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This experiment was performed to evaluate the morphological responses of the gastric epithelial cells and the gastric chief cells of the mouse inoculated with Ehrlich carcinoma cells in the inguinal area following administration of acriflavine-guanosine composition (AG60). Healthy adult ICR mice were divided into normal and experimental groups. In the experimental groups, each mouse was inoculated with 1x10(7) Ehrlich carcinoma cells subcutaneously in the inguinal area. The day following the 7th injection of saline or AG60, each mouse was injected with methyl-3H-thymidine through tail vein. Seventy minutes after the thymidine injection, gastric tissues were taken and fixed in 10% buffered neutral formalin. Deparaffinized sections were coated with autoradiographic emulsion EM-1 and dried, and then placed in a light-tight box. The number of labeled epithelial cells in the gastric mucosae were observed and calculated. And for electron microscopic observation, gastric tissues were prefixed with 2.5% glutaraldehyde-1.5% paraformaldehyde solution, followed by post-fixation with 1% osmium tetroxide solution. The ultrathin sections were stained with uranyl acetate and lead citrate. The size of zymogen granules and mitochondria in the gastric chief cells were observed and calculated. On the autoradiographic study, number of labeled cells in the area of 3.5 mm width (6 micrometer thickness) of mouse gastric mucosae of normal control, tumor control and AG60-treated groups were 319.7+/-66.46, 343.7+/-47.72 and 102.3+/-54.99 respectively. On the electron microscopic study, the size of zymogen granule in the gastric chief cells of normal control, tumor control and AG60-treated groups were 0.74+/-0.208 micrometer, 1.18+/-0.291 micrometer and 0.97+/-0.259 micrometer, respectively. And the mitochondrial size of the gastric chief cells of normal control, tumor control and AG60-treated groups were 0.86+/-0.364 micrometer, 1.02+/-0.466 micrometer and 0.92+/-0.390 micrometer, respectively. And in the AG60 treated group, most chief cells did not show any difference in ultrastructure, except that myelin figures were more frequently observed, in comparison with that of nornmal control group. From the above results, AG60 may suppress the DNA synthesis of the gastric epithelial cells, but does not results severe fine structural defect on the gastric chief cells. These results suggest that AG60 is expected as one of the most effective anticancer drugs.
Adult ; Animals ; Chief Cells, Gastric ; Citric Acid ; DNA ; Electrons ; Epithelial Cells ; Formaldehyde ; Gastric Mucosa ; Humans ; Mice ; Mice, Inbred ICR ; Mitochondria ; Mitochondrial Size ; Myelin Sheath ; Organometallic Compounds ; Osmium Tetroxide ; Polymers ; Secretory Vesicles ; Thymidine ; Veins

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Expression of Aquaporin-3 and Aquaporin-4 in Aquaporin-1 Knockout Mice.

Wan Young KIM ; Young Hee KIM ; Eun Young PARK ; Jin Sun HWANG ; Yu Mi KIM ; Jin KIM

Korean Journal of Anatomy.2008;41(3):163-172.

Recent studies demonstrated impaired urinary concentrating ability in AQP1 knockout mice. To establish of the lack of AQP1 was associated with compensatory changes in other aquaporins, we examined the expression of AQP3 and AQP4 in AQP1 knockout mice. In AQP1 (+/+) mice, there was strong basolateral AQP3 immunostaining in principal cells throughout the collecting duct and strong basolateral AQP4 immunostaining in IMCD cells and principal cells in the medulla. In AQP1 (-/-) mice, there was an increase in AQP3 immunostaining in principal cells in cortex and outer medulla, but no changes in cellular distribution of labeling. In contrast, AQP4 immunostaining was slightly decreased and there was a surprising decrease in cell height and disappearance of immunolabeling of the lateral cell membrane in IMCD cells with only basal labeling remaining. Immunnoblot analysis confirmed the increase in AQP3 expression in cortex (259+/-50%, P<.0.01), outer medulla (607+/-115%, P<0.01) and inner medulla (1,289+/-174%, P<0.0001), and the decrease in AQP4 expression in the inner medulla (31+/-2%, P<0.02) of AQP1 (-/-) compared with AQP1 (+/+) mice (values in AQP1 (-/-) expressed as percentage of AQP1 (+/+)). In summary, AQP1 gene deletion is associated with an upregulation of AQP3 and a downregulation of AQP4. Taken together, these observations suggest that AQP3 and AQP4 are differently regulated and the basolateral water channel expression is upregulated in the cortical and outer medullary collecting duct in AQP1 knockout mice. The significance of the disappererance of AQP4 immunoreactivity in the lateral plasma membrane of IMCD cells in AQP1 knockout mice remains to be established.
Animals ; Aquaporins ; Cell Membrane ; Down-Regulation ; Gene Deletion ; Mice ; Mice, Knockout ; Up-Regulation ; Water

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Correlative Changes of Endothelial Nitric Oxide Synthase and Choline Acetyltransferase in the Hippocampus after Exercise.

Yun Kyung CHO ; Jinji ZI ; Gyu Seong CHOE ; Hye Min KANG ; Junghye KIM ; Heekyung AHN ; Chan PARK

Korean Journal of Anatomy.2008;41(3):185-192.

We found that the expression and activity of endothelial nitric oxide synthase (eNOS) is increased in the hippocampus during exercise (Moon et al., 2006). However, the upstream regulatory factor on the eNOS expression in the hippocampus during exercise has not been clear. In this study, we investigate the role of acetylcholine (ACh) as a regulatory factor for the eNOS expression and activity in the hippocampus during exercise. The results of the present study demonstrate that voluntary wheel running exercise for two weeks increases the expression and activity eNOS. In addition, choline acetyltransferase (ChAT) immnunoreacitvity within the hippocampus was increased after 2 weeks exercise. We further found that the upregulation of ACh with treatment of physostigmine, a booster of ACh releasing, increase the expression and activity of eNOS in the hippocampus. This present study provides the evidence that the upregulation of eNOS during exercise may be mediated by ACh in the hippocampus.
Acetylcholine ; Choline ; Choline O-Acetyltransferase ; Hippocampus ; Nitric Oxide Synthase Type III ; Physostigmine ; Running ; Up-Regulation

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Expression of H(+)-ATPase in Inner Medullary Collecting Duct Cells of Aquaporin-3-Deficient Mice.

Eun Jung LEE ; Wan Young KIM ; Ki Hwan HAN ; Hyang KIM ; Jin KIM

Korean Journal of Anatomy.2003;36(5):443-455.

It has been reported that the decrease in urinary pH observed in AQP1 null mice with a urinary concentrating defect is due to upregulation of H(+)-ATPase in the IMCD. This is thought to be caused by the chronically low interstitial osmolality in these animals. To explore whether increase of H(+)-ATPase expression in the IMCD is associated with changes in the prolonged decrease of interstitial osmolality, we examined the expression of H(+)-ATPase and Na(+)-H(+) exchanger (NHE3) using light and electron microscopic immunocytochemistry in the kidneys of AQP3 null mice which are polyuric and manifest a urinary concentrating defect because of an inability to create a hypertonic medullary interstitium. In both AQP3 (-/-) and AQP1 (-/-) mouse kidneys, type A intercalated cells in cortical and medullary collecting ducts are slightly activated, and strong H(+)-ATPase immunostaining was present in the apical plasma membrane of IMCD cells, whereas no H(+)-ATPase labeling was observed in IMCD cells in wild type mice. No differences of the immunoreactivity for NHE3 in the proximal tubule and thick ascending limb of loop of Henle were observed between AQP3 or AQP1 (-/-) mice and AQP3 (+/+) mouse. These results suggest that the induction of H(+)-ATPase expression in IMCD cells of AQP3 null mice, as well as AQP1 null mice, may be related to their chronically low interstitial osmolality.
Animals ; Cell Membrane ; Hydrogen-Ion Concentration ; Immunohistochemistry ; Kidney ; Loop of Henle ; Mice* ; Osmolar Concentration ; Proton-Translocating ATPases* ; Up-Regulation

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Expression of Activating Transcription Factor 3 in Ischemic Penumbra Region Following Focal Cerebral Ischemia.

Dae Yong SONG ; Kyoung Min OH ; Ji Hye LEE ; Ran Sook WOO ; Yun Jeong LEE ; Jung Tae HAN ; Tai Kyoung BAIK

Korean Journal of Anatomy.2008;41(3):173-183.

It has been demonstrated that some of immediate early genes (IEGs) such as c-Jun or fos are induced immediately following neuronal injury and they play an important role in determining the fate of the injured neurons. Of IEGs, the activating transcription factor 3 (ATF3) is focused by many investigators, because they are expressed in various types of neural insults and have been known to serve a diverse function in both neuronal survival and death. However, little is known about the functional role of ATF3 in ischemic brain injury. So in this study, the authors examined the expression pattern of the activating transcription factor 3 (ATF3) following middle cerebral artery (MCA) occlusion-reperfusion injury. According to the findings obtained by triphenyltetrazolium chloride (TTC) stains, the authors have classified the infarcted area into two regions, the ischemic core region and the ischemic penumbra region. In both regions, many neurons underwent neuronal degeneration, characterized by the shrunken nuclei with eosinophilic perikaryon. The H & E stain also demonstrated the increased number of probable activated astrocytes and microglia in the ischemic brain regions and this was confirmed by GFAP- and OX42-immunohistochemistry. Immunohistochemical study for ATF3 also demonstrated the specific upregulation of ATF3 in the nuclei of neurons under ischemic injury, but not in those of the contralateral regions. Interestingly, the number of the ATF3 positive neurons in the ischemic penumbra regions outnumbered that of the ischemic core regions. Based on many reports that the neuronal death in ischemic penumbra region is caused by programed cell death rather than by necrosis which is main cause of neuronal death in ischemic core region, our results could suggest that the ATF3 is an important IEGs which determine the fate of the ischemic neurons.
Activating Transcription Factor 3 ; Astrocytes ; Brain ; Brain Injuries ; Brain Ischemia ; Cell Death ; Coloring Agents ; Eosinophils ; Genes, Immediate-Early ; Humans ; Microglia ; Middle Cerebral Artery ; Necrosis ; Neurons ; Research Personnel ; Tetrazolium Salts ; Up-Regulation

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