Molecular Changes Induced in Rat Liver by Hemorrhage and Effects of Melanocortin Treatment

Lonati, Caterina; Sordi, Andrea; Giuliani, Daniela; Spaccapelo, Luca; Leonardi, Patrizia; Carlin, Andrea; Ottani, Alessandra; Galantucci, Maria; Grieco, Paolo; Catania, Anna; Guarini, Salvatore

doi:10.1097/aln.0b013e318246ea68

Cited by 11 publications

(6 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The combination with hemorrhage could raise the concern that the inflammatory response might be mainly driven by this component. The interventions induced an increase in heart rate that indicated hemodynamic strain that was not in the range of a hemorrhagic shock ( Lonati et al, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

Acute perioperative stress-induced increase of plaque volume and vulnerability in apolipoprotein E-deficient mice is amenable to statin treatment and IL-6-inhibition

Janssen

Wagner

Demmer

et al. 2015

Disease Models &Amp; Mechanisms

View full text Add to dashboard Cite

Myocardial infarction and stroke are frequent after surgical procedures and consume a considerable amount of benefit of surgical therapy. Perioperative stress, induced by surgery, is composed of hemodynamic and inflammatory reactions. The effects of perioperative stress on atherosclerotic plaques are ill-defined. Murine models to investigate the influence of perioperative stress on plaque stability and rupture are not available. We developed a model to investigate the influence of perioperative stress on plaque growth and stability by exposing apolipoprotein-E-deficient mice, fed a high cholesterol diet for 7 weeks, to a double hit consisting of 30 min of laparotomy combined with a substantial blood loss (approximately 20% of total blood volume; 400 µl). The innominate artery was harvested 72 h after the intervention. Control groups were sham and baseline controls. Interleukin-6 (IL-6) and serum amyloid A (SAA) plasma levels were determined. Plaque load, vascular smooth muscle cell (VSMC) and macrophage content were quantified. Plaque stability was assessed using the Stary score and frequency of signs of plaque rupture were assessed. High-dose atorvastatin (80 mg/kg body weight/day) was administered for 6 days starting 3 days prior to the double hit. A single dose of an IL-6-neutralizing antibody or the fusion protein gp130-Fc selectively targeting IL-6 trans-signaling was subcutaneously injected. IL-6 plasma levels increased, peaking at 6 h after the intervention. SAA levels peaked at 24 h (n=4, P<0.01). Plaque volume increased significantly with the double hit compared to sham (n=8, P<0.01). More plaques were scored as complex or bearing signs of rupture after the double hit compared to sham (n=5-8, P<0.05). Relative VSMC and macrophage content remained unchanged. IL-6-inhibition or atorvastatin, but not blocking of IL-6 trans-signaling, significantly decreased plaque volume and complexity (n=8, P<0.01). Using this model, researchers will be able to further investigate the pathophysiology of perioperative plaque stability, which can result in myocardial infarction, and, additionally, to test potential protective strategies.

show abstract

Section: Discussionmentioning

confidence: 99%

Acute perioperative stress-induced increase of plaque volume and vulnerability in apolipoprotein E-deficient mice is amenable to statin treatment and IL-6-inhibition

Janssen

Wagner

Demmer

et al. 2015

Disease Models &Amp; Mechanisms

View full text Add to dashboard Cite

show abstract

“…It is verified through Cox multifactor survival analysis that LRH1 expression is one of the independent factors influencing prognosis for OS patients (27). Overexpression of LRH1 is an important factor affecting the biological behavior of OS in clinic, which promotes OS progression, and it is closely associated with the role of LRH1 in promoting tumor cell proliferation and metastasis (26). Thus, we provided evidence that downregulation of microRNA-381 upregulated LRH-1/Wnt/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 59%

“…It further reveals that LRH1 can promote genesis, development and metastasis of tumors (12). OS patients with high LRH1 protein expression have remarkably shorter average survival time and average metastasis time compared with those with low LRH1 protein expression, and the difference is of statistical significance (26). It is verified through Cox multifactor survival analysis that LRH1 expression is one of the independent factors influencing prognosis for OS patients (27).…”

Section: Discussionmentioning

confidence: 82%

MicroRNA-381 suppresses the proliferation of osteosarcoma cells through LRH-1/Wnt/β-catenin signaling pathway

Wang

Sun

et al. 2017

Oncol Rep

View full text Add to dashboard Cite

We explored the function of microRNA-381 on osteosarcoma cell growth and anticancer mechanism for clinic treatment. MicroRNA-381 of osteosarcoma patients was decreased, microRNA-381 levels were more downregulated at stages III/IV than those at stage I/II in osteosarcoma patients. Downregulation of microRNA-381 using anti-microRNA-381 mimics increased cell proliferation, decreased LDH activity and apoptosis, and inhibited caspase‑3/9 activities, Bax/Bcl-2 and p53 protein expression in vitro osteosarcoma cells through upregulation of LRH-1/Wnt/β-catenin signaling pathway. Overexpression of microRNA-381 using microRNA-381 mimics inhibited cell proliferation, induced apoptosis and increased LDH activity, caspase‑3/9 activities, expression of Bax/Bcl-2 and p53 protein in osteosarcoma of in vitro model through downregulation of LRH-1/Wnt/β-catenin signaling pathway. Si‑LRH‑1 promoted the anticancer effects of microRNA-381 on osteosarcoma cell growth through Wnt/β‑catenin signaling pathway. Thus, our data suggested that microRNA-381 suppresses the proliferation of osteosarcoma cells through upregulation of LRH-1/Wnt/β-catenin signaling pathway.

show abstract

“…Moreover, RO27-3225 prevents the hemorrhage-induced immunopathological changes in peripheral organs. Treatment with RO27-3225 normalizes hemogasanalysis parameters after hemorrhagic challenge (85).…”

Section: Protective Effects Of Melanocortins In Systemic Inflammationmentioning

confidence: 97%

Activation of Melanocortin Receptors as a Potential Strategy to Reduce Local and Systemic Reactions Induced by Respiratory Viruses

2020

Self Cite

View full text Add to dashboard Cite

The clinical hallmarks of infections caused by critical respiratory viruses consist of pneumonia, which can progress to acute lung injury (ALI), and systemic manifestations including hypercoagulopathy, vascular dysfunction, and endotheliitis. The disease outcome largely depends on the immune response produced by the host. The bio-molecular mechanisms underlying certain dire consequences of the infection partly arise from an aberrant production of inflammatory molecules, an event denoted as “cytokine storm”. Therefore, in addition to antiviral therapies, molecules able to prevent the injury caused by cytokine excess are under investigation. In this perspective, taking advantage of melanocortin peptides and their receptors, components of an endogenous modulatory system that exerts marked anti-inflammatory and immunomodulatory influences, could be an effective therapeutic strategy to control disease evolution. Exploiting the melanocortin system using natural or synthetic ligands can form a realistic basis to counteract certain deleterious effects of respiratory virus infections. The central and peripheral protective actions exerted following melanocortin receptor activation could allow dampening the harmful events that trigger the cytokine storm and endothelial dysfunction while sustaining the beneficial signals required to elicit repair mechanisms. The long standing evidence for melanocortin safety encourages this approach.

show abstract

Molecular Changes Induced in Rat Liver by Hemorrhage and Effects of Melanocortin Treatment

Cited by 11 publications

References 44 publications

Acute perioperative stress-induced increase of plaque volume and vulnerability in apolipoprotein E-deficient mice is amenable to statin treatment and IL-6-inhibition

Acute perioperative stress-induced increase of plaque volume and vulnerability in apolipoprotein E-deficient mice is amenable to statin treatment and IL-6-inhibition

MicroRNA-381 suppresses the proliferation of osteosarcoma cells through LRH-1/Wnt/β-catenin signaling pathway

Activation of Melanocortin Receptors as a Potential Strategy to Reduce Local and Systemic Reactions Induced by Respiratory Viruses

Contact Info

Product

Resources

About