http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Yun, Seung Pil,Han, Yong-Seok,Lee, Jun Hee,Yoon, Yeo Min,Yun, Chul Won,Rhee, Peter,Lee, Sang Hun SPANDIDOS PUBLICATIONS 2017 MOLECULAR MEDICINE REPORTS Vol.16 No.5
<P>Cellular prion protein (PrP<SUP>C</SUP>) can replace other pivotal molecules due to its interaction with several partners in performing a variety of important biological functions that may differ between embryonic and mature stem cells. Recent studies have revealed major advances in elucidating the putative role of PrP<SUP>C</SUP> in the regulation of stem cells and its application in stem cell therapy. What is special about PrP<SUP>C</SUP> is that its expression may be regulated by hypoxia-inducible factor (HIF)-1α, which is the transcriptional factor of cellular response to hypoxia. Hypoxic conditions have been known to drive cellular responses that can enhance cell survival, differentiation and angiogenesis through adaptive processes. Our group recently reported hypoxia-enhanced vascular repair of endothelial colony-forming cells on ischemic injury. Hypoxia-induced AKT/signal transducer and activator of transcription 3 phosphorylation eventually increases neovasculogenesis. In stem cell biology, hypoxia promotes the expression of growth factors. According to other studies, aspects of tissue regeneration and cell function are influenced by hypoxia, which serves an essential role in stem cell HIF-1α signaling. All these data suggest the possibility that hypoxia-mediated PrP<SUP>C</SUP> serves an important role in angiogenesis. Therefore, the present review summarizes the characteristics of PrP<SUP>C</SUP>, which is produced by HIF-1α in hypoxia, as it relates to angiogenesis.</P>
윤제필 ( Je Pil Yun ),박종민 ( Jong Min Park ),윤문식 ( Moon Sik Yun ),김성용 ( Sung Yong Kim ) 한방재활의학과학회 2003 한방재활의학과학회지 Vol.13 No.4
Objective : There were few case reports on the treatment of Herpes Zoster Myelitis by oriental medicine. We experienced one case of a female patient, 33 ages, who had complants; severe neck pain and motor, sensory impairment and headache. Methods : We used acupuncture, negative, physical therapy, chuna, herbal medication. Results and Conclusions :After oriental medical treatments, clinical improvement of the neurologic impairment was noted. We expected that therapeutic value of treatment of Herpes Zoster Myelitis in the oriental medicine will be higher if more clinical studies and researches are accomplished.
Park, Jae-Won,Shin, Yun Kyung,Choen, Yong-Pil 한국발생생물학회 2014 발생과 생식 Vol.18 No.3
Adaptive development of early stage embryo is well established and recently it is explored that the mammalian embryos also have adaptive ability to the stressful environment. However, the mechanisms are largely unknown. In this study, to evaluate the possible role of aquaporin in early embryo developmental adaptation, the expression of aquaporin (AQP) 5 gene which is detected during early development were examined by the environmental condition. To compare expression patterns between in vivo and in vitro, we conducted quantitative RT-PCR and analyzed localization of the AQP5 by whole mount immunofluorescence. At in vivo condition, Aqp5 expressed in oocyte and in all the stages of preimplantation embryo. It showed peak at 2-cell stage and decreased continuously until morula stage. At in vitro condition, Aqp5 expression pattern was similar with in vivo embryos. It expressed both at embryonic genome activation phase and second mid-preimplantation gene activation phase, but the fold changes were modified between in vivo embryos and in vitro embryos. During in vivo development, AQP5 was mainly localized in apical membrane of blastomeres of 4-cell and 8-cell stage embryos, and then it was localized in cytoplasm. However, the main localization area of AQP5 was dramatically shifted after 8-cell stage from cytoplasm to nucleus by in vitro development. Those results explore the modification of Aqp5 expression levels and location of its final products by in vitro culture. It suggests that expression of Aqp5 and the roles of AQP5 in homeostasis can be modulated by in vitro culture, and that early stage embryos can develop successfully by themselves adapting to their condition through modulation of the specific gene expression and localization.
Yun, Seung Pil,Lee, Min Yong,Ryu, Jung Min,Song, Chang Hun,Han, Ho Jae American Physiological Society 2009 American journal of physiology. Cell physiology Vol.296 No.2
<P>17β-Estradiol (E2) is a steroid hormone well known for its roles in the regulation of various cell functions. However, the precise role that E2plays in the proliferation of human mesenchymal stem cells (hMSCs) has not been completely elucidated. In the present study, we examined the effects of E2on cell proliferation and the related signaling pathways using hMSCs. We showed that E2, at ≥10<SUP>−9</SUP>M, significantly increased [<SUP>3</SUP>H]thymidine incorporation after 24 h of incubation, and E2also increased [<SUP>3</SUP>H]thymidine incorporation at >6 h. Also, E2significantly increased the percentage of the cell population in the S phase based on FACS analysis. Moreover, E2increased estrogen receptor (ER), PKC, phosphatidylinositol 3-kinase (PI3K)/Akt, and MAPK phosphorylation. Subsequently, these signaling molecules were involved in an E2-induced increase of [<SUP>3</SUP>H]thymidine incorporation. E2also increased hypoxia-inducible factor (HIF)-1α and VEGF protein levels. These levels of protein expression were inhibited by ICI-182,780 (10<SUP>−6</SUP>M, an ER antagonist), staurosporine and bisindolylmaleimide I (10<SUP>−6</SUP>M, a PKC inhibitor), LY-294002 (10<SUP>−6</SUP>M, a PI3K inhibitor), Akt inhibitor (10<SUP>−5</SUP>M), SP-600125 (10<SUP>−6</SUP>M, a SAPK/JNK inhibitor), and PD-98059 (10<SUP>−5</SUP>M, a p44/42 MAPKs inhibitor). In addition, HIF-1α small interfering (si)RNA and ICI-182,780 inhibited E2-induced VEGF expression and cell proliferation. VEGF siRNA also significantly inhibited E2-induced cell proliferation. In conclusion, E2partially stimulated hMSC proliferation via HIF-1α activation and VEGF expression through PKC, PI3K/Akt, and MAPK pathways.</P>
( Yong Gu Lee ),( Woong Park ),( Sang Hoon Kim ),( Sang Pil Yun ),( Hun Jeong ),( Hyung Jong Kim ),( Dong Ho Yang ) 대한내과학회 2010 The Korean Journal of Internal Medicine Vol.25 No.1
The common causes of rhabdomyolysis include trauma, hypoxia, drugs, toxins, infections and hyperthermia. Operative insults, including direct trauma and ischemia, have the potential to cause the development of rhabdomyolysis. Pneumatic tourniquets used during arthroscopic knee surgery to prevent blood loss have led to many complications such as nerve paralysis and vascular injuries. Rhabdomyolysis can also be caused by prolonged pneumatic tourniquet application without a midapplication release, and also from an increased application pressure, but the actual incidence of this is low. In order to prevent rhabdomyolysis, the clinicians must be aware of such risks and follow strict guidelines for the application time, the midapplication release and also the inflation pressure. Vigorous hydration and postoperative patient surveillance are helpful to prevent rhabdomyolysis. We have recently experienced a case of rhabdomyolysis after the arthroscopic knee surgery, and the rhabdomyolysis could have been associated with the use of a pneumatic tourniquet. (Korean J Intern Med 2010;25:105-109)
Yun, Seung Pil,Yoon, Yeo Min,Lee, Jun Hee,Kook, Minjee,Han, Yong-Seok,Jung, Seo Kyung,Lee, Sang Hun MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.2
<P>Mesenchymal stem cells (MSCs) could be a promising solution in the treatment of various diseases including chronic kidney disease (CKD). However, endoplasmic reticulum (ER) stress induced by ischemia in the area of application limits the integration and survival of MSCs in patients. In our study, we generated ER stress-induced conditions in MSCs using <I>P</I>-cresol. As <I>P</I>-cresol is a toxic compound accumulated in the body of CKD patients and induces apoptosis and inflammation through reactive oxygen species (ROS), we observed ER stress-induced MSC apoptosis activated by oxidative stress, which in turn resulted from ROS generation. To overcome stress-induced apoptosis, we investigated the protective effects of tauroursodeoxycholic acid (TUDCA), a bile acid, on ER stress in MSCs. In ER stress, TUDCA treatment of MSCs reduced ER stress-associated protein activation, including GRP78, PERK, eIF2α, ATF4, IRE1α, and CHOP. Next, to explore the protective mechanism adopted by TUDCA, TUDCA-mediated cellular prion protein (PrP<SUP>C</SUP>) activation was assessed. We confirmed that PrP<SUP>C</SUP> expression significantly increased ROS, which was eliminated by superoxide dismutase and catalase in MSCs. These findings suggest that TUDCA protects from inflammation and apoptosis in ER stress via PrP<SUP>C</SUP> expression. Our study demonstrates that TUDCA protects MSCs against inflammation and apoptosis in ER stress by PrP<SUP>C</SUP> expression in response to <I>P</I>-cresol exposure.</P>