Deleted form of hepatocyte growth factor ameliorates the mortality rate of severe thermal injury in rats

Arisawa, Hirohiko; Yamashita, Yasushi; Ogawa, Hiromi; Masunaga, Hiroaki; Higashio, Kanji

doi:10.1016/s0039-6060(99)70034-6

Cited by 6 publications

(5 citation statements)

References 32 publications

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“…However, most research into the metabolic consequences of a burn injury has been focused toward severe burns, ,− with a only small proportion examining changes in nonsevere burns. ,, In addition, as the incidence of a nonsevere injury is much greater than that of a severe, it is vital to understand how a less-severe injury impacts the systemic metabolic response, and the long-term health consequences of such injury events.…”

Section: Introductionmentioning

confidence: 99%

“…16 Perturbations in circulating lipoproteins, macro-molecular lipid−protein complexes, have also been reported following a burn injury. High-density lipoproteins (HDLs) were reported to be decreased during acute (total serum HDLs) 17 and severe burn injuries, 18 whereas levels of very-low-density lipoproteins (VLDL) and low-density lipoproteins (LDL) were found at higher concentrations in pediatric nonsevere 19 and adult severe burns. 20 The changes identified in lipids and lipoproteins are indicative of burn-induced hypocholesterolemia, hypophospholipidemia and hypertriglyceridemia, which have been associated with morbidity and mortality following a severe burn injury.…”

Section: ■ Introductionmentioning

confidence: 99%

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Nonsevere Burn Induces a Prolonged Systemic Metabolic Phenotype Indicative of a Persistent Inflammatory Response Postinjury

Ryan,

Raby,

Whiley

et al. 2023

J. Proteome Res.

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Globally, burns are a significant cause of injury that can cause substantial acute trauma as well as lead to increased incidence of chronic comorbidity and disease. To date, research has primarily focused on the systemic response to severe injury, with little in the literature reported on the impact of nonsevere injuries (<15% total burn surface area; TBSA). To elucidate the metabolic consequences of a nonsevere burn injury, longitudinal plasma was collected from adults (n = 35) who presented at hospital with a nonsevere burn injury at admission, and at 6 week follow up. A cross-sectional baseline sample was also collected from nonburn control participants (n = 14). Samples underwent multiplatform metabolic phenotyping using 1 H nuclear magnetic resonance spectroscopy and liquid chromatographymass spectrometry to quantify 112 lipoprotein and glycoprotein signatures and 852 lipid species from across 20 subclasses. Multivariate data modeling (orthogonal projections to latent structures-discriminate analysis; OPLS-DA) revealed alterations in lipoprotein and lipid metabolism when comparing the baseline control to hospital admission samples, with the phenotypic signature found to be sustained at follow up. Univariate (Mann−Whitney U) testing and OPLS-DA indicated specific increases in GlycB (p-value < 1.0e −4 ), low density lipoprotein-2 subfractions (variable importance in projection score; VIP > 6.83e −1 ) and monoacyglyceride (20:4) (p-value < 1.0e −4 ) and decreases in circulating anti-inflammatory high-density lipoprotein-4 subfractions (VIP > 7.75e −1 ), phosphatidylcholines, phosphatidylglycerols, phosphatidylinositols, and phosphatidylserines. The results indicate a persistent systemic metabolic phenotype that occurs even in cases of a nonsevere burn injury. The phenotype is indicative of an acute inflammatory profile that continues to be sustained postinjury, suggesting an impact on systems health beyond the site of injury. The phenotypes contained metabolic signatures consistent with chronic inflammatory states reported to have an elevated incidence postburn injury. Such phenotypic signatures may provide patient stratification opportunities, to identify individual responses to injury, personalize intervention strategies, and improve acute care, reducing the risk of chronic comorbidity.

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Section: Introductionmentioning

confidence: 99%

Section: ■ Introductionmentioning

confidence: 99%

Nonsevere Burn Induces a Prolonged Systemic Metabolic Phenotype Indicative of a Persistent Inflammatory Response Postinjury

Ryan,

Raby,

Whiley

et al. 2023

J. Proteome Res.

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“…Perturbations in lipoproteins have also been reported to be perturbed following burn injury. Highdensity lipoproteins (HDLs) that have known benefits to cardiovascular health were found to be decreased during acute (total serum HDLs) 19 and severe burn injuries 20 , whereas levels of potentially atherogenic very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL) were found at higher concentrations in paediatric non-severe and adult severe burns 21 . The changes identified in lipids and lipoproteins may reflect burn-induced hypocholesterolemia, hypophospholipidemia and hypertriglyceridemia, which have been associated with morbidity and mortality following a severe burn injury 22 .…”

Section: Introductionmentioning

confidence: 99%

“…With this knowledge, there is potential to develop metabolic biomarkers predictive in the early stages of long-term complications and to select targets for therapeutic intervention 23 . Most research into metabolic consequences of burns has been targeted towards severe burns 20,[24][25][26][27][28][29][30][31] , with a small proportion examining changes in non-severe burns 8,19,32 . As the incidence of non-severe injury is much greater than severe, it is important to understand how the metabolic perturbations differ between these groups so that therapeutic interventions can be appropriately targeted across the spectrum of injury.…”

Section: Introductionmentioning

confidence: 99%

Non-severe burns induce a prolonged systemic metabolic phenotype indicative of a persistent inflammatory response post-injury

Ryan

Raby

Masuda

et al. 2023

Preprint

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To understand the metabolic consequences following non-severe burns, longitudinal plasma was collected from adults with non-severe burn injuries (n=35) within 48 hours of admission to hospital and at 6 weeks post-surgery, as well as non-burn controls (n=14). Samples were analysed by 1H nuclear magnetic resonance spectroscopy and liquid chromatography-tandem mass spectrometry to quantify 112 lipoprotein, supramolecular phospholipid composite (SPC), GlycB arising from the glycoprotein N-acetylneuraminidino groups and 852 lipid species across 20 chemical subclasses. Alterations in lipoprotein and lipid metabolism were evident in samples taken within 48 hours of admission and found to be sustained at the 6-week timepoint, with increases in GlycB signal (p-value < 0.0001) and the multivariate importance of the apolipoprotein B100/apolipoprotein A1 (ABA1) ratio, as well as decreases in anti-inflammatory phosphatidylcholines, phosphatidylglycerols, phosphatidylinositols and phosphatidylserines. Low circulating high density lipoproteins, and increases in pro-atherogenic low density lipoproteins and monoacylglyceride (20:4) (p-value < 0.0001) are potentially indicative of an increased risk of cardiovascular disease after non-severe burns which requires further investigation.

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“…This deleted variant of HGF (dHGF) differs from the native in its physicochemical and immunological properties, and is more potent in stimulating DNA synthesis for hepatocytes (13). Furthermore, exogenous dHGF enhances not only hepatocyte mitosis but also liver functions such as albumin synthesis and lipogenesis (14,15). Because of these effects, dHGF treatment accelerates hepatic regeneration in 70% hepatectomized rats (16), and prevents liver injuries induced by carbon tetrachloride, dimethylnitrosamine, or D‐galactosamine (17).…”

mentioning

confidence: 99%

Reduction of monocrotaline‐induced hepatic injury by deleted variant of hepatocyte growth factor (dHGF) in rats

Yamashita

Fujise

Imai

et al. 2002

Liver

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Deleted form of hepatocyte growth factor ameliorates the mortality rate of severe thermal injury in rats

Cited by 6 publications

References 32 publications

Nonsevere Burn Induces a Prolonged Systemic Metabolic Phenotype Indicative of a Persistent Inflammatory Response Postinjury

Nonsevere Burn Induces a Prolonged Systemic Metabolic Phenotype Indicative of a Persistent Inflammatory Response Postinjury

Non-severe burns induce a prolonged systemic metabolic phenotype indicative of a persistent inflammatory response post-injury

Reduction of monocrotaline‐induced hepatic injury by deleted variant of hepatocyte growth factor (dHGF) in rats

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