Search PubMed⌕ Search

Biomedical subjects

Y Eto

Publications and source records attributed to Y Eto.

At least 217 records · Page 12Linked to original sources
PubMed1988

Induction of follicle stimulating hormone receptor by erythroid differentiation factor on rat granulosa cell.

Erythroid differentiation factor (EDF), inhibin beta A-homodimer, induced expression of follicle stimulating hormone receptors on rat granulosa cells prepared from diethylstilbestrol primed immature female rats. After 3 day incubation with EDF, the number of FSH receptors on the granulosa cells was increased to about 3.5 times of the control value in a dose dependent manner with an ED50 value of 61 ng/ml. On the other hand, EDF related peptides, i.e., bovine 32K Da inhibin A and TGF beta, had no effect on the FSH receptor induction. The present observation suggests that EDF may play a role in the initiation of the cytodifferentiation of ovarian granulosa cells.

Activins↗
PubMed1988

Identification of a specific receptor for erythroid differentiation factor on follicular granulosa cell.

A cellular receptor for erythroid differentiation factor (EDF) was demonstrated by incubation of 125I-labeled EDF with rat follicular granulosa cell cultures. The specific binding of labeled EDF to the cells showed saturation; Scatchard analysis of binding data indicated a single class of receptors having Kd = 3.4 x 10(-10) M. A large excess of unlabeled EDF reduced labeled EDF binding almost completely, whereas similar doses of inhibin and transforming growth factor type beta, which are quite similar to EDF in protein structure and subunit organization, had no effect; EDF did not share receptors with those factors. EDF receptor (activin A receptor) expression was enhanced in granulosa cells cultured in the presence of follicle-stimulating hormone; follicle-stimulating hormone raised the number of EDF binding sites/cell from 13,000 to 96,000 without altering the binding affinity.

Activins↗
PubMed1988

Accumulation of phosphorus compounds in tissues and cultured skin fibroblasts in patients with hypophosphatasia.

Patients with hypophosphatasia caused by a deficiency of alkaline phosphatase first showed marked accumulation of phosphoethanolamine and other phosphorus compounds in kidney and liver, while in placenta and intestine contents of these compounds were within a normal range. Furthermore, 32P-incorporation in cultured skin fibroblasts of patients with hypophosphatasia was increased about two to three times of control. FPLC chromatographic analysis also indicates that the accumulated phosphorus compounds in hypophosphatasia was smaller molecular phosphorus containing compounds. These data provide new pathophysiological aspect of hypophosphatasia.

Alkaline Phosphatase↗
PubMed1988

Liposome targeting to mouse brain: mannose as a recognition marker.

Liposomes prepared from lecithin:cholesterol:p-aminophenyl-alpha-mannoside (7:2:1, v/v/v) were efficiently incorporated into the mouse brain across the blood brain barrier. Furthermore, liposomes injected intraperitoneally were exclusively distributed into lysosome rich fraction and also taken up by glial cells. These data suggest that blood brain barrier cells and glial cells recognize mannose molecule on the surface of the membrane and can be used for the treatment of brain damage by lysosomal storage disease.

Animals↗
PubMed1988

Erythroid differentiation factor can modulate follicular granulosa cell functions.

The action of human erythroid differentiation factor (EDF) on the functions of rat granulosa cells cultured in a chemically defined medium was investigated. In the presence of FSH that induced LH receptor expression and progesterone synthesis during culture of the cells, EDF augmented both responses in a dose- and time-dependent manner. Unlike FSH, EDF itself did not have such an inducing effect at all. Furthermore, in the absence of FSH, EDF was found to strongly enhance the ability of granulosa cells to produce inhibin. Thus, EDF may play an important role in the regulation of granulosa cell function and differentiation during follicle development.

Animals↗
PubMed1988

Expression of erythroid differentiation factor (EDF) in Chinese hamster ovary cells.

Plasmid DNA containing EDF subunit cDNA and mouse dihydrofolate reductase (DHFR) cDNA was transfected into CHO DHFR- cells by the calcium-phosphate method. DHFR positive transformants secreted recombinant EDF (r-EDF) constitutively in an active form and accumulated it in the conditioned medium. Furthermore, cells which were resistant to methotrexate (MTX : 0.5 microM) secreted r-EDF up to 1 microgram/ml. r-EDF was identical to natural EDF (n-EDF) produced by human acute monocytic leukemia cell line, THP-1, as regards its dimeric structure and a biological activity.

Activins↗
PubMed1988

Clinical and biochemical studies of Japanese neuronal ceroid-lipofuscinosis.

We studied clinical manifestations of Japanese patients with neuronal ceroid-lipofuscinosis (NCL). The onset of the disease and initial symptoms were almost identical to those reported previously in Caucasians. Japanese patients with NCL were not significantly clinically different from Caucasian cases. An atypical case NCL associated with a deficiency of diaminobenzidine peroxidase activity was also presented. Pathogenesis of NCL was studied on the basis of urine dolichol excretion, autofluorescent compounds in urine, thiol protease activities and protein analysis in tissues of NCL patients. Possible biochemical abnormalities in NCL are discussed.

Adolescent↗
PubMed1988

Erythroid differentiation factor is encoded by the same mRNA as that of the inhibin beta A chain.

We have isolated a protein that exhibits a potent differentiation-inducing activity toward mouse Friend erythroleukemia (MEL) cells and human K-562 cells. The protein, designated erythroid differentiation factor (EDF), was found in the culture fluid of human THP-1 cells that had been treated with phorbol 12-myristate 13-acetate. EDF is a homodimer with a Mr of 25,000; the Mr of the monomer is 15,500. cDNA clones encoding the Mr 15,500 subunit of EDF from THP-1 libraries were isolated and sequenced. Surprisingly, the sequence of EDF mRNA is identical to that for the beta A subunit of inhibin, a gonadal protein that suppresses the secretion of pituitary follicle-stimulating hormone. Southern blot analysis indicates that only one gene for EDF/inhibin beta A exists in the human genome. When the EDF subunit cDNA was linked to a simian virus 40 expression vector containing the dihydrofolate reductase gene and transfected into Chinese hamster ovary dihydrofolate reductase negative cells, the transformants began to secrete EDF, demonstrating that the cDNA actually encoded the EDF subunit.

Amino Acid Sequence↗
PubMed1987

Stimulation of FSH release by erythroid differentiation factor (EDF).

The action of erythroid differentiation factor (EDF) on primary culture of rat anterior pituitary cells was examined. EDF stimulates FSH secretion in a dose dependent manner but not of LH secretion. ED50 of EDF for FSH secretion was 5 X 10(-10) M, while ED50 of LHRH for FSH secretion was 5 X 10(-9) M. These data indicate that EDF is a potent agonist for FSH secretion and the biological activity of EDF on anterior pituitary seems to be identical as that of FSH releasing protein (FRP).

Activins↗
PubMed1987

Purification and characterization of erythroid differentiation factor (EDF) isolated from human leukemia cell line THP-1.

We isolated a protein, from a cell line of human origin, which exhibits extensive differentiation inducing activity toward Friend leukemia cells. The protein, called Erythroid Differentiation Factor (EDF), was found in a 4 day culture of THP-1 cells performed in the presence of 4 beta-phorbol 12-myristate 13-acetate(PMA). EDF is a homodimer of a molecular weight of 25,000, with an NH2-terminal sequence identical to that of the beta A-chain of porcine Inhibin. It was suggested that a single protein species is responsible for the activities of both EDF and FRP, a FSH releasing protein isolated from porcine ovarian follicular fluid.

Activins↗
PubMed1987

Expression of amplified cDNA and genomic sequences encoding human interleukin 2 in Chinese hamster ovary cells.

Expression of human interleukin 2 (IL-2) at high levels has been achieved in Chinese hamster ovary (CHO) cells by amplification of transfected sequences. Plasmids containing the human IL-2 cDNA or genomic DNA and mouse dihydrofolate reductase (DHFR) cDNA were transfected into DHFR-negative CHO cells. Transformants expressing DHFR were selected in media lacking nucleosides, and cells which amplified both DHFR and IL-2 genes were obtained by exposure to increasing methotrexate (MTX) concentrations. These cell lines constitutively expressed elevated levels of IL-2 at a concentration of 2 mg/liter. These cell lines continued to produce IL-2 stably through at least 1 month, even in the absence of MTX.

Animals↗
PubMed1987

Pathochemistry, pathogenesis and enzyme replacement in multiple-sulfatase deficiency.

Multiple-sulfatase deficiency (MSD) is now considered to be heterogeneous and could be classified into three or four clinical phenotypes according to the onset of the disease: neonatal, late infantile, juvenile and possibly adult type. Neonatal-type MSD shows severe clinical involvement and practically no arylsulfatase A, B and C activities in cultured skin fibroblasts. Furthermore, arylsulfatase A activity in neonatal-type MSD was not enhanced by the addition of thiosulfate. Therefore, it is distinct from late infantile-type MSD. The degradation of 14C-sulfatide can occur in MSD-cultured skin fibroblasts and was much higher than in late infantile-type MLD. The addition of thiol protease such as leupeptin to cultured MSD skin fibroblasts enhanced arylsulfatase A activity as well as the degradation of 14C-sulfatide. This suggests that the decreased activities of arylsulfatase A is due to an acceleration of the enzyme degradation. Enzyme replacement by the addition of arylsulfatases of different sources (human liver, brain, fungus) was carried out in cultured MSD skin fibroblasts. Human enzymes of arylsulfatase A and B were mostly taken up by MSD cells rather than those of fungus origin. By the exposure to leukocytes to cultured skin fibroblasts, MSD cells corrected arylsulfatase A and B activities.

Adolescent↗
PubMed1987

Partial deficiency of beta-hexosaminidase activity in canine GM2-gangliosidosis.

4-Methylumbelliferyl-N-acetylglucosamine-6-sulfate (4MUGLc6S) which is known to be a specific substrate for human hexosaminidase A was used to determine enzymatic features of canine GM2-gangliosidosis. The enzyme activity using 4MUGlc6S in affected dog brain and liver was less than 20 to 30% of control tissues, whereas total 4-methylumbelliferyl beta-glucosaminidase activity in canine GM2-gangliosidosis was normal or elevated. However, when beta-hexosaminidase was fractionated by DEAE-Sepharose column chromatography, beta-hexosaminidase A like fraction in affected dog tissues was reduced to 20 to 30% of control. These data suggest that canine GM2-gangliosidosis is analogous to human juvenile.

Animals↗