Biomedical subjects

Yoon Hee Chung

Publications and source records attributed to Yoon Hee Chung.

At least 37 records · Page 2Linked to original sources

PubMed2004

A subcellular distribution of estrogen receptor-alpha is changed during artificially induced senescence of PC12 pheochromocytoma cells.

Although estrogen has been considered as a sex hormone for decades, recent reports suggest that estrogen might modulate the development and physiological function of the brain. In addition, the subcellular localization of estrogen receptors (ERs) has shown their presence within both the perinuclear cytoplasm and nuclei, suggesting that these ERs may differ functionally. We, therefore, assayed changes in the subcellular localization of ER-alpha immunoreactivity (IR) in rat pheochromocytoma PC12 cells during the artificial senescence induced by the telomerase inhibitor, 3'-azido-3'-deoxythymidine (AZT). After 2 months of culture with AZT, PC12 cells showed morphological and biochemical characteristics of cellular senescence. In the cells showing artificial senescence, the ER-alpha IR was mainly localized within the cytoplasm, whereas in control cells, ER-alpha IR was found only in the nuclei. Since senescence was induced by AZT, which inhibits the action of telomerase whenever the cells divide, the change in subcellular distribution of ER-alpha IR may be correlated with the length of the telomere.

Animals↗

PubMed2004

Distribution of heat shock protein 108 mRNA during the development of the chicken brain.

The developmental expression of heat shock protein 108 (HSP108) mRNA was mapped in chicken brain using in situ hybridization and reverse transcription-polymerase chain reaction (RT-PCR). RT-PCR showed that HSP108 mRNA increased from embryonic day 5 (E5) to 13 (E13), significantly decreased from E17 to E21 and then increased again at the adult stage. In situ hybridization showed that while intense HSP108 positive (HSP108+) signals were localized in the cerebellum from E7 to E14, the intensities of these signals were significantly decreased at E17. However, at the adult stage, HSP108 expression increased in a cell type dependent manner. A decrease in HSP108 mRNA expression during differentiation was also observed in an in vitro study of brain cells treated with nerve growth factor (NGF).

Age Factors↗

PubMed2004

Immunohistochemical study of the distribution of neuronal voltage-gated calcium channels in the nNOS knock-out mouse cerebellum.

Nitric oxide (NO) participates in synaptic plasticity, neuronal development, and apoptosis. The involvement of NO and ionic calcium in synaptic plasticity imply that NO may exert an effect on Ca2+ channels. Therefore, we investigated changes in the expressions of calcium channel subunits (Cav1.2/alpha1C, Cav1.3/alpha(1D), Cav2.1/alpha1A, and Cav2.2/alpha1B) in nNOS knock-out (-/-) (nNOS((-/-))) mouse cerebellum using an immunohistochemical approach. We found that the immunoreactivities of the Cav1.2 and Cav1.3 subunits were reduced in the cell bodies of Purkinje cells in these mice and that the signal of the Cav1.2 subunit in neurons and of the Cav1.3 subunit in the neuropils of nNOS((-/-)) mice cerebellar nuclei were significantly down-regulated. We show, for the first time, that prolonged NO deficiency in the cerebellum may affect calcium channel protein expressions, especially, of the Cav1.2 and Cav1.3 subunits.

Animals↗

PubMed2004

Region-specific alterations in insulin-like growth factor-I receptor in the central nervous system of nNOS knockout mice.

In the present study, we investigated layer-specific changes in insulin-like growth factor-I (IGF-I) receptor localization in the cerebral cortex, hippocampus and cerebellum of neuronal nitric oxide synthase knockout (nNOS-/-) mice using immunohistochemistry. In the cerebral cortex of control mice, moderately stained cells were seen through the layers II-VI in several cortical regions. In nNOS-/- mice, there was a significant decrease in IGF-I receptor immunoreactivity in the same cortical regions. In the hippocampus of control mice, a distinct immunoreactivity pattern was observed in the CA1-3 areas and dentate gyrus. The immunoreactivity for IGF-I receptor was differentially decreased in each layer in nNOS-/- mice. In nNOS-/- cerebellum, IGF-I receptor immunoreactivity was also significantly decreased in each layer of cerebellar cortex and cerebellar nuclei. To clarify whether decreased expression of IGF-I receptor in nNOS-/- mice was specific, the expression of other receptors for IGF-I was also evaluated. Receptor tyrosine kinase type A (TrkA receptor) and TrkB receptor were differentially decreased in each layer of the hippocampus or cerebellum of nNOS-/- mice. Although further studies of functional features of IGF-I systems in the nNOS-/- mice are required, our first morphological data may provide insights into NO-induced changes in trophic support as well as basic knowledge required for the study of NO-associated neurological diseases.

Animals↗

PubMed2004

Subcellular localization of WD40 repeat 1 protein in PC12 rat pheochromocytoma cells.

The dynamics of actin filament protein is crucial for various physiological processes of the cells. Among the proteins correlating with actin dynamics, a novel 67-kDa WD40 repeat protein 1 (WDR1) was the vertebrate homologue of actin-interacting protein 1 (Aip1). Even though previous studies have provided the clues on the function of WDR1 in specific organs under pathological conditions, the exact subcellular localization of WDR1 is not known. Therefore, in the present study, we undertook to determine the distribution of WDR1 within PC12 pheochromocytoma cells (PC12 cells) using light and electron microscopic techniques. Double immunocytochemistry clearly showed that WDR1 immunoreactivities (IRs) were co-localized with anti-actin antibody, suggesting the involvement of WDR1 in actin dynamics. WDR1 immunoreactivities (IRs) in PC12 cells showed different distribution patterns as nerve growth factor (NGF) concentrations varied. During active proliferation, the distribution of WDR1 IRs seemed to be similar to those found in cortical actin patches, whereas WDR1 IR was observed in cytoplasmic actin cables after PC12 cells were induced to differentiate by treating with NGF. Though further studies are necessary to determine the function of WDR1, the current data represents a first step towards the in vitro study of WDR1 protein.

Actins↗

PubMed2004

Distribution of vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide receptors (VPAC1, VPAC2, and PAC1 receptor) in the rat brain.

To examine the distributions of VIP/PACAP receptors (VPAC1, VPAC2, and PAC1 receptors) in the brain and to identify the cell types that express these receptors, we performed immunohistochemistry and double immunofluorescence in the rat brain with specific antibodies. The immunohistochemistry revealed that the receptors had distinctive, complementary, and overlapping distribution patterns. High levels of the VPAC1 receptor were expressed in the cerebral cortex, hippocampal formation, deep cerebellar nuclei, thalamus, hypothalamus, and brainstem. The VPAC2 receptors were concentrated in the cerebral cortex, hippocampal formation, amygdalar regions, cerebellar cortex, deep cerebellar nuclei, hypothalamus, and brainstem. On the other hand, the PAC1 receptors had a more restricted distribution pattern in the brain, and high levels of the PAC1 receptors were confined to the cerebellar cortex, deep cerebellar nuclei, epithalamus, hypothalamus, brainstem, and white matter of many brain regions. Also, many fibers expressing the PAC1 receptors were observed in various areas, i.e., the thalamus, hypothalamus, and brainstem. The double immunofluorescence showed that the VIP/PACAP receptors were confined to the neuroglia as well as the neurons. All three types of the VIP/PACAP receptors were expressed in the astrocytes, and the PAC1 receptors were also expressed in the oligodendrocytes. These findings indicate that VIP and PACAP exert their functions through their receptors in specific locations in different combinations. We hope that this first demonstration of the distributions of the VIP/PACAP receptors provides data useful in the investigation of the mechanisms of the many functions of VIP and PACAP in the brain, which require further elucidation.

Aging↗

PubMed2004

Age-related changes in erythropoietin immunoreactivity in the cerebral cortex and hippocampus of rats.

Although oxidative stress may influence the fluid properties of blood, resulting in a potential decrement in blood flow and oxygen delivery to the brain during aging, very little is known about age-related changes in Epo expression. Therefore, we examined age-related changes in Epo expression in the cerebral cortex and hippocampus with an immunohistochemical technique. In aged rats, there was a significant decrease in Epo immunoreactivity in the pyramidal cells in the cortical regions. In the hippocampus of adult rats, a distinct immunoreactivity pattern was observed in the CA1-3 areas and dentate gyrus. In aged hippocampus, Epo immunoreactivity was significantly deceased in the pyramidal layer of CA1 regions, and the granule cell layer of dentate gyrus. It was noted that there was distinct pattern of Epo immunoreactivity in the pyramidal layer of CA2-CA3 region of aged rats. Epo immunoreactivity was relatively strong, but was observed only in the periphery of the cytoplasm. The first demonstration of age-related decreases in Epo expression in the cerebral cortex and hippocampus may provide useful data for investigating the pathogenesis of age-related neurodegenerative diseases, suggesting that age-related decreases in Epo may contribute to degenerative events following age-related decreases in brain flow and oxygen supply.

Aging↗

PubMed2004

The distribution of c-myb immunoreactivities in the adult mouse retina.

The myb gene family is composed of three different myb-related genes, A-, B- and c-myb. Among these, the presence of c-myb mRNA in developing and adult retina was previously reported. However, further study on the expression of c-myb in the retina is warranted because the previous study was only performed on developing retinal tissues by in situ hybridization technique. Therefore, in this study, we tried to perform immunohistochemical study, with a focus on the c-myb protein expression in adult retina. Although the cell types were unconfirmed, c-myb protein was likely to have been found in the ganglion, amacrine, horizontal and photoreceptor cells, judging from their locations and morphologies. The experimental data suggested that c-myb immunoreactivities were expressed by the cells in the neural retina, even in the adult stage, especially within some types of cells in specified retinal layers. This suggests that c-myb might play a role in the physiology of the retinal cells, not only in differentiation during retinal development.

Animals↗

PubMed2004

Enhanced expression of erythropoietin in the central nervous system of SOD1(G93A) transgenic mice.

In the present study, we investigated the changes of erythropoietin (Epo) expression in the central nervous system (CNS) of SOD1(G93A) transgenic mice as an in vivo model of amyotrophic lateral sclerosis (ALS). In wild-type SOD1 (wtSOD1) transgenic mice, little immunoreactivity was found in all cortical regions. In the cerebral cortex of symptomatic SOD1(G93A) transgenic mice, there was a significant increase in Epo immunoreactivity. In the hippocampal formation, layer-specific alterations in the staining intensity were observed in the CA1-3 areas and dentate gyrus. Epo immunoreactivity was significantly increased in the midbrain, cerebellar cortex and brainstem of SOD1(G93A) transgenic mice. On the contrary, Epo immunoreactivity was moderately stained in the spinal cord and was not different between wtSOD1 and SOD1(G93A) transgenic mice at the age of 8 weeks, 13 weeks and 18 weeks. In the staining of Epo receptor (EpoR), the changing pattern was similar with that of Epo in the spinal cord and hippocampal formation in wtSOD1 and SOD1(G93A) transgenic mice. Although further studies of functional features of Epo in ALS are needed, the first demonstration of increased immunoreactivity for Epo in the CNS of SOD1(G93A) transgenic mice may provide initial insights into the development of interventional strategies to alleviate motor neuron degeneration in human ALS.

Animals↗

PubMed2004

Postnatal development and age-related changes in the distribution of nitric oxide synthase-immunoreactive neurons in the visual system of rats.

We have determined postnatal development and age-related changes in the distribution of neuronal nitric oxide synthase (nNOS) in the visual system including superior colliculus (SC), dorsal nucleus of lateral geniculate body (dLGB) and visual cortex of rats. In SC, the number and intensity of immunoreactive cells were increased until postnatal day 21 (P21), and were comparably decreased during the following days. Both neurons and neuropil were intensely stained in dLGB at P21, and the staining intensity was decreased in aged rats. The number of nNOS-immunoreactive cells was increased from P7 to P28 and was decreased in aged rats. The first demonstration of different staining patterns in SC, dLGB and visual cortex during the postnatal days and aging suggests that NO may mediate both postnatal refinement and age-associated visual deficits in some brain regions.

Aging↗

PubMed2004

Reactive astrocytes express PARP in the central nervous system of SOD(G93A) transgenic mice.

In the present study, we used the transgenic mice expressing a human Cu/Zn SOD mutation (SOD1(G93A)) as an in vivo model of amyotrophic lateral sclerosis (ALS) and performed immunohistochemical studies to investigate the changes of poly(ADP-ribose) polymerase (PARP) in the central nervous system. In the spinal cord of symptomatic transgenic mice, immunohistochemistry showed intensely stained PARP-immunoreactive glial cells with the appearance of astrocytes, which were confirmed as astrocytes by double-immunofluorescences. In the brainstem and cerebellum, PARP-immunoreactive astrocytes were observed in the medullary and pontine reticular formation, hypoglossal nucleus, vestibular nucleus, cochlear nucleus and cerebellar nuclei. On the contrary, no PARP-immunoreactive glial cells were observed in control mice although PARP-immunoreactive motor neurons were found. In presymptomatic transgenic mice, a few moderately stained neurons were observed, whereas PARP-immunoreactive astrocytes were not detected. The present study provides the first evidence that PARP-immunoreactive astrocytes were found in the central nervous system of symptomatic SOD1(G93A) transgenic mice, suggesting that reactive astrocytes may play an important role in the pathogenesis and progress of ALS.

Animals↗

PubMed2004

Region-specific alterations of neuronal nitric oxide synthase (nNOS) expression in the amygdala of the aged rats.

Although many amygdalar functions are altered by aging, little is known about their mechanisms. As these functions are related with nitric oxide (NO), we examined neuronal nitric oxide synthase (nNOS) expression in the amygdala of the aged rats via immunohistochemical technique. We found that nNOS immunoreactive neurons are decreased in almost all amygdalar areas of the aged rats, while nNOS immunoreactivity of the neuropil is significantly increased in the amygdalar nuclei related with main and accessory olfactory system. These suggest altered levels of NO might provide region-specific mechanisms of many physiological and behavioral deficits of the amygdala developed by aging. However, exact effects of these changes require further elucidation.

Aging↗

PubMed2004

Distribution of neuronal nitric oxide synthase-immunoreactive neurons in the cerebral cortex and hippocampus during postnatal development.

Although many reports have argued a role for nitric oxide (NO) during postnatal development, there has been no combined demonstration in the cerebral cortex and hippocampus. We have investigated the distribution and morphology of neurons and fibers expressing neuronal NO synthase (nNOS) in the cerebral cortex and hippocampal formation of rats during the postnatal development, and correlated these findings with developmental events taking place in these regions. In the cerebral cortex, the nNOS-immunoreactive cells could be divided into two classes : heavily stained neurons and lightly stained neurons. For the lightly stained nNOS-positive neurons, only the cell bodies were observed, whereas for the heavily stained neurons, the cell bodies and their dendrites were visible. During the postnatal days, heavily stained neurons reached their typical morphology in the second week and appeared in all layers except for layer I. In the hippocampus, there was a transient expression of nNOS in the pyramidal cell layer at P3-P7, and this expression disappeared during following days. The adult pattern of staining developed gradually during the postnatal period. This study suggested that these alterations might reflect a region-specific role of NO and a potential developmental role in the postnatal cerebral cortex and hippocampus.

Animals↗

PubMed2003

Immunohistochemical study on the distribution of insulin-like growth factor I (IGF-I) receptor in the central nervous system of SOD1(G93A) mutant transgenic mice.

In the present study, we used the SOD1(G93A) mutant transgenic mice as an in vivo model of ALS and performed immunohistochemical studies to investigate the changes of insulin-like growth factor I (IGF-I) receptor in the central nervous system. IGF-I receptor-immunoreactive astrocytes were detected in the spinal cord, brainstem, central gray and cerebellar nuclei of SOD1(G93A) transgenic mice. In contrast to transgenic mice, no IGF-I receptor-immunoreactive astrocytes were observed in any brain region of wtSOD1 transgenic mice although a few moderately stained neurons were observed. In the hippocampal formation of SOD1(G93A) transgenic mice, IGF-I receptor immunoreactivity was increased in the pyramidal cells of the CA1-3 regions and granule cells of the dentate gyrus. The present study provides the first evidence that IGF-I receptor immunoreactivity was increased in reactive astrocytes in the central nervous system of SOD(G93A) transgenic mice, suggesting that reactive astrocytes may play an important role in the pathogenesis and progress of ALS. The mechanisms underlying the increased immunoreactivity for IGF-I receptor, and the functional implications of these increases, require elucidation.

Amyotrophic Lateral Sclerosis↗

PubMed2003

Immunohistochemical study on the distribution of MnSOD in the central nervous system of the transgenic mice expressing a human Cu/Zn SOD mutation.

In the present study, we used the SOD1(G93A) mutant transgenic mice as an animal model of amyotrophic lateral sclerosis (ALS) and performed immunohistochemical studies to investigate the changes of MnSOD in the central nervous system of transgenic mice at the age of 8, 13, and 18 weeks. In the spinal cord of wild-type SOD1 (wtSOD1) and SOD1(G93A) transgenic mice, MnSOD-immunoreactive neurons were distributed mainly in the anterior horn, although they were also observed in the posterior horn. The staining intensity of MnSOD was significantly increased in the spinal cord of SOD1(G93A) transgenic mice at presymptomatic and symptomatic stage. In the brainstem of symptomatic SOD1(G93A) transgenic mice, significantly increased immunoreactivity for MnSOD was observed in abducens nucleus, facial nucleus, dorsal motor nucleus of vagus, hypoglossal nucleus, medullary and pontine reticular formation, superior and inferior olivary nucleus, and cochlear nucleus. The present study provides the first evidence that MnSOD immunoreactivity was increased in the central nervous system of SOD(G93A) transgenic mice, suggesting that mitochondria may play an important role in the pathogenesis and progress of ALS. The mechanisms underlying the increased immunoreactivity for MnSOD, and the functional implications of these increases, require elucidation.

Amyotrophic Lateral Sclerosis↗

PubMed2003

Immunocytochemical study on the distribution of c-myb in the central nervous system of the transgenic mice expressing a human copper/zinc superoxide dismutase mutation.

Although our previous study showed the constitutive expression of c-myb in neurons, suggesting that this gene might be involved in the normal function of these cells, there were no reports on the expression pattern of c-myb under pathological conditions. In the present study, we first investigated the changes in c-myb immunoreactivities (IRs) in the central nervous system of the transgenic mice expressing a human copper/zinc superoxide dismutase (Cu/Zn SOD) mutation. The distribution of c-myb was enhanced in the various brain regions of transgenic mice expressing a mutated human Cu/Zn SOD gene. Immunohistochemistry showed intensely stained c-myb IR glial cells with the appearance of astrocytes within the various brain regions of transgenic mice such as the gray matter of the midbrain, medulla oblongata and spinal cord. Even though the exact functions of c-myb in the normal and pathological states were not clearly revealed until now, we think that the increase in c-myb expression in the mutant mice could be due to the compensate mechanism of the astrocytes for the reduced defence against superoxide toxicity because the only known function of c-myb was its correlation with the prevention of programmed cell death, which could be deduced from the previous studies.

Animals↗

PubMed2003

Vasoactive intestinal peptide (VIP) and VIP mRNA decrease in the cerebral cortex of nNOS knock-out(-/-) mice.

Although there is much evidence showing that NO regulates the release of VIP in several areas, there is no report about the influence of NO on VIP in the cerebral cortex. We therefore examined changes in VIP expression in the cerebral cortex of nNOS knock-out(-/-) mice using immunohistochemistry and in situ hybridization. The nNOS((-/-)) mice had significantly fewer VIP-immunoreactive neurons than the control mice and the VIP mRNA as well as the VIP-immunoreactivity of the individual neuron was decreased in the nNOS((-/-)) mice. The first demonstration of decrease in VIP expression in the cerebral cortex of nNOS((-/-)) mice may provide useful data for investigating the relation between NO and VIP in the cerebral cortex and the mechanisms of many functions of these two neurotransmitters.

Animals↗

PubMed2003

Reactive astrocytes express cAMP-response-element-binding protein (CREB) binding protein (CBP) in the central nervous system of transgenic mice expressing a human Cu/Zn superoxide dismutase mutation.

In the present study, we used the superoxide dismutase 1(SODI)(G93A) transgenic mice as an in vivo model of amyotrophic lateral sclerosis (ALS) and performed immunohistochemical studies to investigate the changes of cAMP-response-element-binding protein (CREB) binding protein (CBP) in the central nervous system of transgenic mice. The distribution of CBP-immunoreactive neurons was not different between control and transgenic mice, whereas CBP-immunoreactive astrocytes were found only in transgenic mice. CBP-immunoreactive astrocytes were detected in the spinal cord, brainstem, midbrain and cerebellar nuclei of transgenic mice. The present study provides the first evidence that CBP immunoreactive astrocytes were observed in the central nervous system of transgenic mice, suggesting that reactive astrocytes may play an important role in the pathogenesis and progress of ALS.

Amyotrophic Lateral Sclerosis↗