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Dong Kwan Kim  (Kim DK) 4 Articles
Effects of Glucocorticoid on Apoptosis of Human Bone Marrow Osteogenic Stromal Cells.
Ha Young Kim, Duk Jae Kim, Si Yeol Lee, Jeong Soo Hong, Dong Kwan Kim, Ghi Su Kim
J Korean Endocr Soc. 2002;17(1):23-31.   Published online February 1, 2002
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BACKGROUND
Osteoporosis is one of the most serious side effects of long-term glucocorticoid therapy, but the mechanism of glucocorticoid-induced bone loss remains poorly defined. Glucocorticoid induces decreased bone formation and death of isolated segments of bone (osteonecrosis) suggesting that glucocorticoid excess may affect the birth or death rate of bone cells and thereby reduce their numbers. It has been known that reduction in bone formation is due to reduced proliferation in osteoblast precursor cells and reduced matrix synthesis in mature osteoblast. Here, we present evidence for dexamethasone-induced apoptosis on human bone marrow stromal cells (hBMSC). To understand the mechanism of glucocorticoid-induced osteoporosis, we investigated the effects of glucocorticoid on primary cultured hBMSC. METHEODS: Treatment with dexamethasone at the concentration of 10-9 M for 3~5 days significantly decreased cleavage tetrazolium salt WST-1 level/concentration by mitochondrial dehydrogenase in viable cells. Greater decrease was observed with higher concentration of dexamethasone (10-7 M, and 10-5 M). Apoptosis was measured by annexin V binding/propidium iodide using fluorescence-activated cell sorter (FACS) analysis and nuclear morphology stained with the fluorescence dye, Hoechst 33342. RESULTS: The level/concentration of apoptotic hBMSC (annexin V positive / PI negative) was increased with 10-9 M dexamethasone (1.2% to 5.3%) and further increased with 10-7 M, and 10-5 M concentration (11.7% and 12.5%, respectively). The same result was observed with Hoechst 33342 staining. CONCLUSION: These results indicate that glucocorticoid induces apoptosis on osteoblast precursor cell, hBMSC, and may contribute to decrease bone formation
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A Case of Ectopic ACTH Syndrome Caused by Thymic Carcinoid Tumor and Localized by PET.
Jong Chul Won, Sung Kwan Hong, Hyun Ju Lee, Sang Ook Kim, Yun Hee Jeong, Dae Hyuk Moon, Dong Kwan Kim, Kyung Yub Kong, Jae Sung Lee, Ki Soo Kim
J Korean Endocr Soc. 1999;14(4):771-778.   Published online January 1, 2001
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AbstractAbstract PDF
Ectopic ACTH syndrome is frequently caused by lung cancer and uncommonly by other tumors such as thymic carcinoid. For its treatment, early diagnosis and complete resection is irresponsible, but some cases are remained unlocalized in spite of all diagnostic modalities. Here we report a case of ectopic ACTH syndrome which was localized by PET but could not be localized by conventional technique. A tumor at thymic area was ACTH secreting thymic carcinoid which was operated but couldnt resect completly. Glucocorticoid hypersecretion was persisted with chemotherapy, radiotherapy, and ketoconazole treatment. Patient died of sepsis after 12 months of diagnosis.
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Effects of Thyroid Hormone on Preduction of Interleukin-6 and Interleukin-11 in Human Bone Marrow Stromal Cells.
Chul Hee Kim, Dong Kwan Kim, Hong Kyu Kim, Young Ki Song, Ki Soo Kim
J Korean Endocr Soc. 1997;12(4):557-564.   Published online January 1, 2001
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  • 19 Download
AbstractAbstract PDF
BACKGROUND
It is well known that excessive thyroid hormone in the body is associated with bone loss. However, the mechanism by which thyroid hormone affects bone cell metabolism remains unclear. It has been shown that thyroid hormones stimulate osteoclastic bone resorption indirectly via some unknown mediators secreted by osteoblasts, This study was undertaken to determine if interleukin-6 (IL-6) or interleukin-11 (IL-l1) could be the mediator (s) of thyroid hormone-induced bone loss. METHODS: We treated primary cultured human bone rnarrow stromal cells with 3,5,3-triiodo-thyronine (T) and measured basal and interleukin-l (IL-1)-stimulated IL-6/IL-ll production. We also investigated the possible modulating effect of 17B-estradiol (17B-E2.) on thyroid hormone action. RESULTS: T3 at 10 (-12) ~ 10 (-8) M concentration, significantly increased the basal IL-6 production in a dose-dependent manner, and also potentiated the stimulatory effect of IL-1 on IL-6 production. However, T failed to elicit a detectable effect on basal or IL-1-stimulated IL-11 production. Treat#ment with l7B-E2. inhibited IL-1-stimulated IL-6 production, but the effects of T3 on IL-6 production were not affected by 17/B-E. CONCLUSION: These results suggest that thyroid hormone may increase bone resorption by increasing basal IL-6 production and potentiating IL-1-induced IL-6 production from osteoblast-lineage cells, and these effects were independent of estrogen status.
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Effects of Interleukin-6 on mRNA Expression of Alkaline Phosphatase, Osteopontin, Decorin and a1(1)-collagen in Human Bone Marrow Stromal Cells.
Chul Hee Kim, Dong Kwan Kim, Seung Il Park, Kwang Hyun Sohn, Ghi Su Kim
J Korean Endocr Soc. 1996;11(2):156-162.   Published online November 7, 2019
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  • 23 Download
AbstractAbstract PDF
Background
Inter1eukin-6(IL-6) is known to be produced by osteoblastic cells and to have impartant role in regulation of bone remodelling, Most previous studies indicated that IL-6 bas a major role in stimulating osteoclastic resorption by increasing recruitment and proliferation of preosteoclasts. But its autocrine effect on osteoblastic cells has not been well established yet. Therefore, we studied the effects of IL-6 on messenger RNA (mRNA) expression of proteins that are characteristic of osteoblastic cells in human bone marrow stromal (osteoprogenitor) cells (hRMSC). Methods: The expression of mRNAs for alkaline phosphatase, al(1)-collagen, osteopontin and decorin were studied by northern blot analysis after 3 7 days' treatrnent with IL-6 in the concenttation range of 101,000 U/ml. Results: The mRNA levels for any of the osteoblastic proteins studied did not change significantly by IL-6 treatment up to the concentration of 1,000 U/ml. Conclusion: These results suggest that IL-6 does not have a significant role in differentiatian or activities of human bone rnarrow stromal.
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Endocrinol Metab : Endocrinology and Metabolism