Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor

BMC Surgery

Research

Ling Zhang¹  Linping Huang²  Meng Yang²  Jun Liu²  Yao Lu²  Xiaoliang Sun²  Haoyang Ji²  Aiping Song³  Honglei Zhang³  Xin Li⁴  Bo Pang⁵ 

[1] Center of Nephrology, China-Japan Friendship Hospital, 100029, Beijing, China;Department of General Surgery, China-Japan Friendship Hospital, 100029, Beijing, China;Department of Pathology, China-Japan Friendship Hospital, 100029, Beijing, China;Institute of Clinical Medicine Research, China-Japan Friendship Hospital, 100029, Beijing, China;State Key Laboratory of Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, China CDC 155, Changbai Road, Changping, 102206, Beijing, China;

关键词: Calcium-sensing receptor;    Secondary hyperparathyroidism;    Primary hyperparathyroidism;   

DOI  :  10.1186/s12893-023-01928-5

 received in 2022-02-08, accepted in 2023-02-01,  发布年份 2023

来源: Springer

【 摘 要 】

BackgroundDecreased calcium-sensing receptor (CaSR) has been observed in hyperparathyroidism (HPT) without a known mechanism. The purpose of this study was to evaluate the expression of CaSR in primary (PHPT) and secondary (SHPT) subtypes.MethodsImmunohistochemical (IHC) staining and quantitative real-time PCR (qRT-PCR) assay were used to measure the differences in expression of CaSR protein and gene in PHPT and SHPT human samples, compared to matched controls.ResultsCaSR protein was differentially downregulated in SHPT and PHPT compared to normal parathyroid tissues (2.42 ± 0.5 vs. 3.2 ± 0.62, P < 0.05; 1.8 ± 0.83 vs. 3.2 ± 0.62, P < 0.05, respectively). Furthermore, SHPT tissues exhibited significantly higher levels of CaSR mRNA (0.29 ± 0.23 vs. 0.01 ± 0.12, P < 0.05) and protein (2.42 ± 0.5 vs. 1.8 ± 0.83, P < 0.05) than those in PHPT tissue samples.ConclusionDepressed CaSR expression was a critical pathological hallmark of HPT. We found a differential decline of CaSR, in terms of both mRNA and protein levels, in PHPT and SHPT human samples. We think that CaSR dysregulation occurred at the very beginning of disease onset in PHPT, while a similar pathological scenario appeared at the later stage of SHPT. Future studies should be directed to dissect the mechanistic involvement of CaSR in PHPT and SHPT in order to bring treatment precisions in HPT management.

【 授权许可】

CC BY   
© The Author(s) 2023

【 图 表 】

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