[2 cases of congenital adrenal hyperplasia].
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Biomedical subjects
Publications and source records attributed to T Koike.
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In order to clarify the function of P210 bcr/abl oncogene in leukemogenesis, IL-3 dependent murine hematopietic cell line, FDC-P2, was transfected with the plasmid containing cDNA of P210 bcr/abl oncogene (pGD'210) or murine IL-3 (pcDmIL3) by electroporation. Four out of five pGDH210 transfected clones as well as FDC-P2 transfected with pcDmIL3, acquired autonomous proliferation (i.e. lost the requirement for IL-3 supplementation). The expression of bcr/abl oncogene was weak in one clone, which remained dependent on IL-3. Unlike pcDmIL3 transfectants, which secrete IL-3 into the supernatant, IL-3 was not demonstrated in the culture supernatant of pGD'210 transfected FDC-P2. These finding suggest that P210 bcr/abl oncogene is directly associated with autonomous proliferation, which is the first process of leukemogenesis.
Cerebellar granule cells isolated from 7-d-old rats have been shown to die in vitro unless they are continuously exposed to elevated K+ (25 mM). Here we have characterized this neuronal death, and examined whether its major features are shared with those of sympathetic neurons following nerve growth factor (NGF) deprivation. Granule cells underwent active cell death accompanied by morphological features of apoptosis. Brain-derived neurotrophic factor (BDNF), but not NGF, was capable of preventing this neuronal death by acting posttranslationally. Moreover, semiquantitative RT-PCR, Northern blot, and immunoblot analyses showed that trkB, the signal-transducing receptor for BDNF, was upregulated during neuronal death of granule cells in vitro. These results extend recent findings for the role of BDNF in granule cell development, and suggest that BDNF plays a pivotal role on the regulation of the neuronal death/survival of granule cells.