Mi-Kyoung Ha

Publications of Mi-Kyoung Ha

• Expression of mucins on the mucosal surface of lungs of 4-week-old pigs.

  Authors: Chung Hyun Kim, Kichan Lee, Kiwon Han, Yeonsu Oh, Duyeol Kim, Hwi Won Seo, Changhoon Park, Mi-Kyoung Ha, Sung-Hoon Kim, Kyung-Dong Cho, Bog-Hieu Lee, Chanhee Chae

  Veterinary research communications. 02/2011; 35(4):255-60.

  The aim of this study was to determine the immunoreactivity of normal small bronchial, bronchiolar, respiratory bronchiolar, and interalveolar epithelium using antibodies to six mucins: MUC1, MUC2,The aim of this study was to determine the immunoreactivity of normal small bronchial, bronchiolar, respiratory bronchiolar, and interalveolar epithelium using antibodies to six mucins: MUC1, MUC2, MUC4, MUC5AC, MUC5B, and MUC6. The large, gel-forming secreted mucins MUC2, MUC5AC, and MUC5B were widely expressed in the lower respiratory tract. The results of this study demonstrate that these secreted mucins form a gel to cover and protect the mucosal surface in the lower respiratory tract of pigs.

• Emodin inhibits proinflammatory responses and inactivates histone deacetylase 1 in hypoxic rheumatoid synoviocytes.

  Authors: Mi-Kyoung Ha, Young Hoon Song, Soo-Jin Jeong, Hyo-Jung Lee, Ji Hoon Jung, Bonglee Kim, Hyo Sook Song, Jeong-Eun Huh, Sung-Hoon Kim

  Biological & pharmaceutical bulletin. 01/2011; 34(9):1432-7.

  Chronic inflammation of rheumatoid arthritis (RA) is promoted by proinflammatory cytokines and closely linked to angiogenesis. In the present study, we investigated the anti-inflammatory effects ofChronic inflammation of rheumatoid arthritis (RA) is promoted by proinflammatory cytokines and closely linked to angiogenesis. In the present study, we investigated the anti-inflammatory effects of emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) isolated from the root of Rheum palmatum L. in interleukin 1 beta (IL-1β) and lipopolysaccharide (LPS)-stimulated RA synoviocytes under hypoxia. Emodin significantly inhibited IL-1β and LPS-stimulated proliferation of RA synoviocytes in a dose-dependent manner under hypoxic condition. Also, enzyme linked immunosorbent assay (ELISA) revealed that emodin significantly reduced the production of pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α), IL-6 and IL-8], mediators [prostagladin E(2) (PGE(2)), matrix metalloproteinase (MMP)-1 and MMP-13] and vascular endothelial growth factor (VEGF) as an angiogenesis biomarker in IL-1β and LPS-treated synoviocytes under hypoxia. Consistently, emodin attenuated the expression of cyclooxygenase 2 (COX-2), VEGF, hypoxia inducible factor 1 alpha (HIF-1α), MMP-1 and MMP-13 at mRNA level in IL-1β and LPS-treated synoviocytes under hypoxia. Furthermore, emodin reduced histone deacetylase (HDAC) activity as well as suppressed the expression of HDAC1, but not HDAC2 in IL-1β and LPS-treated synoviocytes under hypoxia. Overall, these findings suggest that emodin inhibits proinflammatory cytokines and VEGF productions, and HDAC1 activity in hypoxic RA synoviocytes.