneal cavities. Finally, up-regulation of carrageenan-triggered ICAM-1 expression in the mesenteric microcirculation vessels was abrogated by pretreatment of wild-type mice with 15d-PGJ2, whereas 15d-PGJ2 inhibited F-actin rearrangement process in neutrophils. Taken together these findings demonstrated that 15d-PGJ2 suppresses inflammation-initiated neutrophil migration in a mechanism dependent on NO production in mesenteric tissues.

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“…Mechanisms known to mediate endotoxin tolerance in macrophages that lead to suppression of specific cytokines and inflammatory molecules involve attenuation of NF-κB and AP-1 (activator protein 1) and enhanced expression of the signalling mediators IRAK-M (interleukin-1-receptor-associated kinase M) and SOCS-1 (suppressor of cytokine signalling 1) [48,49]. A case for gene reprogramming can also be made where preconditioning with LPS induces cardiac resistance to ischaemia [50]. In this scenario, exposure to LPS may induce non-specific myocardial adaptations through gene changes (e.g.…”

Section: Reprogramming the Genomic Response To Injury: A Proposed Mecmentioning

confidence: 99%

Toll-like receptors and tolerance to ischaemic injury in the brain

Stevens

Stenzel-Poore

2006

Biochemical Society Transactions

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Ischaemic tolerance in the brain is a powerful adaptive defence that involves an endogenous programme of neuroprotection culminating in marked protection against brain injury from ischaemia. A range of preconditioning stimuli exist that differ in ligand and target characteristics but share the common feature of causing mild stress or insult without inducing overt injury. The protective phenotype that emerges confers tolerance to subsequent exposure to injurious insults. Tolerance to injury is the result of genomic reprogramming, an adaptation comprising regulatory processes that countermand injurious effectors and invoke novel neuroprotective pathways. TLRs (Toll-like receptors) play important roles in sensing potential danger/insult in the form of pathogens as well as endogenous stress molecules that occur in response to mild injury (e.g. heat-shock proteins). Recent studies suggest that TLRs are novel and potent preconditioning targets that offer substantial promise to protect the brain from ischaemic injury.

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Myocardial gene reprogramming associated with a cardiac cross-resistant state induced by LPS preconditioning

Cited by 39 publications

References 32 publications

Bioinformatic identification of novel early stress response genes in rodent models of lung injury

Bioinformatic identification of novel early stress response genes in rodent models of lung injury

Peroxisome Proliferator-Activated Receptor-γ Ligand, 15-Deoxy-Δ12,14-Prostaglandin J2, Reduces Neutrophil Migration via a Nitric Oxide Pathway

Toll-like receptors and tolerance to ischaemic injury in the brain

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