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Original Studies |
Division of Endocrinology and Metabolism, Department of Medicine (M.K., Y.H., K.N.), and the Department of Pathology (A.J.), Kurume University School of Medicine, Kurume 830-0011; the Department of Pathology, Saga Medical University (S.T.), Saga 849-8501; and Koike Hospital (N.K.), Saga 840-0862, Japan
Address all correspondence and requests for reprints to: Yuji Hiromatsu, M.D., Ph.D., Division of Endocrinology and Metabolism, Department of Medicine, Kurume University School of Medicine, 67 Asahimachi, Kurume, 830-0011 Fukuoka, Japan.
Bcl-2 family proteins are important regulators of apoptosis. To clarify a role of apoptosis and the expression of Bcl-2 family proteins in the pathogenesis of subacute thyroiditis (SAT), we evaluated the expression of Bcl-2, Bax, and Bak by immunohistochemistry and apoptosis by in situ end labeling of fragmented DNA in thyroid tissues from 11 patients with SAT. Apoptotic nuclei were found in granulomas, especially in macrophages/histiocytes and lymphocytes, and in the regenerating follicular cells, but were rarely found in the area of fibrosis. The mean (±SD) percentage of apoptotic follicular cells was significantly greater in SAT than that in controls (1.4 ± 0.8% vs. 0.4 ± 0.6%). Bcl-2, Bak, and Bax were strongly expressed in the granulomas and regenerating thyroid follicular cells from patients with SAT. Bcl-2 and Bak, but not Bax, were expressed in follicular cells from normal controls. The percentage of apoptotic cells and the expression of Bax in follicular cells did not correlate with age or serum levels of thyroid hormones, C-reactive protein, or thyroglobulin. These data suggest that apoptosis may be involved in the development of SAT and that Bax expression in regenerating thyrocytes may be important for the recovery of SAT.
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H. Tang, K. Chen, Y. Wei, G. C. Sharp, L. McKee, and H. Braley-Mullen Apoptosis of thyrocytes and effector cells during induction and resolution of granulomatous experimental autoimmune thyroiditis Int. Immunol., December 1, 2000; 12(12): 1629 - 1639. [Abstract] [Full Text] [PDF] |
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