Impact of Burn Injury on Hepatic TGF-??1 Expression and Plasma TGF-??1 Levels

Nishimura, Tetsuro; Nishiura, Teruhiro; deSerres, Suzan; Nakagawa, Takao; Brenner, David A.; Meyer, Anthony A.

doi:10.1097/00005373-200001000-00007

Cited by 15 publications

(9 citation statements)

References 37 publications

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“…Transforming growth factor beta is a multifunctional cytokine with a role in wound repair (Nishimura et al, 2000). It has been observed that receptor expression is increased in epidermis adjacent to a healing wound from Day 2 and decreased from Day 14 (Gold et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

A Study of Burns for Wound Ageing reveals Changes in Unburnt Skin with Implications for Future Research

2005

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Thirty-three punch biopsy sets of burn wound edge and adjacent unburnt skin from burn wounds aged six hours to 23 days were obtained from 18 patients. Immunohistochemical staining was performed for transforming growth factor beta receptor, epidermal growth factor receptor and MIB-1 (which stains the cell cycle associated antigen ki-67) in addition to integrins alpha V, 5 and 3 to assess for temporal patterns that might assist in the ageing of burn wounds. There was an early (12hr-4day) rise in integrin alpha V expression, an increasing expression of transforming growth factor beta receptor from 12 hours onwards, and increased expression of MIB-1 commencing at 2 days. In biopsy samples from the edge of the burn there was a trend for an early (6 hr-4 day) rise in epidermal growth factor receptor expression. There were no discernable changes in integrin alpha 5 or 3. The striking feature was that biopsy samples from the adjacent, unburnt skin showed similar temporal staining patterns. A further study would be required to determine if the effect was generalised or local, but the observation of changes in unburnt tissue implies that careful consideration must be given to selecting control tissue.

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Section: Discussionmentioning

confidence: 99%

A Study of Burns for Wound Ageing reveals Changes in Unburnt Skin with Implications for Future Research

2005

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“…Under the conditions of severe burn injury and sepsis, impaired insulin function could affect liver GCL expression, as has been demonstrated in type II diabetes condition. The signals involve Phosphoinositide 3-kinase/Protein Kinase B/ p70S6 kinase (PI3K/Akt/p70S6K) pathway[ 38 , 39 ] the induced transforming growth factor (TGF)-β1 after burn injury[ 40 ] may also inhibit the transcriptional activity of GCL subunit. Furthermore, GCL subunit can be cleaved by a caspase 3-dependent mechanism under increased apoptosis, which is seen after burn injury[ 41 ] Based on the results of the present study, further mechanistic studies will be directed toward the investigations on the molecular basis for reduced GSH synthesis in the g-glutamyl cycle pathways under the burn injury-induced severe inflammatory state.…”

Section: Discussionmentioning

confidence: 99%

Burn injury differentially alters whole-blood and organ glutathione synthesis rates: An experimental model

Fei

Young

et al. 2013

Burn Trauma

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Previous studies from our laboratories revealed a reduced rate of whole-blood (WB) glutathione (GSH) synthesis in severely burned patients. To determine whether WB GSH metabolism is an indicator of the status of GSH metabolism in one or more of the major organs, we used a burn rabbit model to determine GSH concentrations and rates of synthesis in WB, liver, lungs, kidney, and skeletal muscle. L-[1-13C]-cysteine was infused intravenously for 6 h in rabbits at 3 days post-burn and in sham burn controls. WB and organ 13C-enrichment of cysteine and GSH was determined by gas chromatography/mass spectrometry. Plasma cysteine metabolic flux was increased significantly (P < 0.01) following burn injury. WB, liver, and lung GSH concentrations (P = 0.054, P < 0.05, and P < 0.05, respectively) and fractional rates of GSH synthesis (P < 0.05, P < 0.01, and P < 0.05, respectively) were reduced at 3 days post-burn. Kidney was unaffected. There also appears to be an increased rate of GSH transport out of the liver after burn injury. Hence, there is a differential impact of burn injury on tissue and organ GSH status, with WB qualitatively reflecting the changes in lung and liver. It will be important to determine whether these changes are due to alterations in the intrinsic capacity for GSH synthesis and/or availability of amino acid precursors of GSH.

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“…It was concluded that thermal injury induced hepatic cell apoptosis and proliferation associated with an increase in hepatic NF-kappaB expression and a decrease in hepatic protein concentration. Two important studies investigated possible mediators of liver cells apoptosis [85,86]. The first study focused on transforming growth factor-beta1 (TGF-β1), induced after burn injury, and its contribution to an inhibitory or fatal effect on hepatocytes [85].…”

Section: Livermentioning

confidence: 99%

“…Two important studies investigated possible mediators of liver cells apoptosis [85,86]. The first study focused on transforming growth factor-beta1 (TGF-β1), induced after burn injury, and its contribution to an inhibitory or fatal effect on hepatocytes [85]. The plasma concentration of TGF-β in large ( > 50% total body surface area) burns was significantly increased at 4 h after injury when compared with no injury or medium (25-50% TBSA) burn groups.…”

Section: Livermentioning

confidence: 99%

“…This rise in plasma TGF-β1 was preceded by an increase in hepatic TGF-β1 m-RNA expression at 30 min, 1, 2, and 4 h after burn in the large group. Histologic analysis found greater hepatocyte death in the large burns group than in the medium burns group at 8 h after burn [85]. The second study was conducted by Li and colleague on in vitro cultured hepatocytes from normal guinea pigs.…”

Section: Livermentioning

confidence: 99%

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“Systemic apoptotic response” after thermal burns

Gravante

Delogu

Sconocchia³

2006

Apoptosis

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The systemic pathophysiologic changes following thermal injuries affect multiple organs and body systems leading to clinical manifestations including shock, intestinal alterations, respiratory and renal failure, immunosuppression and others. Recent advances in the comprehension of mechanisms underlying systemic complications of thermal injuries have contributed to uncover part of the cellular and molecular basis that underlie such changes. Recently, programmed cell death (apoptosis) has been considered playing an important role in the development of such pathological events. Therefore, investigators utilizing animal models and clinical studies involving human primates have produced a large body of information suggesting that apoptosis is associated with most of the tissue damages triggered by severe thermal injuries. In order to draw the attention on the important role of apoptosis on systemic complications of thermal injuries, in this review we describe most of these studies, discuss possible cellular and molecular mechanisms and indicate ways to utilize them for the development of therapeutic strategies by which apoptosis may be prevented or counteracted.

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Impact of Burn Injury on Hepatic TGF-??1 Expression and Plasma TGF-??1 Levels

Cited by 15 publications

References 37 publications

A Study of Burns for Wound Ageing reveals Changes in Unburnt Skin with Implications for Future Research

A Study of Burns for Wound Ageing reveals Changes in Unburnt Skin with Implications for Future Research

Burn injury differentially alters whole-blood and organ glutathione synthesis rates: An experimental model

“Systemic apoptotic response” after thermal burns

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