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Articles by M. S Kim
Total Records ( 11 ) for M. S Kim
  M. S Kim , K. Y Wu , V Auyeung , Q Chen , P. A Gruppuso and C. Phornphutkul

Linear growth in children is sensitive to nutritional status. Amino acids, in particular leucine, have been shown to regulate cell growth, proliferation, and differentiation through the mammalian target of rapamycin (mTOR), a nutrient-sensing protein kinase. Having recently demonstrated a role for mTOR in chondrogenesis, we hypothesized that leucine restriction, acting through mTOR, would inhibit growth plate chondrocyte proliferation and differentiation. The effect of leucine restriction was compared with that of the specific mTOR inhibitor, rapamycin. Leucine restriction produced a dose-dependent inhibition of fetal rat metatarsal explant growth. This was accounted by reduced cell proliferation and hypertrophy but not apoptosis. mTOR activity, as reflected by ribosomal protein S6 phosphorylation, was only partially inhibited by leucine restriction, whereas rapamycin abolished S6 phosphorylation. In chondrogenic ATDC5 cells, leucine restriction inhibited cell number, proteoglycan accumulation, and collagen X expression despite minimal inhibition of mTOR. Microarray analysis demonstrated that the effect of leucine restriction on ATDC5 cell gene expression differed from that of rapamycin. Out of 1,571 genes affected by leucine restriction and 535 genes affected by rapamycin, only 176 genes were affected by both. These findings indicate that the decreased chondrocyte growth and differentiation associated with leucine restriction is only partly attributable to inhibition of mTOR signaling. Thus nutrient restriction appears to directly modulate bone growth through unidentified mTOR-independent mechanisms in addition to the well-characterized mTOR nutrient-sensing pathway.

  E. H Koh , M Kim , K. C Ranjan , H. S Kim , H. S Park , K. S Oh , I. S Park , W. J Lee , M. S Kim , J. Y Park , J. H Youn and K. U. Lee

Nitric oxide (NO) stimulates mitochondrial biogenesis. We recently reported that adiponectin synthesis is regulated by mitochondrial function in adipocytes. This study was undertaken to test the hypothesis that endothelial NO synthase (eNOS) plays an important role in adiponectin synthesis by producing NO and enhancing mitochondrial function in adipocytes. We examined the effects of eNOS knockdown on adiponectin synthesis in 3T3-L1 adipocytes and also examined plasma adiponectin levels and the mitochondria in adipose tissue of eNOS knockout (eNOS–/–) mice with and without chronic administration of a NO donor. In cultured 3T3-L1 adipocytes, eNOS siRNA decreased rosiglitazone-induced adiponectin secretion, which was associated with decreases in mitochondrial proteins and biogenesis factors. Plasma adiponectin concentrations were reduced in adult eNOS–/– mice compared with age-matched wild-type mice. Mitochondrial contents in adipose tissue were reduced in eNOS–/– mice, and this was associated with decreased expression of mitochondrial biogenesis factors, increased levels of 8-hydroxyguanosine, a biomarker of oxidative stress, and morphological abnormalities in mitochondria. Rosiglitazone-induced increases in adiponectin expression and mitochondrial content were also reduced significantly in eNOS–/– mice. Chronic administration of a NO donor reversed mitochondrial abnormalities and increased adiponectin expression in adipose tissue of eNOS–/– mice. eNOS plays an important role in adiponectin synthesis in adipocytes by increasing mitochondrial biogenesis and enhancing mitochondrial function.

  C. H Seo , J. R Kim , M. S Kim and K. H. Cho

Motivation: Spatio-temporal regulation of gene expression is an indispensable characteristic in the development processes of all animals. ‘Master switches’, a central set of regulatory genes whose states (on/off or activated/deactivated) determine specific developmental fate or cell-fate specification, play a pivotal role for whole developmental processes. In this study on genome-wide integrative network analysis the underlying design principles of developmental gene regulatory networks are examined.

Results: We have found an intriguing design principle of developmental networks: hub nodes, genes with high connectivity, equipped with positive feedback loops are prone to function as master switches. This raises the important question of why the positive feedback loops are frequently found in these contexts. The master switches with positive feedback make the developmental signals more decisive and robust such that the overall developmental processes become more stable. This finding provides a new evolutionary insight: developmental networks might have been gradually evolved such that the master switches generate digital-like bistable signals by adopting neighboring positive feedback loops. We therefore propose that the combined presence of positive feedback loops and hub genes in regulatory networks can be used to predict plausible master switches.

  W Jin , G. M Kim , M. S Kim , M. H Lim , C Yun , J Jeong , J. S Nam and S. J. Kim

Tropomyosin-related kinase (Trk) C, a member of the Trk family of neurotrophin receptors, has been implicated in the growth and survival of human cancer tissues. Here, we report that TrkC is frequently overexpressed in human breast cancers and plays an essential role in tumor growth and metastasis. Ectopic expression of TrkC in non-malignant mammary epithelial cells suppressed anoikis, which correlated with activation of the Ras-mitogen-activated protein kinase and phosphatidylinositol-3-OH kinase (PI3K)/Akt pathways, and reduced expression of the metastatic regulator Twist. Furthermore, suppression of TrkC expression in highly metastatic mammary carcinoma cells inhibited their growth in vitro, as well as their ability to metastasize from the mammary gland to the lung in vivo. These results have identified TrkC as a critical regulator of breast cancer cell growth and metastasis.

  M. S Kim , C. S Lee , J Hur , H. J Cho , S. I Jun , T. Y Kim , S. W Lee , J. W Suh , K. W Park , H. Y Lee , H. J Kang , D. S Lee , G. Y Koh , H Nakagami , R Morishita , Y. B Park and H. S. Kim

Background— The low engraftment rate of stem/progenitor cells infused via the intracoronary route to the ischemic myocardium is one of the most important factors limiting the efficacy of cell therapy. We investigated the concept of priming peripheral blood stem cells enriched by granulocyte colony-stimulating factor mobilization and apheresis (mobPBSCs) with angiopoietin-1 (Ang1), to enhance the engraftment into the ischemic tissue and neovasculogenic potential.

Methods and Results— The expression of Tie2, the Ang1 receptor, was significantly higher in mobPBSCs than naïve peripheral blood mononuclear cells (19.2±3.0% versus 1.2±0.8% versus 1.2±0.2%; P<0.001 for mobPBSCs from acute myocardial infarction (AMI) patients with granulocyte colony-stimulating factor treatment for 3 days versus peripheral blood mononuclear cells from AMI patients versus peripheral blood mononuclear cells from stable angina patients). After 4 hours of cartilage oligomeric matrix protein (COMP)-Ang1 stimulation, mobPBSCs committed to the endothelial lineage with the induction of CD31 and VE-cadherin expression, mediated by Tie2/Ets-1 pathway. Priming of mobPBSCs with COMP-Ang1 induced the expression of 4β1 and 5β1 integrins, which are also Ets-1 downstream molecules, leading to enhanced adhesion to endothelial cells or fibronectin. In a rabbit ear ischemia/reperfusion model, priming of mobPBSCs with COMP-Ang1 improved first-pass engraftment to the distal vascular bed after intraarterial delivery. In a murine ischemic hind-limb model, intravascular delivery of primed mobPBSCs enhanced both engraftment and neovascularization.

Conclusions— The short-term priming with COMP-Ang1 may be a feasible and promising option to activate mobPBSCs by enhancing differentiation and adhesiveness and to improve the efficacy of cell therapy for ischemic diseases.

  A. M Neubauer , J. A Garcia , J. C Messenger , E Hansis , M. S Kim , A. J.P Klein , G. A.F Schoonenberg , M Grass and J. D. Carroll

Background— Although fixed view x-ray angiography remains the primary technique for anatomic imaging of coronary artery disease, the known shortcomings of 2D projection imaging may limit accurate 3D vessel and lesion definition and characterization. A recently developed method to create 3D images of the coronary arteries uses x-ray projection images acquired during a 180° C-arm rotation and continuous contrast injection followed by ECG-gated iterative reconstruction. This method shows promise for providing high-quality 3D reconstructions of the coronary arteries with no user interaction but requires clinical evaluation.

Methods and Results— The reconstruction strategy was evaluated by comparing the reconstructed 3D volumetric images with the 2D angiographic projection images from the same 23 patients to ascertain overall image quality, lesion visibility, and a comparison of 3D quantitative coronary analysis with 2D quantitative coronary analysis. The majority of the resulting 3D volume images were rated as having high image quality (66%) and provided the physician with additional clinical information such as complete visualization of bifurcations and unobtainable views of the coronary tree. True-positive lesion detection rates were high (90 to 100%), whereas false-positive detection rates were low (0 to 8.1%). Finally, 3D quantitative coronary analysis showed significant similarity with 2D quantitative coronary analysis in terms of lumen diameters and provided vessel segment length free from the errors of foreshortening.

Conclusions— Fully automated reconstruction of rotational coronary x-ray angiograms is feasible, produces 3D volumetric images that overcome some of the limitations of standard 2D angiography, and is ready for further implementation and study in the clinical environment.

  J. A Lee , M. S Kim , J. S Koh , D. H Kim , J. S Lim , C. B Kong , W. S Song , W. H Cho , S. Y Lee and D. G. Jeon

We aimed to understand the biology of osteosarcoma of the flat bone, which is a rare tumor entity.


Cases with osteosarcoma of the flat bone were compared with those of the extremity in order to evaluate their clinicopathologic characteristics. And the influences of heterogeneous treatment modalities on outcome were analyzed.


Tumors of the flat bone comprised 91 (11.3%) of 806 osteosarcoma cases. Eight cases were secondary osteosarcoma associated with previous radiotherapy. Patients with a flat bone tumor were significantly older and more likely to present with metastases at diagnosis than extremity tumor. The proportions of female sex and chondroblastic subtype were higher among flat bone tumors than among extremity tumors. The 5-year overall survival and event-free survival rates were 35.2 ± 5.4% and 24.7 ± 5.5%, respectively. Although age and histologic response to pre-operative chemotherapy were not related to outcome of flat bone tumors, treatment modality influenced the survival. Patients treated surgically had better outcomes than those treated by another means. Radiation therapy did not appear to be an effective local control measure as surgery.


Treatment outcome of the tumor of the flat bone was worse than extremity tumors. Further studies are needed to identify effective local control measures that can substitute for surgery and to determine the biologic characteristics of osteosarcoma of the flat bone.

  J. A Lee , D. H Kim , J. S Lim , J. S Koh , M. S Kim , C. B Kong , W. S Song , W. H Cho , S. Y Lee and D. G. Jeon

Due to the low incidence, treatments for Korean soft tissue Ewing sarcoma patients have been heterogeneous, and reported data are limited. In this study, we retrospectively analyzed soft tissue Ewing cases treated at our institution.


We analyzed the clinicopathologic characteristics and treatment outcome of soft tissue Ewing sarcoma patients and compared with those of skeletal cases.


Twenty-seven soft tissue Ewing sarcoma cases were evaluated. Patients with soft tissue Ewing sarcoma were older than patients with skeletal tumors (P = 0.03), and tended to have metastasis at diagnosis (P = 0.12). However, sex ratios, pathologies, tumor volumes, and histologic response to preoperative chemotherapy were not different in the two groups. The 5-year overall survival (49.0%) and event-free survival (45.6%) of soft tissue Ewing sarcoma patients were similar to those of skeletal tumor patients (51.8% and 46.0%, respectively). Presence of metastasis at diagnosis and poor histologic response to preoperative chemotherapy were associated with an adverse outcome for both groups. Similar to skeletal tumors, central tumor location, pathology and tumor volume tended to be related to the survival of soft tissue Ewing sarcoma. However, age and the use of a modality other than surgery to achieve local control did not influence the survival of soft tissue Ewing sarcoma patients.


Our data could provide a basis to design a collaborative or multinational study targeting Ewing sarcoma family tumors.

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