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Y Oh

Publications and source records attributed to Y Oh.

At least 91 records · Page 5Linked to original sources
PubMed1997

Expression of the amiloride-sensitive sodium channel beta subunit gene in human B lymphocytes.

The amiloride-sensitive, epithelial sodium channel (ENaC) is composed of at least three subunits (alpha, beta, and gamma). This study demonstrates that the ENaC beta subunit gene is expressed in human B cell lines, peripheral blood lymphocytes, and lymph node at the mRNA level. Further, this study shows that both wild-type and mutated alleles of the ENaC beta subunit gene are transcribed in human B lymphocytes derived from an individual affected with Liddle's syndrome, an autosomal dominant form of human hypertension.

Alleles↗
PubMed1997

Ion channels in neuroglial cells.

With the advent of the patch clamp technique, many different types of ion channels have been found in neuroglial cells, including voltage-sensitive ion channels (Na+, Ca2+, K+, and CI- channels), ligand-gated ion channels (glutamate receptor and GABAA receptor), and mechanosensitive ion channels. Most of these ion channels have also been found in excitable cells, and thus excitable and non-excitable cells in the nervous system share a similar repertoire of ion channel gene expression. Various factors, such as different developmental stage or different regions in the brain, are known to influence glial ion channel expression. In addition, glial ion channel expression is influenced by the presence of neurons, suggesting the existence of dynamic mechanism(s) for regulating ion channel expression via cell-to-cell signaling between neurons and glia. In this review, the current understanding of various types of ion channels found in neuroglial cells (i.e., astrocytes, oligodendrocytes, and Schwann cells) is summarized.

Animals↗
PubMed1996

Synthesis and characterization of insulin-like growth factor-binding protein (IGFBP)-7. Recombinant human mac25 protein specifically binds IGF-I and -II.

The mac25 cDNA was originally cloned from leptomeningial cells and subsequently reisolated through differential display as a sequence preferentially expressed in senescent human mammary epithelial cells. The deduced amino acid sequence of the human mac25 propeptide shares a 20-25% identity to human insulin-like growth factor-binding proteins (IGFBPs), suggesting that mac25 could be another member of the IGFBP family. In the present study, we have generated recombinant human mac25 (rh-mac25) in a baculovirus expression system and assessed its affinity for IGFs and have evaluated the pattern of expression of the mac25 gene in human tissues. Binding of 125I-IGF-I and 125I-IGF-II to rh-mac25 was demonstrated by Western ligand blotting after nondenaturing polyacrylamide gel electrophoresis and by affinity cross-linking with as little as 2 nM rh-mac25. Specificity of rh-mac25 binding to 125I-IGFs was demonstrated by competition for rh-mac25 binding with unlabeled IGFs, but not with [QAYLL]IGF-II analog, which has 100-fold less affinity for IGFBPs. In comparison with IGFBP-3, rh-mac25 has at least a 5-6-fold lower affinity for IGF-I and 20-25-fold lower affinity for IGF-II. mac25 mRNA was detectable in a wide range of normal human tissues, with decreased expression in breast, prostate, colon, and lung cancer cell lines. In conclusion, mac25 specifically binds IGFs and constitutes a new member of the IGFBP family, IGFBP-7. Its wider distribution in normal tissue and lower expression in several cancer cells indicate that IGFBP-7 may function as a growth-suppressing factor, as well as an IGF-binding protein.

Gene Expression↗
PubMed1996

Insulin-like growth factor binding protein 3 mediates retinoic acid- and transforming growth factor beta2-induced growth inhibition in human breast cancer cells.

Retinoic acid (RA) is a potent in vitro inhibitor of cell proliferation in various malignant cell lines. The exact mechanisms of its actions, however, are not fully understood. To further elucidate the nature of this inhibition, we investigated the effects of RA in an estrogen receptor-negative human breast cancer cell line, MDA-MB-231. RA (0.01-5 microM) significantly inhibited MDA-MB-231 cell growth by 35-40% as compared with untreated controls. Similar growth inhibitory actions were observed when cells were treated with transforming growth factor beta2 (TGF-beta2), another factor with antiproliferative actions in breast cancer cells. Both RA and TGF-beta2 increased the levels of insulin-like growth factor binding protein (IGFBP) 3 (2-3-fold) and mRNA (1.5-2-fold), whereas IGFBP-4 levels remained essentially unchanged. The direct involvement of IGFBP-3 in cell growth inhibition was further confirmed by its action on cell growth: exogenous IGFBP-3 directly and significantly inhibited MDA-MB-231 cell number by 40%. These results provided circumstantial evidence that IGFBP-3 may mediate RA and TGF-beta2 growth inhibitory actions in human breast cancer cells. To test this hypothesis, we used an antisense IGFBP-3 oligodeoxynucleotide (ODN) which specifically inhibits IGFBP-3 expression. The antisense IGBP-3 ODN dramatically blocked both RA- and TGF-beta2-induced increases in IGFBP-3 protein (90%) and mRNA levels (90%). This effect was not observed when RA- or TGF-beta2-exposed cells were treated with sense IGFBP-3 ODN. Moreover, antisense ODN did not significantly affect IGFBP-4 protein or mRNA levels, strongly supporting the specificity of the antisense IGFBP-3 ODN effect on IGFBP-3 mRNA. This specific effect of antisense IGFBP-3 ODN on IGFBP-3 protein and mRNA levels was accompanied by significant attenuation of the inhibition of cell proliferation attained with RA or TGF-beta2 (approximately 40% of either RA- or TGF-beta2-induced inhibition). The control sense IGFBP-3 ODN did not reduce the growth inhibition observed with either RA or TGF-beta2. These results indicate that IGFBP-3 is an important mediator of RA- and TGF-beta2-induced cell growth inhibition in human breast cancer cells.

Base Sequence↗
PubMed1996

Cell-specific differential expression of Na(+)-channel beta 1-subunit mRNA in the olfactory system during postnatal development and after denervation.

Activity-dependent mechanisms have been implicated in olfactory system development but, although such activity requires ion channels, few reports have described their expression in the olfactory system. We investigated the developmental and denervation-induced regulation of the Na(+)-channel beta 1 subunit (Na beta 1) in rat olfactory bulb (OB) and piriform cortex (PC). In situ hybridization shows that Na beta 1 mRNA expression is upregulated developmentally, but with different time courses in mitral, tufted, and pyramidal cells. In mitral cells, label was detected at postnatal day 4 (P4) and gradually increased to P14. Tufted cells were devoid of Na beta 1 mRNA before P14, when most cells expressed adult levels. In pyramidal cells of PC, Na beta 1 expression was not detectable clearly until P14, with maximal expression at P28. To examine the regulation of Na beta 1 mRNA, we surgically deafferented the OB at P30 and compared the effects on Na beta 1 with those for Na(+)-channel alpha-subunit (Na alpha) mRNAs. Within 5 d of surgery, the Na beta 1 and Na alpha II signals within tufted cells disappeared almost completely. Na beta 1 and Na alpha II expression was decreased in mitral cells to low-to-moderate levels. In pyramidal cells, Na beta 1 mRNA expression was decreased moderately without significant changes in Na alpha II mRNA. Deafferentation had no detectable effects on Na alpha I or III mRNAs in either OB or PC. These data indicate that Na beta 1 mRNA is expressed differentially in subpopulations of cells in the olfactory system during development and after deafferentation and suggest that the expression of Na beta 1 is regulated independently of Na alpha mRNAs via cell-specific and pathway-specific mechanisms.

Animals↗
PubMed1996

Insulin-like growth factor-binding proteins (IGFBPs) and their regulatory dynamics.

The IGFBPs are a family of homologous proteins that have co-evolved with the IGFs and that confer upon the IGF regulatory system both functional and tissue specificity. IGFBPs are not merely carrier proteins for IGFs, but hold a central position in IGF ligand-receptor interactions through influences on both the bioavailability and distribution of IGFs in the extracellular environment. In addition, IGFBPs appear to have intrinsic biological activity independent of IGFs. The current status of research on IGFBPs is reviewed herein. Following a brief introduction to the entire IGF/IGFBP system, separate sections for each of the six cloned mammalian IGFBPs, the most extensive for IGFBP3, cover selected topics that emphasize the dynamics of IGFBPs--that is, their regulation in cells, their functionally important post-translational modifications, and their interactions in the cellular microenvironment--and how these dynamics influence physiological function.

Animals↗
PubMed1996

Transpharyngeal approach to base of tongue tumors: a comparative study.

Tumors of the tongue base have been traditionally removed by resecting the mandible or using a translabial transmandibular approach. These procedures involve significant morbidity including lip and chin scars, malocclusion, compromised deglutition, chronic aspiration, and altered speech articulation. Therefore alternative techniques have been described to minimize the morbidity associated with transmandibular tongue resection. A retrospective analysis of patients with base of tongue tumors treated at the University of California, Los Angeles, Medical Center between 1981 and 1994 was undertaken. Thirteen patients were treated using a transpharyngeal approach compared with 18 patients who underwent a transmandibular resection. There was no difference in terms of survival or tumor-free margins. However, there was a significant difference in function (P < .05). Patients who underwent transpharyngeal resection had significantly better speech and swallowing and less aspiration compared with those who underwent transmandibular resection of tumors.

Adult↗
PubMed1996

Transcriptional and post-translational regulation of insulin-like growth factor-binding protein-5 in rat articular chondrocytes.

The aim of this study was to assess the regulation of insulin-like growth factor-binding proteins (IGFBPs) by IGFs in primary cultures of rat articular chondrocytes (RAC). Employing Western ligand blotting, immunoprecipitation and Northern blot analysis, RAC were found to secrete IGFBP-5 (29 kDa) and IGFBP-4 (24 kDa) as the predominant IGFBPs, as well as IGFBP-2 (32-30 kDa) and IGFBP-3 (43-39 kDa) as the minor species. Treatment of cells with IGF-I and IGF-II resulted in a dose-dependent increase of IGFBP-5 and a small increase in IGFBP-4 in conditioned media (CM). Des(1-3) IGF-I and [Gln6, Ala7, Tyr18, Leu19] IGF-II ([QAYL] IGF-II), which bind to the type 1 IGF receptor but not to IGFBPs, also induced IGFBP-5 peptide, although the increase was less than with IGF-I or IGF-II treatment of RAC. [Leu27] IGF-II, which does not bind to the type 1 IGF receptor but binds to IGFBPs, resulted in little induction of IGFBP-5, while [QAYL-Leu27] IGF-II, which has reduced affinity for both the type 1 IGF receptor and IGFBPs, did not increase IGFBP-5. These data suggest that the increase in IGFBP-5 in CM is modulated by both the type 1 IGF receptor and the interaction between IGFs and IGFBPs. Northern blotting analysis showed that IGF-I, IGF-II and des(1-3) IGF-I treatment of RAC increased steady state levels of IGFBP-5 mRNA, suggesting that the IGF-mediated increase in IGFBP-5 is transcriptionally modulated. Interestingly, the increase in IGFBP-5 peptide levels and mRNA were not parallel, suggesting the possibility of post-translational modifications of IGFBP-5, such as those seen with IGFBP-5 protease. IGFBP-5 protease activity was detectable in untreated CM, whereas treatment with IGF-I and IGF-II partially protected IGFBP-5 from proteolysis. In summary, treatment of RAC with IGF-I and IGF-II results in dose-dependent increases in both IGFBP-5 peptide in the CM and mRNA levels. These changes are mediated by interactions via the type 1 IGF receptor as well as IGFBPs, both transcriptionally and post-translationally.

Animals↗
PubMed1995

Na+ channel beta 1 subunit mRNA expression in developing rat central nervous system.

The sodium channel beta 1 subunit (Na beta 1) is a component of the rat brain voltage-dependent sodium channel. We have used nonradioactive in situ hybridization cytochemical techniques to demonstrate that transcript levels of Na beta 1 are differentially upregulated during postnatal development of several CNS regions, with selective labeling of specific neuronal populations. In the hippocampus, labeling of the pyramidal cell layer (particularly in the CA3 region) and dentate granule cells was initially observed at postnatal day 2 (P2) and P10, respectively, and became progressively more intense with maturation. Labeled cells were first observed in the hilus at P10. In the developing cerebellum, transient labeling was observed in the external granule cell layer beginning at P1 while label increased in the internal granule cell layer up to P21. Purkinje cells showed significant label beginning at P4 and increasing up to P21. Weak signal was seen in neurons of deep nuclei at P1 and increased up to P21. Na beta 1 labeling in the spinal cord was first observed in the ventral horn at P2, and the intensity of labeling in these large motoneurons gradually increased. In addition, there was a ventral-dorsal gradient in this region, with label appearing subsequently in neurons of Rexed laminae IX, VII and VIII, and in the dorsal horn (Rexed laminae I-VI). In these regions, the labeling reached a plateau within the first 2-3 weeks after birth and persisted into the adult rat. The time course and regional heterogeneity of Na beta 1 expression are consistent with the hypothesis that the expression of mature Na+ channels, including Na beta 1, contributes to the development of circuitry that supports complex patterns of electrogenesis.

Animals↗
PubMed1995

Transforming growth factor-beta-induced cell growth inhibition in human breast cancer cells is mediated through insulin-like growth factor-binding protein-3 action.

Most estrogen receptor-negative breast cancer cells, including Hs578T cells, express mRNAs encoding insulin-like growth factor-binding protein (IGFBP)-3, as well as transforming growth factor (TGF)-beta receptors. Our previous studies (Oh, Y., Muller, H. L., Lamson, G., and Rosenfeld, R. G. (1993) J. Biol. Chem. 268, 14964-14971; Oh, Y., Muller, H. L., Pham, H. M., and Rosenfeld, R. G. (1993) J. Biol. Chem. 268, 26045-26048) have demonstrated a significant inhibitory effect of exogenous IGFBP-3 on Hs578T cell growth and existence of IGFBP-3-specific receptors that may mediate those direct inhibitory effect of IGFBP-3. TGF-beta is also a potent growth inhibitor in human breast cancer cells in vitro and regulates IGFBP-3 production in different cell systems, suggesting that IGFBP-3 is a major anti-proliferative factor and a key element for TGF-beta-induced growth inhibition in human breast cancer cells. In support of this hypothesis, we have demonstrated using Hs578T cells that: 1) TGF-beta stimulates IGFBP-3 gene expression and production prior to its inhibition of cell growth, 2) treatment with an IGFBP-3 antisense oligodeoxynucleotide selectively inhibits TGF-beta-induced IGFBP-3 synthesis and cell growth inhibition, and 3) treatment with IGF-II and IGF-II analogs diminish TGF-beta effects by blocking TGF-beta-induced binding of IGFBP-3 to the cell surface. These findings suggest that IGFBP-3 is a major anti-proliferative factor and a key element in TGF-beta-induced growth inhibition in human breast cancer cells.

Amino Acid Sequence↗
PubMed1995

Isolation and characterization of the gene encoding the Drosophila melanogaster transcriptional elongation factor, TFIIS.

We have characterized a genomic clone encoding the Drosophila melanogaster transcriptional elongation factor, TFIIS. The coding region of the TFIIS gene is interrupted by a short intron. The potential promoter region, deduced from the determination of the transcription start point (tsp), lacks distinct TATAAA or CCAAT box consensus sequences. Southern analysis and the in situ hybridization to chromosomes suggests that it is single-copy gene which is localized to the 35B region on the left arm of the second chromosome.

Animals↗
PubMed1995

Differential Na+ channel beta 1 subunit mRNA expression in stellate and flat astrocytes cultured from rat cortex and cerebellum: a combined in situ hybridization and immunocytochemistry study.

Astrocytes have been shown to express voltage-sensitive Na+ channels, but the molecular structure of these channels is not yet known. Recent studies have demonstrated the expression of rat brain voltage-sensitive Na+ channel mRNAs in astrocytes. In this study, we used a combined non-radioactive in situ hybridization/immunocytochemistry method to investigate the expression of voltage-sensitive Na+ channel beta 1 subunit (Na beta 1) mRNA in definitively identified, GFAP-positive astrocytes cultured from two different regions of the rat brain, cerebrum and cerebellum. In general, two morphologically distinct types of GFAP-positive astrocytes were observed in culture: flat, fibroblast-like and stellate, process-bearing. We observed a differential expression of Na beta 1 mRNA in GFAP-positive astrocytes: 1) stellate astrocytes expressed Na beta 1 mRNA, although the level of Na beta 1 mRNA expression was variable, and 2) flat astrocytes generally did not express Na beta 1 mRNA. Moreover, Bergmann-like cells from cerebellum did not express Na beta 1 mRNA, while the granule cells associated with Bergmann-like cell expressed Na beta 1 mRNA. These observations indicate that Na beta 1 mRNA is differentially expressed in rat astrocytes with various morphologies in vitro.

Animals↗
PubMed1995

Differential up-regulation of sodium channel alpha- and beta 1-subunit mRNAs in cultured embryonic DRG neurons following exposure to NGF.

Although the pattern of expression of various sodium channel alpha- and beta-subunits changes as development proceeds, the mechanisms that control the expression of these subunits are not yet understood. To study the role of nerve growth factor (NGF) in modulating the expression of sodium channel subunits, we used in situ hybridization cytochemistry to examine the distribution of sodium channel alpha- and beta 1-subunit mRNAs in embryonic day 16 (E16) dorsal root ganglia (DRG) neurons cultured in the absence or presence of NGE. At 4 days in vitro in the absence of NGF, sodium channel alpha-subunit II mRNA was expressed at low-to-moderate levels in DRG neurons, but the transcripts for sodium channel alpha-subunits I, III and NaG and beta 1-subunit were not detectable. In the presence of NGF, DRG neurons expressed low-to-moderate levels of sodium channel alpha-I, high levels of alpha-II and low levels of alpha-III; NaG mRNA was not detectable. Sodium channel beta 1 mRNA was up-regulated and was expressed at high levels in DRG neurons in NGF-containing media. These observations demonstrate that the NGF exerts a differential up-regulation of sodium channel alpha- and beta-subunit mRNAs in DRG neurons derived from E16 embryos.

Animals↗
PubMed1995

Na+ channel beta 1 subunit mRNA: differential expression in rat spinal sensory neurons.

The brain Na+ channel beta 1 subunit (Na beta 1) mRNA has recently been localized within rat central nervous system where it is expressed at differing levels in different types of neurons. In the present study, we have studied the expression pattern of Na beta 1 mRNA in rat dorsal root ganglion (DRG) neurons using non-radioactive in situ hybridization histochemistry. Na beta 1 mRNA is differentially expressed in adult DRG, with higher levels in intermediate-to-large (> approximately 25 microns in diameter) DRG neurons than in small (< 25 microns) DRG neurons. This cell body size-related Na beta 1 mRNA expression is consistently observed beginning at postnatal day 4 and continues throughout development to adulthood. The present results indicate that (i) Na beta 1 mRNA is expressed in neurons in the peripheral nervous system and (ii) Na beta 1 gene expression is differentially regulated in DRG neurons in relation to their cell body sizes.

Animals↗