Regular ArticleSynthesis and Regulation of Apolipoprotein E during the Differentiation of Human Neuronal Precursor NT2/D1 Cells into Postmitotic Neurons
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Aβ-independent roles of apolipoprotein E4 in the pathogenesis of Alzheimer's disease
2010, Trends in Molecular MedicineCitation Excerpt :In EGFPAPOE reporter mice, in which a cDNA encoding EGFP (enhanced green fluorescent protein) is inserted into the mouse ApoE gene locus immediately following the translation initiation site, CNS neurons express EGFP (representing APOE) in response to excitotoxic injury [47]. APOE is also expressed in primary cultures of human CNS neurons [44] and in many human neuronal cell lines, including SY-5Y, Kelly and NT2 cells [85,86]. Thus, the neuronal expression of APOE is turned on or upregulated in response to stress or injury both in vitro and in vivo.
Deficiency of the housekeeping gene hypoxanthine-guanine phosphoribosyltransferase (HPRT) dysregulates neurogenesis
2010, Molecular TherapyCitation Excerpt :Our present results not only lend the first experimental support to the hypothesis that aberrant development of DA neurons per se may contribute significantly to the pathology of HPRT deficiency in the human, but, even more importantly, we propose that they suggest that a “housekeeping gene” such as HPRT, conventionally considered merely to have important metabolic functions, may also play a vital role in some pathways of mammalian development, including neurogenesis. The human embryonic carcinoma NT2 neuronal differentiation system is a well-established model for studying molecular events during neurogenesis,13,16,17,18 and the model has provided an opportunity in the present study to determine the effect of HPRT expression on in vitro generation and differentiation of DA neurons and other neural cells. Our results demonstrate that HPRT plays a role in the expression of a number of transcription factors known to be necessary or sufficient for the normal development and function of DA neurons.
Pin1 allows for differential Tau dephosphorylation in neuronal cells
2006, Molecular and Cellular NeuroscienceBrain-specific change in alternative splicing of Tau exon 6 in myotonic dystrophy type 1
2006, Biochimica et Biophysica Acta - Molecular Basis of DiseaseApolipoprotein E4 domain interaction occurs in living neuronal cells as determined by fluorescence resonance energy transfer
2004, Journal of Biological ChemistryCitation Excerpt :ApoE4 domain interaction occurs on lipoprotein particles in vitro in human plasma (35, 36) and in vivo in Arg-61 knock-in mice (37), in which domain interaction was introduced into mouse apoE by mutating Thr-61 to Arg. Although it was initially believed that apoE was primarily synthesized by astrocytes in the brain but not by neurons (38), numerous subsequent studies (39–54) have demonstrated that central nervous system neurons also express apoE, albeit at lower levels than astrocytes, under diverse physiological and pathological conditions. Notably, transgenic mice expressing apoE4 specifically in central nervous system neurons are more susceptible to age-induced and excitotoxin-induced neurode-generation (55–57) and behavioral deficits (55, 58) than transgenic mice with similar expression of apoE3.
Astroglial regulation of apolipoprotein E expression in neuronal cells: Implications for Alzheimer's disease
2004, Journal of Biological ChemistryCitation Excerpt :Although our current study does not directly address the mechanisms by which the astrocyte-derived factor or factors regulate the transcription of APOE, we speculate that the factor or factors may trigger a signal pathway, such as the Erk pathway, that leads to activation of certain tissue-specific cis-acting regulatory elements of APOE that might be modified by APOE promoter polymorphisms. Based on the current and previous studies (32-39, 41-47), we hypothesize that acute injury, such as head trauma, or chronic injury, such as damage related to amyloid β deposition or oxidative stress, of the CNS causes astroglial proliferation and activation (astrocytosis), leading to secretion of a factor or factors that activate the Erk pathway and induce neuronal expression of apoE (Fig. 7). Neuronal expression of apoE in response to brain injury probably promotes neuronal repair and remodeling and protects neurons from injury (42, 132-134).
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