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Myung Suk Kim  (Kim MS) 3 Articles
The Effect of Epicatechin on the High Glucose-induced TSP-1 Expression and MMP-2 Activity in Rat Vascular Smooth Muscle Cells.
Gyeong Ryul Ryu, Jung Hoon Kang, Kyong Ja Hong, In Kyung Jeong, Hwa In Jang, Duck Joo Rhie, Shin Hee Yoon, Sang June Hahn, Myung Suk Kim, Yang Hyeok Jo, Myung Jun Kim
J Korean Endocr Soc. 2006;21(4):302-310.   Published online August 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.4.302
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AbstractAbstract PDF
BACKGROUND
The incidence of atherosclerosis is well correlated with the progression of type 2 diabetes mellitus. High plasma glucose in uncontrolled diabetic patients evokes many vascular complications such as atherosclerosis. Specifically, high glucose was reported to induce thrombospondin-1 (TSP-1), which activates matrix metalloproteinase-2 (MMP-2) and leads to the invasion of vascular smooth muscle cells (VSMCs) into the intima. Catechins with antioxidant effects are known to inhibit MMP-2 activity. Therefore, this study was aimed at revealing the effect of epicatechin, one of catechins, on high glucose-induced TSP-1 and the invasiveness of VSMCs. METHODS: VSMCs were primarily isolated from Sprague-Dawley rat aorta. The VSMCs were incubated with different doses (30, 100 and 300 micrometer) of epicatechin under high glucose concentration (30 mM). The TSP-1 protein and mRNA expressions were analyzed by performing Western blotting and Northern blot analyses, respectively. RT-PCR was performed to observe the MMP-2 mRNA expression. Gelatin zymography was performed for the measurement of MMP-2 activity. Invasion assays were performed to evaluate the invasiveness of VSMCs. RESULTS: Epicatechin inhibited the high glucose-induced TSP-1 expression and the MMP-2 activity in a dose-dependent manner. Also, epicatechin inhibited the high glucose-induced invasiveness of VSMCs across the matrix barrier in a dose-dependent fashion. CONCLUSION: Collectively, epicatechin may prevent the high glucose-induced proliferation and invasion of VSMCs by inhibiting the TSP-1 expression and the MMP-2 activity. Therefore, epicatechin appears to play a protective role in the development of atherosclerosis.

Citations

Citations to this article as recorded by  
  • (‐)‐Epicatechin maintains endurance training adaptation in mice after 14 days of detraining
    Maik Hüttemann, Icksoo Lee, Moh H. Malek
    The FASEB Journal.2012; 26(4): 1413.     CrossRef
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Role of Protein kinase C in Desensitization of Somatostatin-induced Calcium Signalling in NG108-15 Cells.
Kyoung Mi Kim, Jong Ho Sung, Myung Jun Kim, Duck Joo Rhie, Yang Hyeok Jo, Sang June Hahn, Myung Suk Kim, Shin Hee Yoon, Bu Seung Kim
J Korean Endocr Soc. 2005;20(4):353-361.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.353
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  • 16 Download
AbstractAbstract PDF
BACKGROUND
Activation of G-protein coupled-somatostatin receptors induces the release of calcium from inositol 1, 4, 5-trisphosphate-sensitive intracelluar stores. G-protein-coupled receptor signaling decreases with prolonged exposure to an agonist. SEBJECTS and METHODS: Fura-2-based digital Ca2+ imaging was used to study the effects of prolonged exposure to an agonist on the somatostatin-induced intracellular Ca2+ concentration([Ca2+]i) increases in NG108-15 cells, which were differentiated with CO2-independent medium and 10micrometer forskolin. RESULTS: Exposure to somatostatin(1micrometer) for 30 min completely desensitized the NG108-15 cells to a second somatostatin-induced response. The cells recovered gradually over 20 min following washout of the somatostatin. The desensitization was not due to depletion of the intracellular Ca2+ stores, and pretreatment for 30 min with bradykinin(100nM), which activates phospholipase C, or DADLE(D-Ala2-D-Leu5 enkephalin, 1microM), which activates phospholipase C, failed to cross-desensitize the somatostatin-evoked [Ca2+]i increases. Treatment with 8-cpt-cAMP(0.1mM) for 30min did not influence the somatostatin-induced[Ca2+]i increases. Phorbol 12, 13-dibutyrate(PdBu, 1microM) blocked the response completely. Down-regulation of PKC due to 24 h exposure of PdBu (1microM) inhibited the somatostatin-induced desensitization. CONCLUSION: Prolonged exposure of somatostatin to NG108-15 cells desensitized the somatostatin-induced release of Ca2+ from the intracelluar store, with protein kinase C also involved in the desensitization.
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A Case of Malignant Insulinoma Treated with Streptozotocin after Surgery.
Yun Chang Jun, Byung Hun Lim, Bong Jung Son, Byung Ik Kim, Man Ho Lee, Sang Jong Lee, Won Kil Pae, Myung Suk Kim
J Korean Endocr Soc. 1994;9(2):150-155.   Published online November 6, 2019
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  • 23 Download
AbstractAbstract PDF
Insulinoma is clinically characterized by fasting hypoglycemia, various neuropsychiatric symptoms, and these caused by secondary to hypoglycemia.Of patients with insulinoma, 80 percent have single benign tumors, 11 percent have multiple benign tumors, 6 percent have single malignant tumors, and the remainder have multiple malignant tumors or islet hyperplasia according to Service's statement.A 42 year-old male chemical engineer who had insulinoma associated with regional lymph node metastasis has been successfully performed with curative resection and consecutive postoperative therapy with streptozotocin.He entered to this hospital because of frequent occasion of bizarre behavior and language, transient unconsiousness and syncopal episode, and sweating associated with hypoglycemia especially in night four months prior to addmission in November 1992. Those symptoms and hypoglycemia were controlled by intravenous glucose injection and/or oral feeding of glucose riched stuffs.No physical abnormalities were found except neuropsychiatric symptoms. On admission the fasting blood glucose level was 10 mg/dl, plasma immunoreactive plasma insulin level was 125.23 uU/ml, and plasma C-peptide level was 10.24 ng/ml, respectively.Abdominal CT was suggestive of retroperitoneal tumor just behind the pancreas. Selective celiac axis angiography demonstrated hypervascular mass supplied by dorsal pancreatic artery which was compatible with insulinoma. Surgical intervention including distal pancreatectomy, as well as splenectomy and parital omental resection were performed successfully. Consecutive postoperative treatment of streptozotocin was done without any side effects.His condition is very good and enjoyed his life with full activity to date.
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