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Guanhua Yu

Publications and source records attributed to Guanhua Yu.

2 recordsLinked to original sources

Differential expression of nerve growth factor transcripts in glia and neurons and their regulation by transforming growth factor-beta1.

Nerve growth factor (NGF) influences neuronal development, function, and response to injury. Using reverse transcriptase polymerase chain reaction, we find that mouse and rat cortex and spinal cord, and both neurons and glia in culture, express NGF mRNA. In the mouse, NGF is regulated by at least two promoters that govern synthesis of four different transcripts, A through D, that are all expressed in the mouse tissues and cells examined. In contrast, rat NGF expression varies with tissue and with cell type: transcript C is expressed strongly in brain but weakly in spinal cord, and transcript D is undetectable in rat central nervous system (CNS). In addition to species- and tissue-specific expression, NGF transcripts also exhibit cell type-specific expression: transcripts B, C and D are expressed in rat astrocytes but poorly or not at all in rat neurons, identifying glia as an important source of NGF in rat. NGF increases sharply after injury. TGF-beta1, which also increases immediately after injury, induces NGF mRNA and protein in rat and mouse glia but not in neurons. Furthermore, transcripts A, B and D, but not C, are upregulated by TGF-beta1 in mouse glia, whereas in rat glia, the major responsive transcript is C. Thus, there may be multiple TGF-beta1-responsive elements in the NGF promoters located upstream of exons 1 and 3 that may differ between mouse and rat. Moreover, NGF transcripts are differentially expressed in a species-, cell type-, and inducer-specific manner. These results have implications for the use of mice versus rats as models for the study of NGF regulation following CNS injury.

Alternative Splicing↗

A new brain-derived neurotrophic factor transcript and decrease in brain-derived neurotrophic factor transcripts 1, 2 and 3 in Alzheimer's disease parietal cortex.

Brain-derived neurotrophic factor (BDNF) supports hippocampal, cortical and basal forebrain cholinergic neurons, which lose function in Alzheimer's disease. In Alzheimer's tissues such as hippocampus and parietal cortex, brain- derived neurotrophic factor mRNA is decreased three- to four-fold compared with controls. However, the molecular mechanism of the down-regulation of BDNF in Alzheimer's disease is unknown. The human brain-derived neurotrophic factor gene has multiple promoters governing six non-coding upstream exons that are spliced to one downstream coding exon, leading to six different transcripts. Here we report an alternate human splice variant within exon 4I for a total of seven transcripts. Previous brain-derived neurotrophic factor mRNA measurements in Alzheimer's disease tissue were done using the downstream coding exon present in all transcripts. Using RT-PCR primers specific for each upstream exon, we observe a significant decrease in three human brain-derived neurotrophic factor mRNA transcripts in Alzheimer's disease samples compared with controls. Transcripts 1 and 3 each exhibit a two-fold decrease, and transcript 2 shows a five-fold decrease. There are no significant differences between control and Alzheimer's disease samples for the other transcripts, including the new splice variant. In rat, both transcripts 1 and 3 are regulated through the transcription factor cAMP response element binding protein, whose phosphorylation is decreased in the Alzheimer's disease brain. This could lead to specific down-regulation of the brain-derived neurotrophic factor transcripts shown here.

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