Comparative proteomic analysis of chief and oxyphil cell nodules in refractory uremic hyperparathyroidism by iTRAQ coupled LC-MS/MS

Li, Shensen; Mao, Jianping; Wang, Mengjing; Ni, Li; Tao, Ye; Huang, Bihong; Chen, Jing

doi:10.1016/j.jprot.2018.02.029

Cited by 7 publications

(7 citation statements)

References 46 publications

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“…Therefore, to identify the critical regulatory factors of oxyphil cell proliferation might be helpful to unravel the pathogenesis and therapeutic target of SHPT. Recently, Li et al (2018) aimed to identify proteins expressed differently in oxyphil compared with chief cells, and eventually found that mitochondrial proteins, consistent with the above results discussed, and metabolisms involving protein synthesis and cell cycle regulation were significantly altered in oxyphil cell. Generally, active vitamin D is used as treatment option but sometime resistance occurs.…”

Section: Proteomics/metabolomics Studies On Ckd-mbdsupporting

confidence: 54%

“…In this study, down-regulated vitamin D binding protein (DBP) might be a potential explanation in the calcitriol treatment resistance by impairing transportation of vitamin D. The critical MIF-CUL1 axis that associated with ubiquitin mediated proteolysis might participate in the proliferation of oxyphil cell due to their significantly altered expression. The results shed light on mitochondria dysfunction in proliferation mechanisms of oxyphil cells, which accelerates the SHPT progression ( Li et al, 2018 ).…”

Section: Proteomics/metabolomics Studies On Ckd-mbdmentioning

confidence: 96%

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Disorders of Calcium and Phosphorus Metabolism and the Proteomics/Metabolomics-Based Research

Sun

et al. 2020

Front. Cell Dev. Biol.

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Section: Proteomics/metabolomics Studies On Ckd-mbdsupporting

confidence: 54%

Section: Proteomics/metabolomics Studies On Ckd-mbdmentioning

confidence: 96%

Disorders of Calcium and Phosphorus Metabolism and the Proteomics/Metabolomics-Based Research

Sun

et al. 2020

Front. Cell Dev. Biol.

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“…The parathyroid glands of healthy adults are comprised predominantly of chief cells, but in conditions such as secondary hyperparathyroidism (SHPT) caused by chronic kidney disease, the relative abundance of a second parathyroid cell type known as oxyphils can increase dramatically ( 11 , 12 ). Parathyroid oxyphils are characterized by high mitochondrial content and appear more abundant in older individuals ( 13 ), but the origin and physiological functions of these cells are unknown.…”

Section: Introductionmentioning

confidence: 99%

Digital spatial profiling of human parathyroid tumors reveals cellular and molecular alterations linked to vitamin D deficiency

Chang

Sosa

et al. 2023

PNAS Nexus

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Primary hyperparathyroidism (PHPT) is a common endocrine neoplastic disorder characterized by disrupted calcium homeostasis secondary to inappropriately elevated parathyroid hormone (PTH) secretion. Low levels of serum 25-hydroxyvitamin D (25OHD) are significantly more prevalent in PHPT patients than in the general population (1-3), but the basis for this association remains unclear. We employed a spatially-defined in situ whole-transcriptomics and selective proteomics profiling approach to compare gene expression patterns and cellular composition in parathyroid adenomas from vitamin D-deficient or vitamin D-replete PHPT patients. A cross-sectional panel of eucalcemic cadaveric donor parathyroid glands were examined in parallel as normal tissue controls. Here, we report that parathyroid tumors from vitamin D-deficient PHPT patients (Def-Ts) are intrinsically different from those of vitamin D-replete patients (Rep-Ts) of similar age and pre-operative clinical presentation. Parathyroid oxyphil cell content is markedly higher in Def-Ts (47.8%) relative to Rep-Ts (17.8%) and normal donor glands (7.7%). Vitamin D-deficiency is associated with increased expression of electron transport chain and oxidative phosphorylation pathway components. Parathyroid oxyphil cells, while morphologically distinct, are comparable to chief cells at the transcriptional level, and vitamin D-deficiency affects the transcriptional profiles of both cell types in a similar manner. These data suggest that oxyphil cells are derived from chief cells and imply that their increased abundance may be induced by low vitamin D status. Geneset enrichment analysis reveals that pathways altered in Def-Ts are distinct from Rep-Ts, suggesting alternative tumor etiologies in these groups. Increased oxyphil content may thus be a morphological indicator of tumor-predisposing cellular stress.

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“…The proportion of oxyphil cells was significantly increased in CKD and had a positive correlation with total PTG weight in SHPT, which suggests that oxyphil cell proliferation is sensitive to PTG stimulation [85]. After calcimimetics treatment, the oxyphil cell content was significantly higher than in the paricalcitol group (a less calcemic analog of calcitriol) [80,86]. In addition, in a retrospective analysis, the proliferation of oxyphil cells was the major pathological progression in SHPT and was highly associated with calcitriol treatment.…”

Section: The Change Of Parathyroid Cells Composition In Shptmentioning

confidence: 99%

The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD

Yeih

Hou

et al. 2018

Nutrients

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In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.

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Comparative proteomic analysis of chief and oxyphil cell nodules in refractory uremic hyperparathyroidism by iTRAQ coupled LC-MS/MS

Cited by 7 publications

References 46 publications

Disorders of Calcium and Phosphorus Metabolism and the Proteomics/Metabolomics-Based Research

Disorders of Calcium and Phosphorus Metabolism and the Proteomics/Metabolomics-Based Research

Digital spatial profiling of human parathyroid tumors reveals cellular and molecular alterations linked to vitamin D deficiency

The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD

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