RT Journal Article
SR Electronic
T1 Excessive proliferation and apoptosis of parathyroid cells contribute to primary hyperparathyroidism in rabbit model
JF Journal of Investigative Medicine
JO J Investig Med
FD BMJ Publishing Group Ltd
SP 1392
OP 1398
DO 10.1136/jim-2021-002184
VO 70
IS 6
A1 Jing-tao Bi
A1 Rong-jie Bai
A1 Hui-li Zhan
A1 Zhan-hua Qian
A1 Li-hua Gong
A1 Ya-qi Liu
A1 Zhi-xue Zheng
A1 Xuan Cai
YR 2022
UL http://hw-f5-jim.highwire.org/content/70/6/1392.abstract
AB 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.No data are available.