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Expression of placenta growth factor mRNA in the rat placenta during mid-late pregnancy
Phil-Ok Koh,Wan-Sung Choi,Gyeong-Jae Cho,Chung-Kil Won 대한수의학회 2005 Journal of Veterinary Science Vol.6 No.3
The placenta is an essential organ that synthesizes several growth and angiogenic factors for its own growth as well as fetal development. It is known that the placenta growth factor (PlGF) is a member of the vascular endothelial growth factor family and is critical for placental growth and fetal development. However, there is little information regarding the expression pattern and cellular localization of PlGF mRNA in rat placenta during pregnancy. The aim of this study was to define the distribution of PlGF mRNA in rat placenta at various gestations. RT-PCR analysis showed that the expression level of PlGF mRNA increased as gestation advanced. Using in situ hybridization histochemistry, positive cells of PlGF mRNA were detected in chorionic villi. PlGF mRNA was expressed in the trophoblast cells and stroma cells surrounding the blood vessels within chorionic villi on day 13 and 15. Also, positive signals of PlGF mRNA were strongly detected in stroma cells of chorionic villi on day 17, 19, and 21. In particular, the density and number of positive signals of PlGF mRNA was significantly increased as gestation advanced. The expression pattern of PlGF mRNA in rat placenta during pregnancy demonstrates that PlGF plays a functional role for placental growth and fetal development during mid-late pregnancy.
Chung, Phil-Sang,He, Peijie,Shin, Jang-In,Hwang, Hee-Jun,Lee, Sang Joon,Ahn, Jin-Chul Landes Bioscience 2009 Cancer Biology & Therapy Vol.8 No.14
<P>Skin phototoxicity is one of the main side effects of photodynamic therapy (PDT). To overcome this problem, some new photosensitizers have been developed with longer absorbance wavelengths and shorter half-life in the body. In this study, we investigated the mechanism of PDT mediated by a new chlorophyll derivative photosensitizer, 9-hydroxypheophorbide alpha (9-HPbD), on AMC-HN-3 cancer cells. Phototoxicity and apoptosis on AMC-HN-3 cells induced by 9-HPbD was exhibited in a time- and dose-dependent manner. Mitochondria and endoplasmic reticulum (ER) were observed as preferential sites of 9-HPbD accumulation. Photoactivation of 9-HPbD-loaded AMC-HN-3 cells led to a rapid generation of reactive oxygen species (ROS) at 30 min, followed by a loss of mitochondrial membrane potential (MMP) at 2 h, translocation of apoptosis-inducing factor (AIF) at 2 h, and the release of cytochrome c at 3 h following PDT. Caspase-12, an important caspase involved in ER-induced apoptosis, and C/EBP homologous protein (CHOP), an ER stress inducible transcription factor, were also upregulated after PDT (3-12 h and 6-12 h, respectively). Subsequently, activation of caspase-9 at 6 h, caspase-3 and PARP at 12 h also occurred in PDT-treated AMC-HN-3 cells. The above observations demonstrate that both mitochondria and ER serve not only as the sites of sensitizer binding, but also the subcellular targets of 9-HPbD-PDT, effective activation of which is responsible for 9-HPbD PDT-induced apoptosis in AMC-HN-3 cells.</P>
Phil-Ok Koh,Chung-Kil Won,Jae-Hyun Cho,Oh-Sung Park,Myeong-Ok Kim,Jin-Hee Sung 한국실험동물학회 2007 Laboratory Animal Research Vol.23 No.2
Severe diabetes in pregnant rats increases the risk for embryonic abnormalities. This study investigated whether diabetes in pregnant rats lead to apoptotic cell death in the placenta. Diabetes was induced by a single intravenous injection of streptozotocin (35 ㎎/㎏) on day 0 of pregnancy, blood and tissue samples were collected on day 20. In the diabetic group, maternal body weight significantly decreased, and TUNEL-positive cells increased in the trophoblast cells within the placental villi. Expression of Bcl-2 and Bcl-XL decreased in the diabetic group, compared to those of control group. While, the levels of Bax and Caspase-3 increased in diabetic group, compared to controls. Our findings demonstrate that streptozotocin-induced diabetes leads the apoptotic cell death of placental tissue through the regulation of Bcl-2 family protein levels, such as Bcl-2, Bcl-XL, and Bax.
Proteomic Analysis of Pancreata from Mini-Pigs Treated with Streptozotocin as Type I Diabetes Models
( Phil Young Lee ),( Sung Goo Park ),( Eun Young Kim ),( Myung Sup Lee ),( Sang J. Chung ),( Sang Chul Lee ),( Dae Yeul Yu ),( Kwang Hee Bae ) 한국미생물 · 생명공학회 2010 Journal of microbiology and biotechnology Vol.20 No.4
Adsorption of Heavy Metal Ions onto Chemically Oxidized Ceiba pentandra (L.) Gaertn. (Kapok) Fibers
Chung, Byung-Yeoup,Cho, Jae-Young,Lee, Min-Hee,Wi, Seung-Gon,Kim, Jin-Hong,Kim, Jae-Sung,Kang, Phil-Hyun,Nho, Young-Chang The Korean Society for Applied Biological Chemistr 2008 Journal of Applied Biological Chemistry (J. Appl. Vol.51 No.1
The physico-chemical properties of kapok fibers were altered via the combination processes of chlorite-periodate oxidation, in order to assess their efficacy as a heavy metal adsorbent. The chemically-oxidized kapok fibers were found to harbor a certain amount of polysaccharides, together with lowered lignin content. This alteration in lignin characteristics was clearly confirmed via FTIR and NBO yield. Moreover, chemically oxidized kapok fibers retained their hollow tube shape, although some changes were noted. The chemically oxidized kapok fibers evidenced elevated ability to adsorb heavy metal ions with the best fit for the Langmuir adsorption isotherm model. Three cycles of adsorption-desorption were conducted with in-between regeneration steps. Our experimental results indicated that chemically oxidized kapok fibers possessed excellent adsorption characteristics, and the modified kapok fibers could be completely regenerated with almost equimolar diluted sodium hydroxide. Pb, Cu, Cd and Zn ions evidenced adsorption rates of 93.55%, 91.83%, 89.75%, and 92.85% on the chemically oxidized kapok fibers. The regeneration efficiency showed 73.58% of Pb, 71.55% of Cu, 66.87% of Cd, and 75.00% of Zn for 3rd cycle with 0.0125N NaOH.
Chung, Soon-Hyo,Ha, Heon-Phil,Jung, Woo-Sang,Byun, Ji-Young The Iron and Steel Institute of Japan 2006 ISIJ international Vol.46 No.10
<P>An <I>ab initio</I> study was carried out on interface energies, misfit strain energies, and electron structures at coherent interfaces between bcc Fe and MCs (NaCl structure, M=V, Nb, Ta). The interface energies at relaxed interfaces Fe/VC, Fe/NbC, and Fe/TaC were −0.120, −0.169 and −0.158 J/m<SUP>2</SUP>, respectively. Influence of bond energy was estimated using the discrete lattice plane/nearest neighbor broken bond (DLP/NNBB) model. It was found that the dependence of interface energy on the type of carbide was closely related to changes of the bond energies between Fe, M and C atoms before and after formation of the interfaces Fe/MC. The misfit strain energies in Fe/VC, Fe/NbC, and Fe/TaC systems were 0.086, 0.891 and 0.827 eV per 16 atoms (Fe; 8 atoms and MC; 8 atoms), respectively. The misfit strain energy became larger when difference of lattice parameters between the bulk Fe and the bulk MCs increased.</P>
Sung, Jin-Hee,Cho, Eun-Hae,Cho, Jae-Hyeon,Won, Chung-Kil,Kim, Myeong-Ok,Koh, Phil-Ok The Society ; Maruzen Co. [distributor] 2012 The Journal of veterinary medical science Vol.74 No.11
<P>Ferulic acid plays a neuroprotective role in cerebral ischemia. The aim of this study was to identify the proteins that are differentially expressed following ferulic acid treatment during ischemic brain injury using a proteomics technique. Middle cerebral artery occlusion (MCAO) was performed to induce a focal cerebral ischemic injury in adult male rats, and ferulic acid (100 mg/kg) or vehicle was administered immediately after MCAO. Brain tissues were collected 24 hr after MCAO. The proteins in the cerebral cortex were separated using two-dimensional gel electrophoresis and were identified by mass spectrometry. We detected differentially expressed proteins between vehicle- and ferulic acid-treated animals. Adenosylhomocysteinase, isocitrate dehydrogenase [NAD(+)], mitogen-activated protein kinase kinase 1 and glyceraldehyde-3-phosphate dehydrogenase were decreased in the vehicle-treated group, and ferulic acid prevented the injury-induced decreases in these proteins. However, pyridoxal phosphate phosphatase and heat shock protein 60 were increased in the vehicle-treated group, while ferulic acid prevented the injury-induced increase in these proteins. It is accepted that these enzymes are involved in cellular metabolism and differentiation. Thus, these findings suggest evidence that ferulic acid plays a neuroprotective role against focal cerebral ischemia through the up- and down-modulation of specific enzymes.</P>
Chung, Tae Nyoung,Kim, Jin Hee,Choi, Bo Young,Chung, Sung Phil,Kwon, Sung Won,Suh, Sang Won unknown 2015 Stem cells translational medicine Vol.4 No.2
<P>Global cerebral ischemia (GCI) is the leading cause of a poor prognosis even after successful resuscitation from cardiac arrest. Therapeutic induction of hypothermia (TH) is the only proven therapy-and current standard care-for GCI after cardiac arrest; however, its application has been significantly limited owing to technical difficulties. Mesenchymal stem cells (MSCs) are known to suppress neuronal death after cerebral ischemia. The prevention of blood-brain barrier (BBB) disruption has not been suggested as a mechanism of MSC treatment but has for TH. We evaluated the therapeutic effect of MSC administration on BBB disruption and neutrophil infiltration after GCI. To evaluate the therapeutic effects of MSC treatment, rats were subjected to 7 minutes of transient GCI and treated with MSCs immediately after reperfusion. Hippocampal neuronal death was evaluated at 7 days after ischemia using Fluoro-Jade B (FJB). BBB disruption, endothelial damage, and neutrophil infiltration were evaluated at 7 days after ischemia by immunostaining for IgG leakage, Rat endothelial antigen-1, and myeloperoxidase (MPO). Rats treated with MSCs showed a significantly reduced FJB+ neuron count compared with the control group. They also showed reduced IgG leakage, endothelial damage, and MPO+ cell counts. The present study demonstrated that administration of MSCs after transient GCI provides a dramatic protective effect against hippocampal neuronal death. We hypothesized that the neuroprotective effects of MSC treatment might be associated with the prevention of BBB disruption and endothelial damage and a decrease in neutrophil infiltration.</P>