Possible role of CRF peptides in burn-induced hypermetabolism

Chance, William T.; Dayal, Ramesh; Friend, Lou Ann; Sheriff, Sulaiman

doi:10.1016/j.lfs.2005.05.083

Cited by 11 publications

(7 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A degree of receptor specificity was also suggested by these studies, with antisense ODN knockdown or pharmacological blockade of CRF type 1 receptor having no significant effect on REE in burned or control rats. These results are consistent with our previous observations showing that a biochemical lesion of hypothalamic CRF receptors using a saporin-CRF conjugate significantly reduced the hypermetabolic response in burned rats (Chance et al, 2006). In addition, in Chance et al (2006), it appeared that hypothalamic CRF R-2 expression was reduced by the saporin-CRF treatment in burned rats.…”

Section: Discussionsupporting

confidence: 93%

“…These results are consistent with our previous observations showing that a biochemical lesion of hypothalamic CRF receptors using a saporin-CRF conjugate significantly reduced the hypermetabolic response in burned rats (Chance et al, 2006). In addition, in Chance et al (2006), it appeared that hypothalamic CRF R-2 expression was reduced by the saporin-CRF treatment in burned rats. The present study strongly suggests that the mediation of burn-induced hypermetabolism is through the CRF 2 receptor.…”

Section: Discussionsupporting

confidence: 93%

“…Conversely to what was observed with CRF R-1 blockade, both antisense ODN knockdown and receptor blockade of CRF R-2 effectively reduced burn-induced hypermetabolism. These results are similar to our previous report (Chance et al, 2006) in which biochemical lesion of CRF receptors using a saporin-CRF conjugate significantly reduced REE in burned rats and decreased expression of CRF R-2 mRNA. The biochemical results of the present experiment employing RIA and PCR appear to support the roles of a urocortin and CRF R-2 in mediating burn-induced hypermetabolism.…”

Section: Discussionsupporting

confidence: 92%

“…CRF R-2, however, exhibits a reasonable density in hypothalamic areas (Reul and Holsboer, 2002), including the arcuate nucleus (ARC), paraventricular nucleus (PVN), and ventromedial hypothalamus (VMH). In a previous study (Chance et al, 2006), we observed significantly reduced resting energy expenditure (REE) in burned rats following biochemical lesioning of hypothalamic CRF receptors by ivt injection of a saporin-CRF conjugate. Analysis of hypothalamic CRF receptor mRNA by PCR suggested that the concentration of CRF R-2 was decreased in burned rats treated with the saporin-CRF conjugate.…”

Section: Introductionmentioning

confidence: 90%

See 3 more Smart Citations

Mediation of burn-induced hypermetabolism by CRF receptor-2 activity

et al. 2007

Self Cite

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 90%

See 2 more Smart Citations

Mediation of burn-induced hypermetabolism by CRF receptor-2 activity

et al. 2007

Self Cite

View full text Add to dashboard Cite

“…More recent research confirmed disturbance of the hypothalamic–pituitary–adrenal axis in severely burned patients. Hypothalamic peptides and receptors of the corticotropin releasing factor family have been identified as putative mediators of severe burn-induced hypermetabolism [ 69 , 70 ]. Serum prolactin has been found to correlate with burn severity [ 29 ] and, further downstream, temporary adrenal insufficiency has been reported in the early stages of severe burn trauma [ 71 ], which was associated with higher mortality rates [ 72 ].…”

Section: Disturbance Of Hormonal Stress Responsementioning

confidence: 99%

Bench-to-bedside review: Burn-induced cerebral inflammation – a neglected entity?

et al. 2009

View full text Add to dashboard Cite

Severe burn injury remains a major burden on patients and healthcare systems. Following severe burns, the injured tissues mount a local inflammatory response aiming to restore homeostasis. With excessive burn load, the immune response becomes disproportionate and patients may develop an overshooting systemic inflammatory response, compromising multiple physiological barriers in the lung, kidney, liver, and brain. If the blood-brain barrier is breached, systemic inflammatory molecules and phagocytes readily enter the brain and activate sessile cells of the central nervous system. Copious amounts of reactive oxygen species, reactive nitrogen species, proteases, cytokines/chemokines, and complement proteins are being released by these inflammatory cells, resulting in additional neuronal damage and life-threatening cerebral edema. Despite the correlation between cerebral complications in severe burn victims with mortality, burn-induced neuroinflammation continues to fly under the radar as an underestimated entity in the critically ill burn patient. In this paper, we illustrate the molecular events leading to blood-brain barrier breakdown, with a focus on the subsequent neuroinflammatory changes leading to cerebral edema in patients with severe burns. IntroductionSevere burn injury remains a significant health issue for society and a life-threatening event for the victim. Each year, more than 1.2 million people in the United States alone suffer burn injuries [1]; some 100,000 of these patients are hospitalized, accounting for a total of 2 million hospital days [2]. Thermal injuries mainly affect patients younger than 50 years of age [3] and remain one of the leading causes of childhood deaths, according to the Children's Burn Awareness Program. While the overall mortality has been reported to be 5%, it rapidly increases with advancing age and burn size up to 96% [3]. Most fatalities (65%) seem to be linked to burn-induced multiple organ failure, and 93% of burn patients present with clinical signs of the systemic inflammatory response syndrome before succumbing to their injuries [4].One of the critically impaired yet frequently overlooked organs in severe burn victims is the brain, despite the fact that cerebral complications in severe burn victims have been shown to highly correlate with mortality [5]. Hypoxic brain injury has been found as a primary cause of death in up to 10% of severe burn patients in an age-dependent manner [6]. The present review focuses on the neuroinflammatory changes occurring after severe burn injury and on the molecular mechanisms involved in their pathogenesis. Breakdown of the blood-brain barrier and development of cerebral edemaUnder physiological conditions, the blood-brain barrier (BBB) tightly regulates the molecules that enter the brain tissue. During the systemic inflammatory response syndrome, sepsis, or severe burn injury, however, this physical barrier between the systemic circulation and the cerebral parenchyma can be seriously compromised.When peripheral tissues are ex...

show abstract

Early Manipulation of Metabolic Changes due to Severe Burns in Children

Norbury

Jeschke

Herndon

Intensive Care Medicine

View full text Add to dashboard Cite

Possible role of CRF peptides in burn-induced hypermetabolism

Cited by 11 publications

References 40 publications

Mediation of burn-induced hypermetabolism by CRF receptor-2 activity

Mediation of burn-induced hypermetabolism by CRF receptor-2 activity

Bench-to-bedside review: Burn-induced cerebral inflammation – a neglected entity?

Early Manipulation of Metabolic Changes due to Severe Burns in Children

Contact Info

Product

Resources

About