http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Oh, Hwanhee,Ryu, Je-Hwang,Jeon, Jimin,Yang, Siyoung,Chun, Churl-Hong,Park, Hongryeol,Kim, Hyung Joon,Kim, Woo-Shin,Kim, Hong-Hee,Kwon, Young-Guen,Chun, Jang-Soo Mary Ann Liebert, Inc 2012 Journal of bone and mineral research Vol.27 No.6
<P>Developing cartilage serves as a template for long-bone development during endochondral ossification. Although the coupling of cartilage and bone development with angiogenesis is an important regulatory step for endochondral ossification, the molecular mechanisms are poorly understood. One possible mechanism involves the action of Dickkopf (DKK), which is a family of soluble canonical Wnt antagonists with four members (DKK1-4). We initially observed opposite expression patterns of Dkk1 and Dkk2 during angiogenesis and chondrocyte differentiation: downregulation of Dkk1 and upregulation of Dkk2. We examined the in vivo role of Dkk1 and Dkk2 in linking cartilage/bone development and angiogenesis by generating transgenic (TG) mice that specifically express Dkk1 or Dkk2 in chondrocytes, hypertrophic chondrocytes, or endothelial cells. Despite specific expression pattern during cartilage development, chondrocyte- and hypertrophic chondrocyte-specific Dkk1 and Dkk2 TG mice showed normal developmental phenotypes. However, Dkk1 misexpression in endothelial cells resulted in defects of endochondral ossification and reduced skeletal size. The defects are caused by the inhibition of angiogenesis in developing bone and subsequent inhibition of apoptosis of hypertrophic chondrocytes and cartilage resorption.</P>
Recombinant TRPV1 as a Potential Material for Detecting Several Agonists with FET Sensor
Siyoung HA,Oh Seok KWON 한국생물공학회 2021 한국생물공학회 학술대회 Vol.2021 No.4
The Transient Receptor Potential Vanilloid 1 (TRPV1) channel is an appear target for the treatment of pain with a unique expression profile in marginal nociceptors and the ability to show various activation. Several agonists of endogenous and exogenous nature have been described for ion channel. TRPV1 initially identified as the receptor for interaction with capsaicin, temperature greater than 43 °C, acidic conditions and leads to a painful, burning sensation. Based on this, the objective of this study was to test the antigenic potential of the recombinant TRPV1 protein for subsequent use in diagnostic tests. The TRPV1 expressed in the Escherichia coli strain BL21 was conformed from experimentally using ELISA and Western blotting and then the recombinant TRPV1 were applied with the surface of receptor to detect target material and improve sensing performance. Finally, we demonstration of the liquid-ion gated system based GFET biosensor for detection of TRPV1 receptor’s agonists, with highly sensitivity, selectivity and rapid responses in real-time.
Siyoung Ha,Oh Seok Kwon 한국진공학회 2021 한국진공학회 학술발표회초록집 Vol.2021 No.2
The ACE2 is an appear target for the spike SI protein on Coronavirus specifically SARS-CoV and SARS-CoV-2. The expression of ACE2 in cortical neurons and glials makes them susceptible to SARS-CoV and CoV-2 attack, a possible basis for the occurrence of olfactory syndrome and neurological deficits seen in COVID-19. When the Spike SI protein binds to the enzymatic domain of ACE2 on the cell surface, viruses and enzymes are transfected into the cell. Based on this, the objective of this study was to test the antigenic potential of the recombinant ACE2 protein for subsequent use in diagnostic test.
Hypoxia-inducible factor-2α is a catabolic regulator of osteoarthritic cartilage destruction
Yang, Siyoung,Kim, Jonghwan,Ryu, Je-Hwang,Oh, Hwanhee,Chun, Churl-Hong,Kim, Byoung Ju,Min, Byoung Hyun,Chun, Jang-Soo Nature Publishing Group 2010 Nature medicine Vol.16 No.6
<P>Osteoarthritic cartilage destruction is caused by an imbalance between anabolic and catabolic factors. Here, we show that hypoxia-inducible factor-2 alpha (HIF-2 alpha, encoded by EPAS1) is a catabolic transcription factor in the osteoarthritic process. HIF-2 alpha directly induces the expression in chondrocytes of genes encoding catabolic factors, including matrix metalloproteinases (MMP1, MMP3, MMP9, MMP12 and MMP13), aggrecanase-1 (ADAMTS4), nitric oxide synthase-2 (NOS2) and prostaglandin-endoperoxide synthase-2 (PTGS2). HIF-2 alpha expression was markedly increased in human and mouse osteoarthritic cartilage, and its ectopic expression triggered articular cartilage destruction in mice and rabbits. Moreover, mice transgenic for Epas1 only in chondrocytes showed spontaneous cartilage destruction, whereas heterozygous genetic deletion of Epas1 in mice suppressed cartilage destruction caused by destabilization of the medial meniscus (DMM) or collagenase injection, with concomitant modulation of catabolic factors. Our results collectively demonstrate that HIF-2 alpha causes cartilage destruction by regulating crucial catabolic genes.</P>
Yang, Siyoung,Ryu, Je-Hwang,Oh, Hwanhee,Jeon, Jimin,Kwak, Ji-Sun,Kim, Jin-Hong,Kim, Hyun Ah,Chun, Churl-Hong,Chun, Jang-Soo H. K. Lewis 2015 Annals of the rheumatic diseases Vol.74 No.3
<P><B>Objective</B></P><P>Hypoxia-inducible factor 2α (HIF-2α), encoded by <I>Epas1</I>, causes osteoarthritic cartilage destruction by regulating the expression of matrix-degrading enzymes. We undertook this study to explore the role of nicotinamide phosphoribosyltransferase (NAMPT or visfatin) in HIF-2α-mediated osteoarthritic cartilage destruction.</P><P><B>Methods</B></P><P>The expression of HIF-2α, NAMPT and matrix-degrading enzymes was determined at the mRNA and protein levels in human osteoarthritis (OA) cartilage, mouse experimental OA cartilage and primary cultured mouse chondrocytes. Experimental OA in mice was induced by destabilisation of the medial meniscus (DMM) surgery or intra-articular injection of Ad-<I>Epas1</I> or Ad-<I>Nampt</I> in wild-type, <I>Epas1</I><SUP>+/−</SUP>, <I>Epas1</I><SUP>fl/fl</SUP>;<I>Col2a1-Cre</I> and <I>Col2a1-Nampt</I> transgenic (TG) mice. Primary cultured mouse chondrocytes were treated with recombinant NAMPT protein or were infected with adenoviruses.</P><P><B>Results</B></P><P>We found that the <I>Nampt</I> gene is a direct target of HIF-2α in articular chondrocytes and OA cartilage. NAMPT protein, in turn, increased mRNA levels and activities of MMP3, MMP12 and MMP13 in chondrocytes, an action that was necessary for HIF-2α-induced expression of catabolic enzymes. Gain-of-function studies (intra-articular injection of Ad-<I>Nampt; Col2a1-Nampt</I> TG mice) and loss-of-function studies (intra-articular injection of the NAMPT inhibitor FK866) demonstrated that NAMPT is an essential catabolic regulator of osteoarthritic cartilage destruction caused by HIF-2α or DMM surgery.</P><P><B>Conclusions</B></P><P>Our findings indicate that NAMPT, whose corresponding gene is a direct target of HIF-2α, plays an essential catabolic role in OA pathogenesis and acts as a crucial mediator of osteoarthritic cartilage destruction caused by HIF-2α or DMM surgery.</P>