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

Abstract Background Decreased 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. Methods Immunohistochemical (IHC) staining and qua...

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Main Authors: Xin Li, Yao Lu, Ling Zhang, Aiping Song, Honglei Zhang, Bo Pang, Jun Liu, Xiaoliang Sun, Haoyang Ji, Linping Huang, Meng Yang
Format: Article
Language:English
Published: BMC 2023-02-01
Series:BMC Surgery
Subjects:
Online Access:https://doi.org/10.1186/s12893-023-01928-5
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author Xin Li
Yao Lu
Ling Zhang
Aiping Song
Honglei Zhang
Bo Pang
Jun Liu
Xiaoliang Sun
Haoyang Ji
Linping Huang
Meng Yang
author_facet Xin Li
Yao Lu
Ling Zhang
Aiping Song
Honglei Zhang
Bo Pang
Jun Liu
Xiaoliang Sun
Haoyang Ji
Linping Huang
Meng Yang
author_sort Xin Li
collection DOAJ
description Abstract Background Decreased 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. Methods Immunohistochemical (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. Results CaSR 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. Conclusion Depressed 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.
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spelling doaj.art-274afad519e04588a32e086b4be11da02023-02-12T12:03:29ZengBMCBMC Surgery1471-24822023-02-012311510.1186/s12893-023-01928-5Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptorXin Li0Yao Lu1Ling Zhang2Aiping Song3Honglei Zhang4Bo Pang5Jun Liu6Xiaoliang Sun7Haoyang Ji8Linping Huang9Meng Yang10Institute of Clinical Medicine Research, China-Japan Friendship HospitalDepartment of General Surgery, China-Japan Friendship HospitalCenter of Nephrology, China-Japan Friendship HospitalDepartment of Pathology, China-Japan Friendship HospitalDepartment of Pathology, China-Japan Friendship HospitalState Key Laboratory of Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, China CDC 155Department of General Surgery, China-Japan Friendship HospitalDepartment of General Surgery, China-Japan Friendship HospitalDepartment of General Surgery, China-Japan Friendship HospitalDepartment of General Surgery, China-Japan Friendship HospitalDepartment of General Surgery, China-Japan Friendship HospitalAbstract Background Decreased 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. Methods Immunohistochemical (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. Results CaSR 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. Conclusion Depressed 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.https://doi.org/10.1186/s12893-023-01928-5Calcium-sensing receptorSecondary hyperparathyroidismPrimary hyperparathyroidism
spellingShingle Xin Li
Yao Lu
Ling Zhang
Aiping Song
Honglei Zhang
Bo Pang
Jun Liu
Xiaoliang Sun
Haoyang Ji
Linping Huang
Meng Yang
Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor
BMC Surgery
Calcium-sensing receptor
Secondary hyperparathyroidism
Primary hyperparathyroidism
title Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor
title_full Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor
title_fullStr Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor
title_full_unstemmed Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor
title_short Primary and secondary hyperparathyroidism present different expressions of calcium-sensing receptor
title_sort primary and secondary hyperparathyroidism present different expressions of calcium sensing receptor
topic Calcium-sensing receptor
Secondary hyperparathyroidism
Primary hyperparathyroidism
url https://doi.org/10.1186/s12893-023-01928-5
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