Expression of TGFβ2 but Not TGFβ1 Correlates with the Deposition of Scar Tissue in the Lesioned Spinal Cord

Lagord, Catherine; Berry, Martin; Logan, Ann

doi:10.1006/mcne.2002.1121

Cited by 119 publications

(108 citation statements)

References 50 publications

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“…This expression pattern is in line with experimental studies revealing an early and maintained increase of TGF-b at the mRNA and protein levels following experimental crush and contusion injuries of the adult rat spinal cord. 8,10,19 Furthermore, the cell types demonstrating TGF-b1 immunoreactivity following human SCI (that is, macrophages, some astrocytes and neurons) also show a striking similarity to what has already been identified at the mRNA levels in experimental animals. 8,10,19 In the postmortem human SCI samples TGF-b1 expression remained elevated for up to 10 months; however, the longest time point of TGF-b1 elevation demonstrated in experimental animals was 54 days after injury.…”

Section: Discussionsupporting

confidence: 56%

“…8,10,19 Furthermore, the cell types demonstrating TGF-b1 immunoreactivity following human SCI (that is, macrophages, some astrocytes and neurons) also show a striking similarity to what has already been identified at the mRNA levels in experimental animals. 8,10,19 In the postmortem human SCI samples TGF-b1 expression remained elevated for up to 10 months; however, the longest time point of TGF-b1 elevation demonstrated in experimental animals was 54 days after injury. 8 Therefore, the early and prolonged upregulation of TGF-b1 after experimental SCI appears to correlate with the events that take place following humans SCI.…”

Section: Discussionsupporting

confidence: 56%

“…9 This distribution pattern is similar to that obtained using experimental animals, where TGF-b1 and TGF-b2 could be found in neurons and astrocytes of the adult rodent spinal cord. 8,13 The function of both cytokines in the normal CNS is presently not clear. In vitro and in vivo studies have demonstrated a neuroprotective and growth promoting effect of TGF-b on a number of neuronal populations 14,15 as well as both growth-inhibitory and growth-promoting effects on astrocytes (depending on their phenotype when exposed to the TGF-b 16 ).…”

Section: Discussionmentioning

confidence: 99%

“…4,5 In a number of CNS pathologies of experimental animals and humans (including inflammatory disorders, degenerative diseases and traumatic injuries) TGF-b1 and TGF-b2 are rapidly and abundantly expressed. [6][7][8][9] In experimental SCI, TGF-b isoforms were shown not only to be involved in the early inflammatory response but also to play a central role in the formation of the scar at the lesion site. 8,10 However, the extent to which experimental SCI induced changes of TGF-b expression reflect the events taking place following human SCI remains unknown.…”

Section: Introductionmentioning

confidence: 99%

“…[6][7][8][9] In experimental SCI, TGF-b isoforms were shown not only to be involved in the early inflammatory response but also to play a central role in the formation of the scar at the lesion site. 8,10 However, the extent to which experimental SCI induced changes of TGF-b expression reflect the events taking place following human SCI remains unknown. Thus, the present investigation was undertaken to determine the spatio-temporal pattern of TGF-b1 and TGF-b2 expression in samples of postmortem human spinal cord, taken from patients who died at a range of survival times following severe traumatic SCI.…”

Section: Introductionmentioning

confidence: 99%

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TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

et al. 2007

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Study design: Immunohistochemical investigation in control and lesioned human spinal cords. Objectives: To assess the spatial and temporal expression patterns of transforming growth factor-b1 and -b2 (TGF-b1 and TGF-b2) in the human spinal cord after traumatic injury. Setting: Germany, Aachen, Aachen University Hospital. Methods: Sections from human spinal cords from 4 control patients and from 14 patients who died at different time points after traumatic spinal cord injury (SCI) were investigated immunohistochemically. Results: In control cases, TGF-b1 was confined to occasional blood vessels, intravascular monocytes and some motoneurons, whereas TGF-b2 was only found in intravascular monocytes. After traumatic SCI, TGF-b1 immunoreactivity was dramatically upregulated by 2 days after injury (the earliest survival time investigated) and was detected within neurons, astrocytes and invading macrophages. The staining was most intense over the first weeks after injury but gradually declined by 1 year. TGF-b2 immunoreactivity was first detected 24 days after injury. It was located in macrophages and astrocytes and remained elevated for up to 1 year. In white matter tracts undergoing Wallerian degeneration, there was no induction of either isoform. Conclusion: The early induction of TGF-b1 at the point of SCI suggests a role in the acute inflammatory response and formation of the glial scar, while the later induction of TGF-b2 may indicate a role in the maintenance of the scar. Neither of these TGF-b isoforms appears to contribute to the astrocytic scar formation in nerve fibre tracts undergoing Wallerian degeneration.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

et al. 2007

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Myelin‐associated glycoprotein alters the neuronal secretome and stimulates the release of TGFβ and proteins that affect neural plasticity

et al. 2022

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Myelin‐associated glycoprotein (MAG) and Nogo inhibit neurite outgrowth by binding to receptors such as NgR1, PirB and LRP1, and they have also been shown to induce phosphorylation of Smad2, a key intermediate in the transforming growth factor β (TGFβ) signalling pathway. In this study, we determined that MAG and Nogo do not transactivate the TGFβ receptor through their canonical receptors or discoidin domain receptor 1, which we identified as a novel receptor for MAG and Nogo. Instead, MAG and Nogo promoted Smad2 phosphorylation by stimulating secretion of TGFβ. Proteomic analysis of the neuronal secretome revealed that MAG also regulated the secretion of proteins that affect central nervous system plasticity—inducing the secretion of S100A6, septin‐7 and neurofascin 186, while inhibiting the secretion of frataxin, MAP6, syntenin‐1 and GAP‐43. This represents a novel function for MAG that has broad implications for the treatment for spinal cord injury.

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The microanatomy of spinal cord injury: A review

et al. 2014

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Spinal cord injury is a highly prevalent condition associated with significant morbidity and mortality. The pathophysiology underlying it is extraordinarily complex and still not completely understood. We performed a comprehensive literature review of the pathophysiologic processes underlying spinal cord injury. The mechanisms underlying primary and secondary spinal cord injury are distinguished based on a number of factors and include the initial mechanical injury force, the vascular supply of the spinal cord which is associated with spinal cord perfusion, spinal cord autoregulation, and post-traumatic ischemia, and a complex inflammatory cascade involving local and infiltrating immunomodulating cells. This review illustrates the current literature regarding the pathophysiology behind spinal cord injury and outlines potential therapeutic options for reversing these mechanisms.

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Expression of TGFβ2 but Not TGFβ1 Correlates with the Deposition of Scar Tissue in the Lesioned Spinal Cord

Cited by 119 publications

References 50 publications

TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

TGF-β1 and TGF-β2 expression after traumatic human spinal cord injury

Myelin‐associated glycoprotein alters the neuronal secretome and stimulates the release of TGFβ and proteins that affect neural plasticity

The microanatomy of spinal cord injury: A review

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