Expression of endothelin-1 system in a pig model of endotoxic shock

Forni, Monica; Mazzola, Silvia; Ribeiro, Luciana A.; Pirrone, Federica; Zannoni, Augusta; Bernardini, Chiara; Bacci, Maria Laura; Albertini, M.

doi:10.1016/j.regpep.2005.07.001

Cited by 42 publications

(34 citation statements)

References 32 publications

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“…The increase began after 1 h of treatment and continued for 4 h, confirming that LPS is a strong stimulus for ET-1 mRNA induction. In contrast, LPS did not influence the gene expression levels of ECE-1, ET A , or ET B , in contrast to our previous results (Forni et al 2005) in which LPS treatment at 4 h decreased their expression levels. These conflicting results suggest, together with the trends observed in the sham group, a possible effect of the anesthesiological/surgical protocol.…”

Section: Discussioncontrasting

confidence: 99%

“…Real-time quantitative PCR was performed using an iCycler thermocycler (Bio-Rad). Specific porcine primers for ET-1, ECE-1, ET A , ET B , and hypoxanthine phosphoribosyltransferase (HPRT, housekeeping gene) were designed, and real-time PCR (SYBR green I) was performed as previously described (Forni et al 2005). Relative gene expression levels were calculated using the 2 −ΔΔCT method (Applied Biosystems User Bulletin #2, 2001) relative to the control T0.…”

Section: Methodsmentioning

confidence: 99%

“…The roles of the ET system's key components (ET-1, ECE-1, ET A , and ET B ) in sepsis are not yet fully clarified. Our previous study in a porcine model (Forni et al 2005) showed that an LPS infusion (lasting 4 h) induced opposite effects on the various components of the ET-1 system in the lung: an increase of ET-1 mRNA and a decrease in the mRNA levels of the other components. Since ET-1 peptide has a short half-life (15-20 min) (Galiè et al 2004), the aim of the present research was to evaluate lung ET system expression levels at different times after LPS treatment during porcine endotoxic shock.…”

mentioning

confidence: 94%

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Pulmonary kinetic expression of the endothelin system in a swine model of endotoxic shock

et al. 2010

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Endothelin (ET)-1 is a potent vasoconstrictor peptide involved in the derangement of respiratory mechanics during endotoxic shock. We measured the kinetics of pulmonary mRNA expression of the key components of the ET system [i.e., ET-1, ET-converting enzyme (ECE), and ETA and ETB receptors] by quantitative real-time reverse transcriptase-polymerase chain reaction in a swine model of endotoxic shock (0, 1, 2, 3, and 4 h of continuous LPS infusion at 40 microg/kg/hour; sham group, 4 hour saline infusion). A significant increase in mRNA expression levels was observed for ET-1 in LPS-treated piglets; the increase began as early as 1 hour. In contrast, no significant variations were observed for the ECE, ETA, or ETB genes. Small gene expression differences observed with respect to our previous results suggest a possible effect of the anesthesia or surgical protocol on ET system regulation.

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Section: Discussioncontrasting

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 94%

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Pulmonary kinetic expression of the endothelin system in a swine model of endotoxic shock

et al. 2010

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“…Previously, Forni et al (2005) reported that LPS infusion evokes a large increase in plasma concentration of ET-1, and an increase in heart ET-1, ETA-R and ETB-R mRNA level. Therefore, a detrimental effect of endotoxin is partially a result of overproduction of ET-1.…”

Section: Discussionmentioning

confidence: 93%

The influence of ETA and ETB receptor blockers on LPS-induced oxidative stress and NF-κB signaling pathway in heart

Piechota-Polańczyk¹,

Kleniewska²,

Gorąca³

2012

gpb

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Abstract. The aim of this study was to assess whether an endothelin-A receptor (ETA-R) blocker, BQ123, or an endothelin-B (ETB-R) receptor blocker, BQ788, influences nuclear factor kappa beta (NF-κB) pathway, free radical generation, tumor necrosis factor-alpha (TNF-α) concentration, and glutathione redox system in hearts obtained from lipopolysaccharide (LPS)-induced endotoxic rats. The study was performed on rats divided into groups: 1) saline, 2) saline + LPS (15 mg/kg), 3) BQ123 (1 mg/kg b.w.) + LPS, 4) BQ123 (0.5 mg/kg b.w.) + LPS, 5) BQ788 (3 mg/kg b.w.) + LPS. The ETA-R and ETB-R antagonists were injected i.v. 30 min before LPS administration. In rats, BQ123 caused a significant decrease in TBARS (p < 0.05) but not in H 2 O 2 concentration. It also decreased tissue protein level and improved tissue redox status (p < 0.01). Only a dose of 1 mg/kg decreased TNF-α concentration (p < 0.05). BQ788 lowered TBARS, H 2 O 2 and protein concentration (p < 0.05; p < 0.02; p < 0.001, respectively), however, it did not affect TNF-α concentration. Neither ETA-R nor ETB-R blockers influenced LPS-induced increase in p65 subunit level and activation of NF-κB pathway. Our results demonstrated that ETA-R blockage is more effective in inhibiting free radical generation and improving heart antioxidant properties than ETB-R blockage under oxidative stress. NF-κB pathway is not incorporated in ETA-R and ETB-R influence on ROS production.

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“…Studies have shown that LPS stimulates the synthesis of ET-1 both in vivo and in vitro (Ohta et al 1990;Forni et al 2005;Zaedi et al 2006). Furthermore, the use of a nonselective endothelin receptor antagonist, tezosentan, has been shown to limit various hemodynamic abnormalities associated with endotoxemia, including pulmonary edema (Kuklin et al 2004;Rossi et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Preferential recruitment of neutrophils by endothelin-1 in acute lung inflammation induced by lipopolysaccharide or cigarette smoke

Bhavsar

Liu²,

Patel³

et al. 2008

COPD

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This study examined the role of endothelin-1 (ET-1) in recruiting infl ammatory cells to the lung after induction of injury with either lipopolysaccharide (LPS) or cigarette smoke. Hamsters injected with either ET-1 or its precursor peptide (Big ET-1) prior to treatment with LPS or cigarette smoke had markedly increased concentrations of neutrophils in bronchoalveolar lavage fl uid (BALF) despite a reduction in total numbers of BALF leukocytes. Furthermore, the effect of ET-1 on smoke-exposed animals was reversed by addition of an endothelin-A receptor antagonist. These results are consistent with preferential recruitment of neutrophils by ET-1, and suggest that inhibition of this proinfl ammatory mediator may decrease acute pulmonary infl ammation associated with cigarette smoke and other pulmonary toxins.

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Expression of endothelin-1 system in a pig model of endotoxic shock

Cited by 42 publications

References 32 publications

Pulmonary kinetic expression of the endothelin system in a swine model of endotoxic shock

Pulmonary kinetic expression of the endothelin system in a swine model of endotoxic shock

The influence of ETA and ETB receptor blockers on LPS-induced oxidative stress and NF-κB signaling pathway in heart

Preferential recruitment of neutrophils by endothelin-1 in acute lung inflammation induced by lipopolysaccharide or cigarette smoke

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