Abstract
CD4(+) T cells play a crucial role in the pathogenesis of acquired aplastic anemia (AA). Tcf-1 gene regulates T cell development and function, and it is significantly upregulated in the bone marrow CD4(+) T cells from patients with acquired AA. To explore the role of Tcf-1 in the pathogenesis of AA, we knocked down Tcf-1 gene in CD4(+) T cells of AA patients and studied the effects of Tcf-1 silencing on its downstream gene expression. Upon transfection of psiRNA into marrow CD4(+) T cells from bone marrow of aplastic anemia patients, the expression of Tcf-1 was significantly knocked down; consequently, expressions of c-Myc and CD44 were also significantly reduced. Our results suggest that Tcf-1 may contribute to pathogenesis of AA by regulating downstream gene expression such as c-myc and CD44.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Adult
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Anemia, Aplastic / physiopathology*
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Bone Marrow Cells / cytology
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Bone Marrow Cells / physiology*
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CD4-Positive T-Lymphocytes / cytology
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CD4-Positive T-Lymphocytes / physiology*
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Cell Separation
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Cells, Cultured
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Female
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Gene Expression*
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Gene Silencing
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Humans
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Hyaluronan Receptors / genetics
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Hyaluronan Receptors / metabolism
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Male
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Middle Aged
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Proto-Oncogene Proteins c-myc / genetics
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Proto-Oncogene Proteins c-myc / metabolism
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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T Cell Transcription Factor 1 / genetics*
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T Cell Transcription Factor 1 / metabolism*
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Young Adult
Substances
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CD44 protein, human
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Hyaluronan Receptors
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MYC protein, human
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Proto-Oncogene Proteins c-myc
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RNA, Messenger
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T Cell Transcription Factor 1
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TCF7 protein, human