Jae-Sang Park

Publications (3)6.15 Total impact

• Article: Texture direction of combined microgrooves and submicroscale topographies of titanium substrata influence adhesion, proliferation, and differentiation in human primary cells.

  Byung Jin Im, Suk Won Lee, Namsik Oh, Myung Hyun Lee, Jong Ho Kang, Richard Leesungbok, Sang Cheon Lee, Su Jin Ahn, Jae Sang Park
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  ABSTRACT: This study aimed to identify the optimal micro- and submicroscale topographies of titanium (Ti) substrata that would most significantly influence adhesion, proliferation, and other activities of these cells. Truncated V-shaped microgrooves in 60 μm-wide and 10 μm-deep cross-sections with 0°, 30°, 60°, or 90° angles between the microgrooves and ridge-top submicroscale texture were created on the Ti substrata (designated NE60/10-0°, NE60/10-30°, NE60/10-60° and NE60/10-90°, respectively). Ground titanium with submicroscale texture but with no microgrooves was used as the control substratum, NE0. Scanning electron microscopic observation and the assays determining the cell adhesion, cell proliferation and osteoblast differentiation were performed. Cells more actively migrated into the microgrooves on NE60/10-30° than into the microgrooves on any other substrata tested, suggesting that the cells utilise the increased surface area of the substrata at the microscale level. NE60/10-0° and NE60/10-30° substrata generally enhanced adhesion, proliferation, alkaline phosphatase activity, and osteoblast differentiation of human primary cells when compared to other Ti substrata, and significant correlations were observed between these cellular activities. Here, we show that the contact guidance of human primary cells grown on Ti substrata can be controlled more by specific submicroscale textures on ridge tops than by the dimensions of surface microgrooves only. Also, the degree of angles created between the submicroscale textures and microgrooves on Ti substrata significantly affect cell adhesion, proliferation and differentiation in human primary cells.
  Archives of oral biology 12/2011; 57(7):898-905. · 1.65 Impact Factor
• Article: SIRT1 modulates high-mobility group box 1-induced osteoclastogenic cytokines in human periodontal ligament cells.

  Young-Suk Kim, Young-Man Lee, Jae-Sang Park, Suk-Keun Lee, Eun-Cheol Kim
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  ABSTRACT: Bone resorptive cytokines contribute to bone loss in periodontal disease. However, the involvement of SIRT1 in high-mobility group box 1 (HMGB1)-induced osteoclastic cytokine production remains unknown. The aim of this study was to investigate the role of SIRT1 in the responses of human periodontal ligament cells to HMGB1 and to identify the underlying mechanisms. The effect of HMGB1 on osteoclastic cytokine expression and secretion, and the regulatory mechanisms involved were studied by ELISA, reverse transcription-polymerase chain reaction, and Western blot analysis. HMGB1 upregulated the mRNA expression levels of the osteoclastic cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-11, and IL-17. In addition, HMGB1 upregulated RANKL mRNA expression, and SIRT1 mRNA and protein expression. The upregulation of these cytokines by HMGB1 was attenuated by pretreatment with inhibitors of p38 mitogen-activated protein kinase and NF-κB, as well as neutralizing antibodies against Toll-like receptors 2 and 4. Inhibition of SIRT1 by sirtinol or SIRT1 siRNA blocked the HMGB1-stimulated expression of RANKL and cytokines. These results suggest that the inhibition of SIRT1 may attenuate HMGB1-mediated periodontal bone resorption through the modulation of osteoclastogenic cytokine levels in human periodontal ligament cells.
  Journal of Cellular Biochemistry 12/2010; 111(5):1310-20. · 2.87 Impact Factor
• Article: Endoplasmic reticulum stress is involved in hydrogen peroxide induced apoptosis in immortalized and malignant human oral keratinocytes.

  Seung-Ki Min, Sun-Kyung Lee, Jae-Sang Park, Jun Lee, Jun-Young Paeng, Sang-Im Lee, Hwa-Jeong Lee, Youngho Kim, Hyun-Ock Pae, Suk-Keun Lee, Eun-Cheol Kim
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  ABSTRACT: Although hydrogen peroxide may play an important role in the development of cancer, it can be an efficient inducer of apoptosis in cancer cells; the exact mechanism by which this action occurs is not completely understood in oral cancer cells. In this study, the mechanisms by which H(2)O(2) inhibited growth and induced apoptosis were differentially investigated using HPV-immortalized human oral keratinocytes (IHOK) and oral cancer cells (HN4). H(2)O(2) treatment sensitively and dose-dependently induced growth inhibition and typical apoptosis in IHOK and HN4 cells, as demonstrated by a decreased level of cell viability, an increased population of cells in the sub-G(0)/G(1) phase, ladder formation of the genomic DNA, chromatin condensation and accumulation of Annexin V(+)/PI(+) cells. Furthermore, the expression of Bax, p53 and p21(WAF1/CIP1) increased, whereas the expression of Bcl-2 decreased in immortalized and malignant keratinocytes that were treated with H(2)O(2). In addition, cytochrome-c from the mitochondria was observed in H(2)O(2)-treated IHOK and oral cancer cells, and this was accompanied by the activation of caspase-3 and -9. Additionally, H(2)O(2) treatment induced upregulation of CHOP, GRP78 and several representative endoplasmic reticulum (ER) stress-responsive proteins, including heme oxygenase-1. Overall, these results suggest that H(2)O(2) triggers apoptosis via the mitochondrial and ER stress pathway in IHOK and HN4 cells, and that increasing the cellular levels of H(2)O(2) sufficiently may lead to selective killing of oral cancer cells and therefore be therapeutically useful.
  Journal of Oral Pathology and Medicine 09/2008; 37(8):490-8. · 1.63 Impact Factor