11:10-12:00, Rm 103

OthersU-18-25Suppressed expression of Hsp60 by siRNA affects mitochondrialprotein’s transportSung-Hun Bae, Gun-Hyun Park, Myung-Jin Kim, Jae-Hyoung Park and You-JinHwangDivision of Biological science, Gachon University of Medicine and Science, Inchon 406-799, KoreaMitochondria usually exist in cell at large number, produce ATP by oxidativephosphorylation and play important role at lipid metabolism and apoptosis. Furthermore,they carry out many functions for living cell. Mitochondria can divide into threecompartments outter membrane, intermembrane space and matrix. These compartmentshas its indigenous protein subunits and these proteins are necessary for normal functionsof mitochondria. One of these proteins, Hsp60 function like chaperon. Hsp60 binds withCytochrome b2 and maintains its structure unfolding. In this way, Cytochrome b2 can betransported to intermembrane space where its final destination. Not only Cytochrome b2,but many enzymes, functional protein precursors are the main target of Hsp60. Whenthese precursors bind with Hsp60, it maintains precursors’s state folding or unfolding totransport it appropriate site. In this study, we use siRNA that suppresses expression ofHsp60 to know how it affects mitochondria and cell. We carried out western blotting ofnon-Hsp60 cell protein and control cell protein. After compare two results, we found thatthere are some differences.U-18-28Topical application of Polygonum multiflorum extract induces hairgrowth of resting hair follicles through upregulating Shh and betacateninexpression in C57BL/6 miceHye-Jin Park, Nannan Zhang and Dong Ki ParkDepartment of Bioscience and Biotechnology, Konkuk University, 1 Hwayang-dong, Kwangjin-gu,Seoul 143-701, KoreaEthnopharmacological relevance: Polygonum multiflorum has traditionally been used fortreating patients suffering from baldness and hair loss in East Asia. Aim of the study: Thepresent study sought to investigate the hair growth promoting activities of Polygonummultiflorum and its mechanism of action. Materials and methods: The Polygonummultiflorum extract was topically applied to the shaved dorsal skin of telogenic C57BL6/Nmice. To determine the effect of Polygonum multiflorum extract in telogen to anagentransition, the expression of beta-catenin and Sonic hedgehog (Shh) was determined byimmunohistochemistry analysis. Results: Polygonum multiflorum extract promoted hairgrowth by inducing anagen phase in telogenic C57BL6/N mice. In Polygonum multiflorumextract treated group, we observed increase in the number and the size of hair folliclesthat are considered as evidence for anagen phase induction. Immunohistochemicalanalysis revealed that earlier induction of beta-catenin and Shh were observed inPolygonum multiflorum extract treated group compared to that in control group.Conclusion: These results suggest that Polygonum multiflorum extract promotes hairgrowth by inducing anagen phase in resting hair follicles.U-18-26Reactive oxygen species mediates mitochondrial DNA deletion viaimpairment of mitochondria biogenesis in ionizing radiation-inducedcellular senescenceHyeon-Soo Eom, Hae-Ran Park, Changhyun Roh, Uhee JungAdvanced Radiation Technology Institute (ARTI), Korea Atomic Energy Research Institute(KAERI), 1266 Jeonbuk, KoreaMitochondrial DNA(mtDNA) deletion is a well-known marker for oxidative stress andaging. MtDNA biogenesis genes, nuclear respiratory factor-1(NRF-1) and mitochondrialtranscription factor A(TFAM) are essential for maintenance of mtDNA. Considering thatoxidative stress can affect mitochondrial biogenesis, we hypothesized that change ofmitochondrial biogenesis by ionizing radiation(IR)-induced reactive oxygen species(ROS)may cause mtDNA deletion. IR increased the intracellular ROS level, senescenceassociatedβ-galactosidase(SA-β-gal) activity and mtDNA common deletion(4977bp), anddecreased expression of NRF-1 and TFAM mRNA in IMR-90 cells. To confirm theincreased ROS level is essential for mtDNA deletion and change of mitochondrialbiogenesis in irrated cells, the effects of N-acetylcysteine(NAC) on irrated cells wereexamined. NAC significantly attenuated the IR-induced ROS increase, mtDNA deletionand SA-β-gal activity, and increased expression of NRF-1 and TFAM mRNA. Theseresults suggest that ROS is a key mediator of mtDNA deletion via change of mitochondriabiogenesis gene in cellular senescence induced by IR. [This work was supported byNuclear R&D Program of Ministry of Education, Science and Technology, Republic ofKorea (Grant no. 2007-2000091).]U-18-27Cathepsin B is increased by high glucose stimulus in human peritonealmesothelial cellsNam Hee Jung¹and Jin Hyun Jun¹ , ², Su Ah Sung*¹Eulji Medi Bio Research Institute, Gyeonggi do 461-713, ²Department of Bio-Medical LaboratoryScience, Eulji University, Gyeonggi do 461-713, Department of Internal Medicine and Division ofNephrology, Eulji Medical Center, Seoul 139-872, Korea *CorrespondBackground. Peritoenal dialysis (PD) is a life saving treatment for end stage renal diseasepatients. However, the chronic exposure to high glucose of PD solutions causesperitoneal fibrosis which is associated with change in solute transport rate and with ultrafiltrationfailure. In peritoneal fibrosis, previous studies about the extracelluar matrixdegradation were limited in the matrix metalloproteinase. Cathepsin B, a potentlysosomal cystein protease, degrades extracellular matrix. Its activity was higher in theaneurismal aortic wall than in aortic wall of patients with occlusive disease. We aimed toevaluate whether cathepsin B secretion is increased by glucose stimulation in humanperitoneal mesothelial cells (HPMC) Methods. HPMCs were obtained by commercial cellline (MeT-54) and primary culture obtained from the pieces of human omentum duringelective gastric surgery. The mesothelial cell characterization was confirmed by thecobblestone appearance. The activity of cathepsin B was measured in supernatant of theconditioned cells (control, mannitol 83.3mM and 236.1mM, glucose 83.3mM (1.5%) and236.1mM (4.5%), and LPS 5ug/ml) at 6 hour by ELISA. Results. The secretion ofcathepsin B is much increased with the osmotic (1.26 and 1.54 ng/mL), glucose stimuli(1.00 and 2.13 ng/ml) and LPS treatment (1.33 ng/mL) than control (0.87ng/ml) byconcentration dependent pattern. Conclusion. Cathepsin B is secreted by HPMC and itsexcretion is increased by high glucose stimulus. Its role in peritoneal fibrosis need to bestudied by further iv vivo studies.344 Korean Society for Biochemistry and Molecular BiologyU-18-29Constitutive overexpression ofId-1 in mammary glands of transgenicmice results in precocious and increased formation of terminal end buds,enhanced alveologenesis, delayed involutionDONG-HUI SHIN¹, SI-HYONG JANG¹, BYEONG-CHEOL KANG², HYUN-JUN KIM¹,SEUNG HYUN OH³, AND GU KONG¹ , ⁴ , *¹Department of Pathology, College of Medicine, Hanyang University, Seoul, Korea, ²Departmentof Laboratory Animal Medicine, College of Medicine, Seoul National University, Seoul, Korea,³Division of Basic and Applied Sciences, National Cancer Center, Gyeonggi-do, Korea, ⁴Institutefor Bioengineering and Biopharmaceutical Research, Hanyang University, Seoul, KoreaInhibitor of differentiation-1 (Id-1) has been shown to play an essential role in cellproliferation, invasion, migration, and anti-apoptosis. However, the effect of Id-1 inmammary gland development remains unknown. Here, we generated MMTV-Id-1transgenic mice to study the role of Id-1 in mammary gland development. In virgin mice,Id-1 overexpression led to precocious development and delayed regression of terminalend buds compared with wild-type mice. The number of BrdU, β-catenin and cyclin D1-positive cells were increased in Id-1 transgenic mice. Id-1 transgenic mice had morelobulated and prominent alveolar budding than wild-type mice and had significantlygreater counts of lobuloalveolar structures in early pregnancy. Moreover, Id-1 regulatedthe Bcl-2 and Bax expression, and resulted in delay of apoptotic peak during involution.We also found that Id-1 was able to modulate expression of the regulators of Wnt/βcateninsignaling such as phospho-Akt, BMP2, FGF3, and RAR-βin tubuloalveolardevelopment of mammary glands. Taken together, our results suggest that Id-1 plays apivotal role in mammary gland development through Wnt signaling-mediated accelerationof precocity and alveologenesis and Bcl-2 family members-mediated delay of involution.U-18-30The changed expression of CXCR2-related chemokine by FGF2 in theosteoblast and endothelial cells supports the migration of hematopoieticstem and progenitor cellKyung-Ae Yoon¹, Hye-Sim Cho¹and Je-Yoel Cho¹ , *¹Department of Biochemistry, School of Dentistry, Kyungpook National University, Daegu, KoreaThe maintenance of stem cells requires a specific microenviroment. HSC (hematopoietic stem cell)niche could mainly distinguish the osteoblast (OB) niche that maintains a quiescent HSCmicroenviroment and the vascular niche that regulates the proliferation, differentiation, andmobilization of HSC. SDF-1-CXCR4 signaling is essential for hematopoiesis. Recent reportshowed that the reduction of SDF-1 were affected the expression of OB niche-related factors inbone marrow (BM) stromal cells of the conditioned knockout mice model and systemicadministration of FGF2 failed normal hematopoiesis in the BM by the reduced SDF-1. However,FGF2 signaling was important regulator of endothelial cell angiogenesis by increased SDF-1.Therefore, we hypothesized FGF2 induces a change of HSCs migration in BM and investigatedimportant factors of HSCs migration using microarray chip. We firstly confirmed FGF2 decreasedthe expression of HSC niche-related genes in the primary OB but not in C166 cells. We selectedthe changed gene that function in extracellular region during FGF2 treatment by gene chipanalysis. We were confirmed selected genes by qRT-PCR and identified CXCR2-relatedchemokine candidate. Chemotaxis assay showed this selected chemokine induced the migration ofhematopoietic stem and progenitor cells (HSPCs). According to these results, FGF2 induced thechange of chemokine expression and finally this difference between OB and C166 cells affectedthe migration of HSPCs in the BM. To investigate mechanism about the different of CXCR2-relatedchemokine expression by FGF2, we are sure to FGFR type. This work was supported by the KoreaScience and Engineering Foundation (KOSEF) grant funded. (Grant NO. 2009-0077615)