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Excessive proliferation and apoptosis of parathyroid cells contribute to primary hyperparathyroidism in rabbit model
  1. Jing-tao Bi1,
  2. Rong-jie Bai2,
  3. Hui-li Zhan2,
  4. Zhan-hua Qian2,
  5. Li-hua Gong3,
  6. Ya-qi Liu1,
  7. Zhi-xue Zheng1,
  8. Xuan Cai1
  1. 1Department of General Surgery, Beijing Jishuitan Hospital, Beijing, China
  2. 2Department of Radiology, Beijing Jishuitan Hospital, Beijing, China
  3. 3Department of Pathology, Beijing Jishuitan Hospital, Beijing, China
  1. Correspondence to Rong-jie Bai, Department of Radiology, Beijing Jishuitan Hospital, Beijing 100035, China; bairongjie{at}126.com

Abstract

To explore the molecular pathogenesis of primary hyperparathyroidism (PHPT), we investigated the proliferation and apoptosis of parathyroid cells in a rabbit model of diet-induced PHPT. A total of 120 adult Chinese rabbits were randomly divided into normal diet (Ca:P, 1:0.7) group (control group) or a high-phosphate diet (Ca:P, 1:7) group (experimental group). The thyroid and parathyroid complexes were harvested for 1-month interval from month 1 to month 6. The expression of proliferation markers, including proliferating cell nuclear antigen (PCNA) and cyclin-D1, and B cell lymphoma-2 (Bcl-2), were evaluated by immunohistochemistry in thyroid and parathyroid tissues. Apoptosis was quantified by DNA-fragment terminal labeling. Our results demonstrated that parathyroid cells in the experimental group started proliferating from the end of the 2nd month, the expression of PCNA, Bcl-2, and cyclin-D1 were significantly higher in the PHPT group than those of the control group (p<0.05). Furthermore, the apoptosis index (AI) was positively correlated with the glandular cell count and expression of PCNA in the 6th month in the PHPT group. Overall, our results suggested that excessive proliferation and apoptosis of parathyroid cells may contribute to the pathogenesis of PHPT through PCNA-related, Bcl-2-related, and cyclin-D1-related pathways.

  • apoptosis
  • cell cycle
  • disease models, Animal
  • cell proliferation

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Footnotes

  • Contributors R-jB is corresponding author who is responsible for concept, design, definition of intellectual content, literature search, experimental studies, data analysis, and statistical analysis. J-tB is responsible for manuscript preparation, manuscript editing, and manuscript review. Other authors are responsible for literature search, experimental studies, and data acquisition. H-lZ and Z-hQ are responsible for specimen collection and preparation of the rabbit model. L-hG is responsible for the pathological graphic analysis. Y-qL, Z-xZ and XC are responsible for manuscript transplantation and review. R-jB is responsible for the overall content as guarantor.

  • Funding This study was supported by the National Natural Science Foundation of China (grant number 82171921, 81071130), Beijing Natural Science Foundation of China (grant number 7202063, 7102082).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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