- GLP-1 Can Protect Proinflammatory Cytokines Induced Beta Cell Apoptosis through the Ubiquitination.
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Dong Mee Lim, Ju Young Kim, Kang Woo Lee, Keun Young Park, Byung Joon Kim
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Endocrinol Metab. 2011;26(2):142-149. Published online June 1, 2011
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DOI: https://doi.org/10.3803/EnM.2011.26.2.142
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 Abstract
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- BACKGROUND
Proinflammatory cytokines are one of the causes of diabetes mellitus. However, the exact molecular mechanism by which proinflammatory cytokines induce beta-cell death remains to be clearly elucidated. Glucagon-like peptide-1 (GLP-1) affects the stimulation of insulin secretion and the preservation of beta-cells. Additionally, it may exert an antiapoptotic effect on beta cells; however, the mechanism underlying this effect has yet to be demonstrated. Therefore, we investigated the protective effects of GLP-1 in endoplasmic reticulum (ER)-mediated beta-cell apoptosis using proinflammatory cytokines. METHODS: To induce ER stress, hamster insulin-secreting tumor (HIT)-T15 cells were treated using a mixture of cytokines. Apoptosis was evaluated via MTT assay, Hoechst 33342 staining, and annexin/propidium iodide (PI) flow cytometry. The mRNA and protein expression levels of ER stress-related molecules were determined via PCR and Western blotting, respectively. Nitric oxide was measured with Griess reagent. The levels of inducible nitric oxide synthase (iNOS) mRNA and protein were analyzed via real-time PCR and Western blot, respectively. iNOS protein degradation was evaluated via immunoprecipitation. We pretreated HIT-T15 cells with exendin (Ex)-4 for 1 hour prior to the induction of stress. RESULTS: We determined that Ex-4 exerted a protective effect through nitric oxide and the modulation of ER stress-related molecules (glucose-regulated protein [GRP]78, GRP94, and CCAAT/enhancer-binding protein homologous protein [CHOP]) and that Ex-4 stimulates iNOS protein degradation via the ubiquitination pathway. Additionally, Ex-4 also induced the recovery of insulin2 mRNA expression in beta cells. CONCLUSION: The results of this study indicate that GLP-1 may protect beta cells against apoptosis through the ubiquitination pathway.
- A Case of Malignant Pleural Effusion with Pleural Metastasis in a Patient with Papillary Thyroid Carcinoma.
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Ju Young Kim, Dae Won Park, Jin O Na, Byoung Yeon Hwang, Dong Lim Kim, Dong Hyun Shin, Sin Gon Kim, Kyung Mook Choi, Sei Hyun Baik, Dong Seop Choi, Sung Jin Cho, Nan Hee Kim
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J Korean Endocr Soc. 2002;17(2):269-274. Published online April 1, 2002
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Abstract
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- Papillary thyroid carcinomas comprise approximately 80 percent of all thyroid cancers, but haves a good prognosis, with overall survival rates at 10 years of about 80 to 95 percent. They spreads through the lymphatic system, and the lung is the most frequent metastasis site. If distant metastasis is present, the overall survival rate is about 40 percent. Although malignant pleural effusion, with pleural metastasis is a rare complication in patients with papillary thyroid carcinoma, the development of malignant pleural effusion is an extremely adverse prognostic indicator. We recently experienced a case of malignant pleural effusion with papillary thyroid carcinoma. A 54-year-old woman was admitted to the hospital because of dyspnea. A chest X-ray showed massive pleural effusion in the right hemithorax. Previously total thyroidectomy, and iodine-131 therapy had been performed, but a local recurrence and pulmonary metastasis developed 5 years later, accompanied by malignant pleural effusion with pleural metastasis. We performed diagnostic thoracentesis, which confirmed a metastatic papillary thyroid carcinoma. This patient was a rare case of paplillary thyroid carcinoma, in which the disease was represented by a rapid deterioration with malignant pleural effusion. So we report this case with a review of the literature.
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