http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Kim, Eung Kweon,Lee, Ga-Hyun,Lee, Boram,Maeng, Yong-Sun Hindawi 2017 Stem cells international Vol.2017 No.-
<P>Homeostasis and regeneration of corneal epithelia are sustained by limbal epithelial stem cells (LESCs); thus, an LESC deficiency is a major cause of blindness worldwide. Despite the generally promising results of cultivated LESC transplantation, it has been limited by variations in long-term success rates, the use of xenogeneic and undefined culture components, and a scarcity of donor tissues. In this study, we identified the culture conditions required to expand LESCs <I>in vitro</I> and established human limbus-derived highly proliferative ABCG2<SUP>+</SUP>/ABCB5<SUP>+</SUP> double-positive LESCs. These LESCs exhibited the LESC marker profile and differentiated into corneal epithelial cells. In addition, cultured LESCs expressed high levels of the stem cell markers Sox2, Oct4, c-Myc, and Klf4, had high telomerase activity, and had stable, normal genomes. These results suggest that our novel cultivation protocol affects the phenotype and differentiation capacity of LESCs. From the limbus, which contains a heterogenous cell population, we have derived highly proliferative ABCG2<SUP>+</SUP>/ABCB5<SUP>+</SUP> double-positive cells with the ability to differentiate into corneal epithelial cells. This study opens a new avenue for investigation of the molecular mechanism of LESC maintenance and expansion <I>in vitro</I> and may impact the treatment of corneal disease, particularly corneal blindness due to an LESC deficiency.</P>
Kim, Bong-Yoon,Olzmann, James A,Choi, Seung-Il,Ahn, So Yeon,Kim, Tae-Im,Cho, Hyun-Soo,Suh, Hwal,Kim, Eung Kweon American Society for Biochemistry and Molecular Bi 2009 The Journal of biological chemistry Vol.284 No.29
<P>The 5q31-linked corneal dystrophies are heterogeneous autosomal-dominant eye disorders pathologically characterized by the progressive accumulation of aggregated proteinaceous deposits in the cornea, which manifests clinically as severe vision impairment. The 5q31-linked corneal dystrophies are commonly caused by mutations in the TGFBI (transforming growth factor-beta-induced) gene. However, despite the identification of the culprit gene, the cellular roles of TGFBI and the molecular mechanisms underlying the pathogenesis of corneal dystrophy remain poorly understood. Here we report the identification of periostin, a molecule that is highly related to TGFBI, as a specific TGFBI-binding partner. The association of TGFBI and periostin is mediated by the amino-terminal cysteine-rich EMI domains of TGFBI and periostin. Our results indicate that the endogenous TGFBI and periostin colocalize within the trans-Golgi network and associate prior to secretion. The corneal dystrophy-associated R124H mutation in TGFBI severely impairs interaction with periostin in vivo. In addition, the R124H mutation causes aberrant redistribution of the mutant TGFBI into lysosomes. We also find that the periostin-TGFBI interaction is disrupted in corneal fibroblasts cultured from granular corneal dystrophy type II patients and that periostin accumulates in TGFBI-positive corneal deposits in granular corneal dystrophy type II (also known as Avellino corneal dystrophy). Together, our findings suggest that TGFBI and periostin may play cooperative cellular roles and that periostin may be involved in the pathogenesis of 5q31-linked corneal dystrophies.</P>
Comparison of Corneal Deposits After LASIK and PRK in Eyes With Granular Corneal Dystrophy Type II
Kim, Tae-im,Kim, Terry,Kim, Sun Woong,Kim, Eung Kweon SLACK, Inc. 2008 Journal of refractive surgery Vol.24 No.4
<P>PURPOSE: To compare the characteristics of corneal deposits in eyes with granular corneal dystrophy type II (Avellino corneal dystrophy) after LASIK and photorefractive keratectomy (PRK). METHODS: Patients with heterozygous granular corneal dystrophy type II were examined with slit-lamp microscopy for recurrence of granular corneal dystrophy type II after uneventful LASIK and PRK surgery. One particular case involved bilateral incomplete flaps after LASIK, resulting in excimer laser ablation under the flap in one area and surface ablation in another area of both eyes. Deoxyribonucleic acid sequencing analysis in all patients confirmed the heterozygous status of granular corneal dystrophy type II. RESULTS: An abundance of coarse, white opacities consistent with granular corneal dystrophy type II were observed along the interface in all of the LASIK cases. In comparison, only a mild increase in opacities was noted in the PRK cases. In the LASIK case with bilateral incomplete flaps, abundant opacities were present in both corneas along the interface of the LASIK flap, and a minimal increase of stromal opacities was noted where no LASIK flap was present. CONCLUSIONS: Exacerbation of granular corneal dystrophy type II deposits occurred in the corneal stroma to a much greater degree after LASIK compared to surface ablation surgery.</P>
Kim, Sun Woong,Lee, Hwan Young,Kim, Tae-im,Shin, Kyoung-Jin,Yang, Woo Ick,Kim, Eung Kweon S. Karger AG 2009 Ophthalmologica Vol.223 No.6
<P><I>Aims:</I> To investigate the survival of donor-derived cells in a successfully grafted corneal button 10 years after penetrating keratoplasty for lattice dystrophy. <I>Methods:</I> In 1996, a 48-year-old male with lattice corneal dystrophy underwent penetrating keratoplasty 3 times in the right eye within a 3-month interval. Nine years and 7 months later, the patient underwent a fourth penetrating keratoplasty. After surgery, the previous graft was analyzed to determine the origin of the cells. The epithelium and endothelium were removed, and then the button was dissected into 5 stromal blocks measuring 2 × 1.8 mm. Tissues underwent forensic genotyping using 16 markers (amelogenin for sex chromosomes and 15 autosomal short tandem repeats). Patient buccal tissue DNA was used as a control. <I>Results:</I> The epithelium and buccal tissue contained identical DNA (i.e. recipient DNA). Similarly, the most peripheral stromal tissue contained only recipient DNA. In contrast, the most central stromal tissue only contained DNA of nonrecipient origin (presumably donor), while the stromal tissue between the periphery and center contained both recipient and nonrecipient DNA. <I>Conclusions:</I> The corneal stroma was infiltrated by surrounding recipient-derived keratocytes from the periphery. Therefore, more donor-derived cells had survived in the central stroma.</P><P>Copyright © 2009 S. Karger AG, Basel</P>
Kim, Tae-im,Lee, Hun,Hong, Hye Kyoung,Kim, Kyu Seo,Choi, Seung-Il,Maeng, Yong-Sun,Kim, Eung Kweon Masson Pub. USA 2015 Cornea Vol.34 No.8
PURPOSE:: To investigate the effects of tranilast, an inhibitor of chemical mediators and fibroblast proliferation, on the expression of transforming growth factor-beta (TGF-&bgr;)-induced protein (TGFBIp) in wild-type (WT) and homozygous (HO) granular corneal dystrophy type 2 corneal fibroblasts. METHODS:: Cell proliferation and cytotoxicity were measured by Cell Counting Kit-8 and lactate dehydrogenase assay. Western blotting and real-time polymerase chain reaction were used to determine changes in the expression of TGFBIp and TGFBI mRNA. We determined the effects of tranilast on phosphorylated Smad2 (pSmad2) and pSmad3, wound-healing, and expression of alpha-smooth muscle actin (α-SMA), type I collagen, and integrins. RESULTS:: High concentrations of tranilast decreased proliferation of corneal fibroblasts but did not cause elevation of lactate dehydrogenase, except at 1.0 mM tranilast. TGF-&bgr; increased the expression of TGFBIp and TGFBI mRNA in WT and HO corneal fibroblasts. Cotreatment of corneal fibroblasts with tranilast and TGF-&bgr; reduced the levels of TGFBIp and TGFBI mRNA. In addition, application of tranilast reduced pSmad2 in WT and HO corneal fibroblasts and pSmad3 in HO corneal fibroblasts, both of which were increased initially by TGF-&bgr;. Tranilast delayed wound healing and reduced the expression of α-SMA, type I collagen, and some of integrins in WT and HO corneal fibroblasts. CONCLUSIONS:: Application of tranilast in WT and HO corneal fibroblasts inhibited the expression of TGFBIp by blocking TGF-&bgr; signaling. Thus, tranilast may be useful in delaying or preventing the recurrence of corneal opacity in TGFBI-linked corneal dystrophies if clinical studies confirm these findings.
조권문 ( Kweon Moon Jo ),김재원 ( Jae Won Kim ),임지은 ( Ji Eun Lim ),황종하 ( Jong Ha Hwang ),김해중 ( Hai Joong Kim ),김탁 ( Tak Kim ),이응석 ( Eung Seok Lee ),신진우 ( Jin Woo Shin ) 대한산부인과학회 2003 Obstetrics & Gynecology Science Vol.46 No.6
Uterine papillary serous carcinoma (UPSC) has been recognized as an aggresive tumor with early and deep myometrial invasion, frequent lympho-vascular space involvement, and a high relapse rate. It has also been shown that deep myometrial invasion cannot p