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Youn Kyoung SEO ; Chae Soo SHIN ; Jong Heon KIM ; Young June YOU ; Doo Jin PAIK

Korean Journal of Physical Anthropology.2003;16(4):301-311. doi:10.11637/kjpa.2003.16.4.301

Prolonged ischemic-reperfusion induces cellular damages and apoptosis in rat skeletal muscle. Reactive oxygen species generated during reperfusion time induce expression of various genes and apoptosis. Among apoptosis-related gene products, Bcl-2 and Bax regulate the apoptotic response by inhibiting and promoting cell death, respectively. The purpose of this study was to observe the age-related alertation of expression profile of Bcl-2 and Bax in rat tibialis anterior muscle and soleus muscle following ischemia-reperfusion. 9 weeks, 30 weeks, and 65 weeks old male Sprague-Dawley rats were divided into control and ischemia groups. Ischemia group was divided into 3 subgroups based on reperfusion time. For ischemia, left commom iliac artery was occulded for 4 hours using rodent vascular clamps. The animals were sacrificed at hours 0, 3 and 24 after onset of reperfusion and tibialis anterior and soleus muscles were removed. Muscle tissues were embedded in paraffin and 6 micrometer sections were made. The expression level of Bcl-2 and Bax were examined using immunohistochemical methods. The results obtained were as follows; 1. In control group, immunoreactivities (IMRs) of Bcl-2 and Bax were weak or moderate in 30 weeks old rats and were trace in 9 and 65 weeks old rat. 2. In control group, IMRs of Bcl-2 and Bax in tibialis anterior muscle were more higher than those in soleus muscle, but not significantly. 3. In ischemia group, IMRs of Bax were increased with aging. 4. In ischemia group, IMR of Bax in tibialis anterior muscle was higher than that in soleus muscle. These results suggested that the increased IMR of Bax may be related to increasing of ischemic injury, and both old skeletal muscle and tibialis anterior muscle are susceptabile to ischemic injury of rat skeletal muscle.
Male ; Humans ; Rats ; Animals

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Youn Kyoung SEO ; Chae Soo SHIN ; Jong Heon KIM ; Young June YOU ; Doo Jin PAIK

Korean Journal of Physical Anthropology.2003;16(4):291-299. doi:10.11637/kjpa.2003.16.4.291

Prolonged ischemic-reperfusion induces cellular damages and apoptosis in rat skeletal muscle. Such injury takes place in the phase of reperfusion following ischemia induction in part via regulating of apoptosis-related gene inductions. The present study was performed to examine the age-related alertation of expression of apoptosis in rat tibialis anterior and soleus muscles following ischemia-reperfusion. 9 weeks, 30 weeks, and 65 weeks old male Sprague-Dawley rats were divided into 2 groups such as controls and ischemia. For ischemia, left commom iliac artery was occulded for 4 hours using rodent vascular clamps. The tibialis anterior and soleus muscles were removed 0, 3, and 24 hours after onset of reperfusion. Muscle samples were embedded in paraffin and 6 micrometer sections were made. The apoptotic reactions was detected using TUNEL methods. The results obtained were as follows; 1. In control groups, the number of apoptosis was increased with aging, but not significantly. 2. In ischemia groups, the number of apoptosis was increased at 3 hours after ischemia, and decreased at 24 hours after ischemia. 3. In ischemia groups, the number of apoptosis was increased with aging. 4. In ischemia groups, the number of apoptosis in the tibialis anterior muscle was higher than that in soleus muscle. These results suggested that the ischemic injury of the rat skeletal muscle is increased with aging and that tibialis anterior muscle is more susceptabile to ischemic injury than soleus muscle.
Male ; Humans ; Rats ; Animals

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Changes of Apoptosis Inducing Factor in the Rat Brain with Ischemic Injury Induced by Middle Cerebral Artery Occlusion.

Young Il LEE

Korean Journal of Physical Anthropology.2003;16(4):279-289. doi:10.11637/kjpa.2003.16.4.279

It is well known that cerebral ischemia induces apoptotic neuronal cell death along with necrosis. Apoptosis is characterized by several morphological nuclear changes including chromatin condensation and nuclear fragmentation. These changes are triggered by the activation of members of caspase family, caspase activated DNase, and several novel proteins. A novel gene, the product of which caused chromatin condensation and DNA fragmentation, was recently identified, cloned, and designated apoptosis inducing factor (AIF). AIF is a mitochondrial flavoprotein (prosthetic group: flavin adenine dinucleotide) with significant homology to plant ascorbate reductase and bacterial NADH oxidase, and is normally confined to the mitochondrial space. In a variety of different apoptosis-inducing conditions, AIF translocates through the outer mitochondrial membrane to the cytosol and the nucleus. Thus, similar to cytochrome c, AIF is a phylogenetically old, bifunctional protein with an oxidoreductase function and a second apoptogenic function. In this study, to investigate changes of AIF expression levels in the rat brain during various time periods (6, 12, 18, 24 hrs) of ischemic insults, we performed permanent middle cerebral artery (MCA) occlusion model using male SD rats and the extent of ischemic injury was measured by 2% TTC (2, 3, 5-triphenyl tetrazolium chloride) staining. There were numerous TUNEL-positive neuronal cell nuclei, which implies apoptotic cell death in the areas with ischemic insult. Western blot analysis was performed with separate samples (cytosolic fraction & mitochondrial fraction). This method was designed to investigate if the expression of AIF is really increased during ischemic injury, or the increased AIF activity is caused by its release from the mitochondrial inter-membrane space to cytosol. In the immunohistochemical study using polyclonal anti-AIF antibody revealed overall distribution of AIF in the rat brain including cerebral cortex, basal ganglia and also in hippocampus that is especially sensitive to ischemia. There was apparently increased AIF immunoreactivity in the nucleus accumbens of ischemia-induced hemisphere compared to contralateral control hemisphere. Our results seem to be the first evidence on the involvement of AIF in the apoptotic neuronal cell loss with ischemic insult and will provide some clues to the pathophysiology of neuronal apoptosis induced by ischemic insult. Further researches will reveal functional relationship between AIF and other factors involved in chromatin condensation and degradation and whether AIF itself will be useful as a caspase-independent, Bcl-2-independent death inducer.
Male ; Humans ; Rats ; Animals

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Attenuated Ceramide-induced Neuronal Apoptosis by Acanthopanax senticous.

Do Yeon LEE ; Dae Seong KIM ; Dong Suep SOHN ; Sung Su KIM ; Kyung Yong KIM ; Won Bok LEE

Korean Journal of Physical Anthropology.2003;16(4):267-277. doi:10.11637/kjpa.2003.16.4.267

Both Acanthopanax senticosus and Acorus gramineus Soland are typical Oriental herbs. They have been used as a tonic, anti-rheumatic, anti-inflammatory, anti-stress, anti-cancer agent. But, it is still unclear how they effectively regulate their various biological properties. Ceramide is emerging as a second messenger of apoptotic cell death and there is increasing evidence that ceramide is involved in neurodegenerative disease and the process of senescence. The present study investigated the different effects of A. senticosus and A. gramineus on ceramide-induced apoptosis in human neuroblastoma SK-N-SH cells. We showed that ceramide induced apoptosis through the mediation of reactive oxygen species(ROS) production and A. senticosus, as an effective antioxidant, significantly inhibited the increase of ROS generation, thereby preventing apoptosis. Furthermore, an increase of caspase activity (apoptosis executors) resulted from ceramide reduced by A. senticosus. But A. gramineus had almost no protective effects. These results implicate that ROS play on important roles in ceramide-induced apoptosis, also A. senticosus protects effectively via inhibition of ROS generation by ceramide through selective pathway.
Humans ; Neuroblastoma

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Development of In Vitro Blood-Brain Barrier Model with Bovine Brain Microvessel Endothelial Cells.

Dong Suep SOHN ; Kyung Yong KIM ; Dae Jin KIM ; Ki Jeong KIM ; In Ja LIM ; Sung Su KIM ; Won Bok LEE ; Dae Joong KIM ; Seung Kyu BANG ; Hee Sang LEE

Korean Journal of Physical Anthropology.2003;16(4):257-265. doi:10.11637/kjpa.2003.16.4.257

The in vitro blood-brain barrier (BBB) model was established with bovine brain microvessel endothelial cells (BBMECs). The characteristics of BBMECs were identified by morphological and functional studies. BBMECs began to grow as spindle shaped cells and distinctly formed the monolayer of whirling appearance by 6 to 7 days after plating. Transendothelial electrical resistance (TEER) of the monolayer increased through 11 days and then started to decrease. The gamma-GTP activity (1791.5+/-397.8 nmol/min/mg of protein) and alkaline phosphatase activity (15.0+/-7.8 micromol/min/mg of protein) were high. BBMECs in culture were characterized by the binding of anti-vWF, anti-ZO-1, anti-vimentin, and anti-fibronectin antibodies. They failed to react with anti-GFAP, anti-GalC, and antineurofilament 160/200 kD antibodies, markers for astrocyte, oligodendrocyte, and neuron, respectively. Decreasing order of the permeability through the BBMEC monolayers of paracellular transport model drugs was mannitol, sucrose, and PEG-4000. The permeability of transcellular transport model drugs, progesterone and propranolol was much higher than that of paracellular transport model drugs. The BBMECs cultured on porous membrane have been qualified as an in vitro BBB model and also can be used for the BBB transport study in the drug development and for the BBB transport mechanism of drugs.

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Postnatal Development of Transforming Growth factor-alpha-immunoreactive Neurons in the Diencephalon of the Rat.

Young Lan PARK ; Hong Soon KIM ; Jae Wook OH ; Jong Joong KIM ; Jeong Seok MOON ; Sang Bong JEONG ; Yoon Young CHUNG

Korean Journal of Physical Anthropology.2003;16(4):233-255. doi:10.11637/kjpa.2003.16.4.233

Transforming growth factor-alpha (TGF-alpha) immunoreactivity during postnatal development was examined in the rat diencephalon using immunohistochemistry. The time of appearance and localization of TGF-alpha immunoreactivity was slightly different in many areas of diencephalon during postnatal development. At birth, TGF-alpha immunoreactivity was mainly evident in thalamic medial, median and parafascicular thalamic nucleus of intralaminar nuclei. In addition, TGF-alpha immunoreactivity was clearly evident at the first postnatal week in most hypothalamic nuclei. Therefore, TGF-alpha immunoreactivity was found at postnatal days 7 in most diencephalic nuclei excepting the vental posterior thalamic nuclei, metathalamus and epithalamus. The quantitative increase of number was first apparent in the midline structures of thalamus in the first postnatal week. And then TGF-alpha-immunoreactive cells progressively increased throughout diendephalon by postnatal days 15. Adult patterns were reached at postnatal days 20. These results indicate that TGF-alpha-immunoreactive cells were first appeared in thalamic midline structures, increased progressively in the first two postnatal weeks, and followed mediolateral gradient. In addition to maturation of TGF-alpha-immunoreactive cells requires a relatively prolonged period of time to achieve an adult configuration. Also, the early appearance of TGF-alpha immunoreactivity in most diencephalic nuclei may be related to the early appearance of EGFR immunorecativity in many other brain regions. Taken together, these findings suggest that TGF-alpha immunoreactivity correlated with the appearance of the related functional activity in the different regions of diencephalon.
Adult ; Male ; Female ; Humans ; Rats ; Animals

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Study on the Bcl-2 Expression in Korean Fetal Development Using a Tissue-array Technique.

Young Bok YOO ; Young Il LEE ; Byung Lan LEE

Korean Journal of Physical Anthropology.2003;16(4):225-232. doi:10.11637/kjpa.2003.16.4.225

Apoptosis is a genetically programmed cell death that is required for morphogenesis during embryogenic development and for tissue homeostasis in adult organisms. Although apoptosis is important in the development, expression of apoptosis-related genes has been studied mostly in the cancers and neurodegenerative diseases. We intended to obtain the basic data in order to understand the role of the apoptosis-related genes including bcl-2 in the apoptosis in the human development. Immunohiostochemistry for Bcl-2 was performed using Korean fetal lung, kidney, thymus, placenta, testis, small intestine, pancrease, skin, urinary bladder tissues in the 14~30 weeks of the human development. Our results showed that Bcl-2 appeared in early stages of human development in the lung, kidney, thymus, placenta, small intestine, pancreas. As differentiation grew, expression of Bcl-2 decreased and had the tendency of localizing in the bronchial epitheliums, tubular epitheliums, Bowman's epithelium, lymphocytes, synchytial trophoblasts, intestinal epitheliums, ganglionic cells, ductal epitheliums of pancreas. We suggested that in the early stages when differentiation didn't occur cell death was suppressed, in the late stages when differentiation was achieving cell death increased to remove the innecessary portions of the organs to protect the specific cells of the organs having functions. For the efficiency of the experiment, a high-throughput technique, a tissue-array method was applied which contributed to save time, money and labor without performance errors. Tissue-array technique will be useful to fasten the developmental studies.
Adult ; Male ; Female ; Humans

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Immunohistochemical and Electron Microscopic Study on the Depigmentation Effect of Melanoston.

Ho Sam CHUNG ; Chul OH ; Byung Chan KANG ; Ho Kwon JUNG

Korean Journal of Physical Anthropology.2003;16(4):213-224. doi:10.11637/kjpa.2003.16.4.213

The present study was designed to address whether melanoston which was extracted from yeast was able to induce depigmentation of the skin in guinea pigs. The activity of tyrosinase which participates in the synthesis of melanin pigment residing in melanocytes of guinea pig's epidermis was assessed using immunohistochemical staining methods with anti-tyrosinase antibody. To determine whether melanoston affects the processes of melanin synthesis in melanosome of melanocytes, melanoston-applied skin was examined by electron microscopy following immunogold tagging methods. We obtained results as follows: 1. The activity of tyrosinase was the lowest 3 weeks after application of 0.1 and 0.01% melanoston on the skin of guinea pigs. 2. The frequency of immunogold particles distributed in melanocytes and keratinocytes was lowest 3-4 weeks after application of 0.5 and 0.1% melanoston. Thus, these results suggest that melanoston has a potential to inhibit synthesis and distribution of melanin in the epidermis.

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Database Linkage Study on the Demographic Characteristics of Korean Cadaver Donors.

Young Il LEE

Korean Journal of Physical Anthropology.2003;16(4):205-211. doi:10.11637/kjpa.2003.16.4.205

In the past, all cadaver dissections for the education of medical students were performed with one who has sickened and died unidentified by the roadside. Recently, needs for cadaver donations are increasing more and more due to decrease of unidentified dead bodies with economical development and improvement of environment. However, in spite of increasing cadaver donations, demographic studies on the cadaver donors haven't been performed until now. In this study, demographic characteristics such as sex, age, cause of death, and educational level on 107 cadaver donors from 1998 to 2000 were investigated and compared them to the data from 'annual report on the cause of death statistics' published by national statistical office. Male cadaver donors occupied 71.9% (77 persons) and female occupied 28.1% (30 persons). Age related proportions revealed 16.8% with ages over 70, 23.4% with ages from 60 to 69, 28.0% with ages from 50 to 59, 17.8% with ages from 40 to 49, 10.3% with ages from 30 to 39, and only 3.7% with ages less than 30. Most frequent causes of death among the cadaver donors were diseases from malignant neoplasm (35.7%) and circulatory system (33.9%). Educational levels above high-school graduation occupied 49.5% among cadaver donors whereas proportion of educational levels above high-school graduation among overall dead persons in 1998 was only 19.7%. Results from this study could be practiced as important basic data base for the expansion of cadaver donation campaigns and organized regular future studies on the demographic characteristics of cadaver donors.
Female ; Male ; Humans

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Bcl-2 Family and Caspases are Involved in CoCl2-Induced Apoptosis of PC12 Cells.

Ji Yeon JUNG ; Hee Ju PARK ; Sun Hun KIM ; Won Jae KIM

Korean Journal of Physical Anthropology.2006;19(2):137-148. doi:10.11637/kjpa.2006.19.2.137

Hypoxic/ischemic condition induces the neuronal apoptotic events, consequently resulting in neuronal damages. Cobalt chloride (CoCl2) could mimic the hypoxic condition including the production of reactive oxygen species (ROS). This study aimed to investigate the roles of Bcl-2 family and caspases as central regulators of apoptosis, in CoCl2-induced apoptosis of PC12 cells. Cell viability was determined by MTT assay and DNA fragmentation was detected by DNA laddering. The expression levels of Bcl-2, Bax, Bid, cytochrome c and Fas/APO-1 were determined by RT-PCR or Western blotting analysis in CoCl2-treated PC12 cells. Caspase-9 and caspase-3 activities were assessed using spectrophotometry and caspase-8 activity was measured with fluorospectrocytometry. Administration of CoCl2 decreased viability of cells in a dose- and time-dependent manner. Furthermore, fragmentation of the genomic DNA and apoptotic bodies were induced in CoCl2-treated PC12 cells. Bcl-2, an anti-apoptotic Bcl-2 family, was downregulated, whereas Bax, pro-apoptotic molecule, was upregulated in CoCl2-treated cells. Treatment of CoCl2 augumented the release of cytochrome c into the cytoplasm and increase of caspase-8, -9, and -3 activities. In addition, CoCl2 upregulated Fas and downregulated pro-Bid, which are known to be correlated with death receptor-mediated apoptotic signaling pathway. Therefore, these results suggest that Bcl-2 family and caspase play crucial roles in CoCl2-induced apoptosis through mitochondria- and death receptor-dependent pathways in PC12 cells.
Animals ; Apoptosis* ; Blotting, Western ; Caspase 3 ; Caspase 8 ; Caspase 9 ; Caspases* ; Cell Survival ; Cobalt ; Cytochromes c ; Cytoplasm ; DNA ; DNA Fragmentation ; Humans ; Mitochondria ; Neurons ; PC12 Cells* ; Reactive Oxygen Species ; Spectrophotometry

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