Modulation of prion protein gene expression by growth factors in cultured mouse astrocytes and PC-12 cells

Lazarini, Françoise; Castelnau, Pierre; Chermann, Jean-François; Deslys, Jean‐Philippe; Dormont, Dominique

doi:10.1016/0169-328x(94)90055-8

Cited by 31 publications

(17 citation statements)

References 35 publications

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“…EGF has been shown to increase PrP gene expression in cultured mouse astrocytes (Lazarini et al, 1994). We have also demonstrated that EGF increases PrP C -related mRNA synthesis in the SC of Cbl-D rats and, together with Cbl, contributes to maintaining SC and CSF PrP C levels within the normal range (Scalabrino et al, 2012).…”

Section: Regulation Of Prp C -Related Mrnasmentioning

confidence: 91%

Relationships between cobalamin, epidermal growth factor, and normal prions in the myelin maintenance of central nervous system

Scalabrino

Veber

Tredici

2014

The International Journal of Biochemistry & Cell Biology

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Section: Regulation Of Prp C -Related Mrnasmentioning

confidence: 91%

Relationships between cobalamin, epidermal growth factor, and normal prions in the myelin maintenance of central nervous system

Scalabrino

Veber

Tredici

2014

The International Journal of Biochemistry & Cell Biology

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“…Nevertheless, several studies indicated that PrP c could contribute to several distinct processes, including lymphocyte activation, synaptic transmission, cell adhesion, signaling, and apoptosis (for review, see Linden et al, 2008). Other works also suggested that PrP c could be involved in the neuronal differentiation of PC12 cells triggered by either interleukin-6 or nerve growth factor, as shown by increased expression of PrP c mRNA levels (Lazarini et al, 1994). Consistent with a pivotal link between NGF and PrP c , PrP c mRNA expression was also increased after intracerebral injection of this growth factor in cholinergic neurons (Mobley et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

p53-Dependent Transcriptional Control of Cellular Prion by Presenilins

Vincent¹,

Sunyach²,

Orzechowski³

et al. 2009

J. Neurosci.

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The presenilin-dependent ␥-secretase processing of the ␤-amyloid precursor protein (␤APP) conditions the length of the amyloid ␤ peptides (A␤) that accumulate in the senile plaques of Alzheimer's disease-affected brains. This, together with an additional presenilinmediated -secretase cleavage, generates intracellular ␤APP-derived fragments named amyloid intracellular domains (AICDs) that regulate the transcription of several genes. We establish that presenilins control the transcription of cellular prion protein (PrP c ) by a ␥-secretase inhibitor-sensitive and AICD-mediated process. We demonstrate that AICD-dependent control of PrP c involves the tumor suppressor p53. Thus, p53-deficiency abolishes the AICD-mediated control of PrP c transcription. Furthermore, we show that p53 directly binds to the PrP c promoter and increases its transactivation. Overall, our study unravels a transcriptional regulation of PrP c by the oncogene p53 that is directly driven by presenilin-dependent formation of AICD. Furthermore, it adds support to previous reports linking secretase activities involved in ␤APP metabolism to the physiology of PrP c .

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“…19,20) Research indicates that PrP mRNA levels increase in response to neurotrophic factors, 21) cytokines, 22,23) and hormones. 18,24) Migration inhibitory factor-related protein (MRP8) fragment stimulates PrP C expression, and platelet derived growth factor has an opposite effect, acting as a suppressor in human fibroblasts.…”

mentioning

confidence: 99%