Biphasic transforming growth factor-β production flanking the pro-inflammatory cytokine response in cerebral trauma

Rimaniol, Anne-Cécile; Lekieffre, D.; Serrano, A.; Masson, Annie; Bénavidès, J.; Zavala, Flora

doi:10.1097/00001756-199512000-00032

Cited by 21 publications

(14 citation statements)

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“…wound healing. Although TGF-b expression was not examined in the present study, our finding of sequential CTGF 1 cell accumulation, similar to reported TGF-b 1 accumulation (Logan et al, 1992;Rimanol et al, 1995) suggests an analogous cascade during CNS wound healing. This is supported by the fact, that unlike many tissues, the normal adult CNS does contain only rare amounts of the TGF-b 1 isoform, which is selectively upregulated in astrocytes contributing to scar formation after injury (Logan and Berry, 1993).…”

Section: Differential Cellular Accumulation Of Ctgfsupporting

confidence: 88%

Differential Cellular Accumulation of Connective Tissue Growth Factor Defines a Subset of Reactive Astrocytes, Invading Fibroblasts, and Endothelial Cells Following Central Nervous System Injury in Rats and Humans

Schwab¹,

Beschorner²,

Nguyen³

et al. 2001

Journal of Neurotrauma

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In brain injury, the primary trauma is followed by a cascade of cellular and molecular mechanisms resulting in secondary injury and scar formation. Astrogliosis and expression of transforming growth factor beta (TGF-beta) are key components of scar formation. A cytokine mediating the effects of TGF-beta is connective tissue growth factor (CTGF), a fibrogenic peptide encoded by an immediate early gene with suggested roles in tissue regeneration and aberrant deposition of extracellular matrix. In order to investigate CTGF in traumatic lesions, we evaluated 20 human brains with traumatic brain injury (TBI) and 18 rat brains with stab wound injury. Compared to remote areas and unaltered control brains, CTGF+ cells accumulated in border zones of the traumatic lesion site (p < 0.0001). In the direct peri-lesional rim, CTGF expression was confined to invading vimentin+, GFAP- fibroblastoid cells, endothelial and smooth muscle cells of laminin+ vessels, and GFAP+ reactive astrocytes. In the direct peri-lesional rim, CTGF+ astrocytes (>80%) co-expressed the activation associated intermediate filaments nestin and vimentin. In injured rat brains, numbers of CTGF+ cells peaked at day 3 and 7 and decreased to almost base level 3 weeks postinjury, whereas in humans, CTGF+ cells remained persistently elevated up to 6 months (p < 0.0001). The restricted accumulation of CTGF+-reactive astrocytes and CTGF+ fibroblastoid cells lining the adjacent laminin+ basal lamina suggests participation of these cells in scar formation. Furthermore, peri-lesional upregulation of endothelial CTGF expression points to a role in blood-brain barrier function and angiogenesis. In addition, CTGF appears to be a sensitive marker of early astrocyte activation.

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Section: Differential Cellular Accumulation Of Ctgfsupporting

confidence: 88%

Differential Cellular Accumulation of Connective Tissue Growth Factor Defines a Subset of Reactive Astrocytes, Invading Fibroblasts, and Endothelial Cells Following Central Nervous System Injury in Rats and Humans

Schwab¹,

Beschorner²,

Nguyen³

et al. 2001

Journal of Neurotrauma

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“…The mechanisms that regulate many of these changes remain to be established and an improved understanding can lead to strategies to halt the tissue destruction that occurs after brain trauma. Increasingly, it has become apparent that significant amounts of inflammatory cytokines are produced within the injured CNS, even that following an acute non-immune trauma to this tissue (Woodroofe et al, 1991;Minami et al, 1992;Taupin et al, 1993;Rimaniol et al, 1995;Rostworowski et al, 1997). The production of inflammatory cytokines occurs promptly, with levels of transcripts encoding IL-1␤ being elevated by 15 min of corticectomy injury (Herx et al, unpublished data), and prominent by 3 hr (Rostworowski et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Traumatic injury to the CNS results in the production of inflammatory cytokines via both intrinsic (by microglia, astrocytes, and even neurons) and extrinsic means (by infiltrating macrophages, lymphocytes, and other leukocytes) (Woodroofe et al, 1991;Taupin et al, 1993;Rimaniol et al, 1995). We have found an increase in interleukin (IL)-1 transcripts by 3 hr, the earliest period studied, after CNS trauma to adult mice (Rostworowski et al, 1997).…”

mentioning

confidence: 98%

Interleukin-1 is a key regulator of matrix metalloproteinase-9 expression in human neurons in culture and following mouse brain trauma in vivo

et al. 2000

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“…In animal models of TBI, a biphasic course of TGF-β production has been reported. An initial peak of TGF-β was seen at 30 min post-injury and a second peak at 48 hr time when pro-inflammatory cytokine signaling had resolved [49][55]. After the initial cytokine response and microglia and PMN activation, TBI results in increased circulating neutrophils as early as 3.5 hr after impact [50, 51].…”

Section: Discussionmentioning

confidence: 99%

Global assessment of oxidized free fatty acids in brain reveals an enzymatic predominance to oxidative signaling after trauma

Anthonymuthu

Kenny

Amoscato

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Traumatic brain injury (TBI) is a major health problem associated with significant morbidity and mortality. The pathophysiology of TBI is complex involving signaling through multiple cascades, including lipid peroxidation. Oxidized free fatty acids, a prominent product of lipid peroxidation, are potent cellular mediators involved in induction and resolution of inflammation and modulation of vasomotor tone. While previous studies have assessed lipid peroxidation after TBI, to our knowledge no studies have used a systematic approach to quantify the global oxidative changes in free fatty acids. In this study, we identified and quantified 244 free fatty acid oxidation products using a newly developed global liquid chromatography tandem-mass spectrometry (LC-MS/MS) method. This methodology was used to follow the time course of these lipid species in the contusional cortex of our pediatric rat model of TBI. We show that oxidation peaked at 1 hr after controlled cortical impact and was progressively attenuated at 4 and 24 hr time points. While enzymatic and non-enzymatic pathways were activated at 1 hr post-TBI, enzymatic lipid peroxidation was the predominant mechanism with 15-lipoxygenase (LOX) contributing to the majority of total oxidized fatty acid content. Pro-inflammatory lipid mediators were significantly increased at 1 and 4 hr after TBI with return to basal levels by 24 hr. Anti-inflammatory lipid mediators remained significantly increased across all three time points, indicating an elevated and sustained anti-inflammatory response following TBI.

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Biphasic transforming growth factor-β production flanking the pro-inflammatory cytokine response in cerebral trauma

Cited by 21 publications

References 0 publications

Differential Cellular Accumulation of Connective Tissue Growth Factor Defines a Subset of Reactive Astrocytes, Invading Fibroblasts, and Endothelial Cells Following Central Nervous System Injury in Rats and Humans

Differential Cellular Accumulation of Connective Tissue Growth Factor Defines a Subset of Reactive Astrocytes, Invading Fibroblasts, and Endothelial Cells Following Central Nervous System Injury in Rats and Humans

Interleukin-1 is a key regulator of matrix metalloproteinase-9 expression in human neurons in culture and following mouse brain trauma in vivo

Global assessment of oxidized free fatty acids in brain reveals an enzymatic predominance to oxidative signaling after trauma

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