Purpose: In the pathogenesis of the primary hyperparathyroidism (PHPT), dysregulation has been observed in extracellular signal-regulated 1/2 (ERK 1/2), c-Jun N-terminal kinase (JNK), and phosphatidylinositol 3 kinase (PI3K) pathways. Progranulin (PGRN) is a glycoprotein found in many tissues and has been observed to activate MAPK, JNK, PI3K pathways in multiple studies. We aim to investigate the progranulin expression in parathyroid adenomas and establish its relationship with clinical parameters and comorbidities in patients with PHPT.
Methods: 182 cases were included in our study, consisting of 102 patients with PHPT and 80 controls. All cases with PHPT were operated and parathyroid adenomas were pathologically confirmed. The PGRN staining patterns were examined by applying anti-granulin (anti-GRN) antibody at 1/300 dilution to the parathyroid samples of the cases.
Results: Within the patient group, negative staining was observed in 59 (57.8%) samples, mild staining in 26 (25.5%) samples, and strong staining in 17 (16.7%) samples. In the control group, all samples showed strong staining. There was a significant decrease in PGRN staining in the patient group compared to the control group (p < 0.001). There was no significant relationship between the degree of PGRN staining and age, biochemical parameters in patients with PHPT. Patients were compared in terms of PHPT-related complications and PGRN expression, no significant difference was observed.
Conclusion: Our findings show that adenomas expressed lower PGRN compared to normal parathyroid tissue, suggesting that PGRN expression loss may play an important role in pathogenesis of parathyroid adenomas.
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