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Biomedical subjects

A Fujimori

Publications and source records attributed to A Fujimori.

At least 145 records · Page 8Linked to original sources
PubMed1990

Release of calcitonin gene-related peptide (CGRP) from capsaicin-sensitive vasodilator nerves in the rat mesenteric artery.

The effect of perivascular nerve stimulation (PNS) and capsaicin treatment on the release of calcitonin gene-related peptide (CGRP) was examined by radioimmunoassay (RIA) in isolated, perfused rat mesenteric arteries. In the preparation precontracted by methoxamine and treated with guanethidine, an adrenergic neuron blocker, PNS and capsaicin induced vasodilator responses and increase of CGRP-like immunoreactivity (CGRP-LI) in the perfusate in a frequency-dependent manner. The CGRP-LI released by capsaicin was identified as CGRP and its oxidized form by high-performance liquid chromatography coupled with RIA. After the tissue was treated with capsaicin, PNS didn't cause both the vasodilator response and the increase of CGRP-LI in the perfusate. These findings suggest that CGRP plays a neurotransmitter role in capsaicin-sensitive vasodilator nerves in rat mesenteric arteries.

Animals↗
PubMed1990

Evidence for spontaneous conversion of Mex- to Mex+ in human lymphoblastoid cells.

A series of human lymphoblastoid cell lines (LCLs) called Mex- were defined by Sklar and Strauss on the basis of their inability to remove O6-methylguanine from DNA. Instability of Mex- has previously been shown as a population phenotype of LCLs. We examined whether Mex- as a cellular phenotype is spontaneously convertible or not. At the population doubling number (PDN) 23 after recloning, two out of 15 independent subcultures derived from a Mex- LCL, AT1-1, were found to contain a small fraction of Mex+ cells after treatment with 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU). Three Mex+ subclones were identified without exposure to ACNU among 486 subclones from replica plating of an expanded Mex- clone (PDN30). The rate of spontaneous conversion was estimated to be in the range of 10(-8)-10(-7) per cell per generation by the fluctuation analyses on two Mex- subclones. These results strongly support the hypothesis that Mex- as a cellular phenotype is spontaneously convertible to Mex+.

Cell Line↗
PubMed1990

Nongenomic activation of the calcium message system by vitamin D metabolites in osteoblast-like cells.

1,25-dihydroxycholecalciferol (1,25(OH)2D3) rapidly affects calcium (Ca2+) transport in several cell systems, suggesting physiological actions independent of genomic activation. To test this hypothesis, we studied immediate to early effects (0.5-300 sec) of 1,25(OH)2D3 on cytosolic Ca2+ [Ca2+]i in single osteogenic sarcoma ROS 17/2.8 cells loaded with fura-2. An acute rise in [Ca2+]i was observed in 40% of the cells following addition of 1,25(OH)2D3, with a threshold concentration of 10(-11) M. In most cases, the [Ca2+]i rise was transient, with return to baseline within 1 min; less frequently a more prolonged effect was observed, with variable recovery times. 25-hydroxycholecalciferol (25(OH)D3) reproduced the effect of 1,25(OH)2D3 on [Ca2+]i, with equal potency and similar responses, whereas 24,25-dihydroxycholecalciferol, 1 alpha-hydroxycholecalciferol, and 22 oxa-1,25(OH)2D3 were not effective. 1,25(OH)2D3 also increased [Ca2+]i in ROS 24/1 cells, which are defective of receptors for the vitamin D metabolites. At high doses (10(-8)-10(-7) M) of 1,25(OH)2D3 the [Ca2+]i rise in ROS 17/2.8 cells was due to both influx of extracellular Ca2+ and release of Ca2+ from intracellular stores, as the effect was only partially inhibited by Ca2(+)-channel blockade by nifedipine. At low doses (10(-9)-10(-10) M), the effect was entirely dependent on extracellular Ca2+. 1,25(OH)2D3 also increased the production of inositol 1,4,5 trisphosphate (Ins(1, 4, 5)P3) and diacylglycerol, at a threshold dose of 10(-9) M, indicating activation of phospholipase C (PLC). In two thirds of the cells studied, a second addition of 1,25(OH)2D3 within 5 min to cells prestimulated with equimolar doses of the vitamin D metabolite resulted in a [Ca2+]i transient of higher amplitude than the first, a phenomenon occurring at all doses of the hormone, and associated with production of Ins(1, 4, 5)P3. This response amplification was not produced by 25(OH)D3, and pretreatment with 1 alpha(OH)D3 did not significantly enhance 1,25(OH)2D3-induced production of Ins(1, 4, 5)P3. In conclusion, activation of the Ca2+ message system by vitamin D metabolites is a rapid, nongenomic effect; 1,25(OH)2D3 specifically activates both PLC and dihydropyridine-sensitive Ca2+ channels, and "primes" the cells to respond with an enhanced [Ca2+]i rise to a subsequent homologous stimulation; the presence of both the 1 alpha and 25 hydroxyl groups is necessary to express the full hormonal action of vitamin D on [Ca2+]i.

Animals↗
PubMed1989

Neurogenic vasodilation and release of calcitonin gene-related peptide (CGRP) from perivascular nerves in the rat mesenteric artery.

The effect of perivascular nerve stimulation (PNS) on the release of calcitonin gene-related peptide (CGRP) was examined by radioimmunoassay (RIA) in isolated, perfused rat mesenteric arteries. The released CGRP-like immunoreactivity (CGRP-LI) was identified to be CGRP itself and its oxidized form by combined analysis with RIA and high performance liquid chromatography. CGRP-LI was localized in the perivascular nerves of the large mesenteric artery and its branches. In the preparation precontracted by methoxamine, and perfused with a solution containing guanethidine, an adrenergic neuron blocker, PNS induced vasodilator responses and an increase of CGRP-LI in the perfusate in a frequency-dependent manner. Both the responses were attenuated by tetrodotoxin (10(-6) M), suggesting that they were neurogenic in origin. Removal of Ca2+ from the perfusing solution also abolished the PNS-induced release of CGRP-LI. These findings suggest that CGRP plays a transmitter role in the neurogenic vasodilation in the rat mesenteric vascular bed.

Animals↗
PubMed1989

Cyclooxygenase inhibitors enhance cell growth in an osteoblastic cell line, MC3T3-E1.

To elucidate the significance of endogenous prostaglandin E2 (PGE2) in osteoblastic cell function, we studied the effects of cyclooxygenase inhibitors on cell growth and alkaline phosphatase (ALP) activity in MC3T3-E1 cells. UMR-106 cells were also used as references in our experiments. MC3T3-E1 cells, cultured in alpha-minimal essential medium containing 10% fetal bovine serum, were shown to produce PGE2, which was markedly suppressed in the presence of indomethacin. Addition of indomethacin resulted in an increase in DNA content and [3H]thymidine incorporation. A similar growth stimulatory effect was observed when structurally different cyclooxygenase inhibitors, that is, acetyl salicylic acid (ASA), flurbiprofen, and piroxicam, were added. These cyclooxygenase inhibitors, however, differed in their effects on ALP activity. Indomethacin and ASA enhanced ALP activity, whereas flurbiprofen and piroxicam suppressed it. We then examined the effects of exogenous addition of PGE2. Although exogenous PGE2 at 6 x 10(-6) M slightly stimulated cell growth, it inhibited cell growth at 6 x 10(-8) M and 6 x 10(-7) M. ALP activity was reduced in a dose-dependent fashion by exogenous PGE2. These results suggest that PGE2 produced by MC3T3-E1 may be suppressing cell proliferation and that cyclooxygenase inhibitors, per se, may stimulate cell growth by inhibiting endogenous PGE2 production in MC3T3-E1 cells. UMR-106 cells also produced PGE2, although less than MC3T3-E1 cells. In UMR-106 cells, the cyclooxygenase inhibitors did not influence DNA content or ALP activity as distinctly as in MC3T3-E1 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗