No abstract available.
Parathyroid Hormone-Related Protein

No abstract available.
Hand* ; Parathyroid Hormone-Related Protein*

Hypercalcemia of malignancy due to metastatic gastric adenocarcinoma is extremely rare; in fact, to the best of our knowledge, only three case reports of hypercalcemia associated with metastatic gastric adenocarcinoma have been published in the literature to date. Herein, we report a rare case involving a 61-year-old African-American female who had hypercalcemia at initial presentation and who was later diagnosed with poorly differentiated gastric adenocarcinoma with extensive liver metastases, without bone involvement. She was found to have elevated parathyroid hormone-related peptide and normal parathyroid hormone levels. Despite aggressive treatment, she died within a few months of diagnosis.
Adenocarcinoma* ; Diagnosis ; Female ; Humans ; Hypercalcemia* ; Liver ; Middle Aged ; Neoplasm Metastasis ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein

Hypercalcemia is one of the most common paraneoplastic syndromes and believed to occur through two general mechanisms, one humoral and the other local. The former mechanism has been termed humoral hypercalcemia of malignancy (HHM) and has been associated with the secretion of various cytokines, including parathyroid hormone-related protein (PTHrP). PTHrP beats sttuctural and functional similarities to PTH and seems to play a key role in the pathogenesis of HHM. We experienced the case of HHM associated with hepatoma, a rare cause of HHM, in 48 year-old male. We found no evidence of bone metastasis. In this case, contrary to our general acknowledgment, serum 1,25 (OH)D concentration was elevated. We report this case with a brief review of related literatures.
Carcinoma, Hepatocellular* ; Cytokines ; Humans ; Hypercalcemia* ; Male ; Middle Aged ; Neoplasm Metastasis ; Paraneoplastic Syndromes ; Parathyroid Hormone-Related Protein*

In cancer patient, hypercalcemia may develop. The mechanism is local osteolysis by metastasis of cancinoma, or secretion of hormone such as PTHrP (parathyroid hormone related peptides). Bone metastasis in carcinoma of uterine cervix is uncommon. In this report, we present a case of hypercalcemia caused by metastasis of cervical carcinoma to the right acetabulum with a brief review of the literature.
Acetabulum* ; Cervix Uteri ; Female ; Humans ; Hypercalcemia* ; Neoplasm Metastasis* ; Osteolysis ; Parathyroid Hormone-Related Protein

OBJECTIVETo investigate the effect of parathyroid hormone related protein (PTHrP) on proliferation of human osteoblasts (MG-63) under the circumstance of tension force in vitro.

METHODSAn apparatus was designed and fabricated by which force was loaded onto the cultured cells in vitro. Reverse transcription-polymerase chain reaction (RT-PCR) was used for measuring the expression of PTHrP mRNA and c-fos mRNA. The effect of tension force and different PTHrP dose(0, 0.01, 0.1, 1 nmol/L) on the proliferation of human osteoblasts were examined using flow cytometry.

RESULTSVarious forces of the mechanical stretching exerted different influences on the intensities of the mRNA' expression. The strain of 12% induced the most remarkable mRNA' expression. The mitogenesis happened in the group with tension force (12%) combined with PTHrP was more active than that in the group with PTHrP or tension' force only. Tension force combined with PTHrP induced significantly more c-fos mRNA than that of tension force only.

CONCLUSIONThe mechanical stretching can inevitably influence the expression of PTHrP mRNA. The most active mitogenesis happened in the group with tension force combined with PTHrP. The effect may be related with the signaling pathways of c-fos.

OBJECTIVETo investigate the regulatory mechanism of parathyroid hormone-related protein (PTHrP) in proliferation and differentiation of chondrocytes of condyle in fetal mouse.

METHODSChondrocytes of condyle in fetal mouse were separated and cultured in vitro, the influence of PTHrP on proliferation and differentiation was observed.

RESULTSAfter two weeks' culture in 0.01 nmol/L, 0.1 nmol/L, 1 nmol/L, 10 nmol/L human PTHrP, there was significant difference in the number of cartilage nodule formed between experiment group and control group (P<0.05), and there was no significant difference in 0.01 nmol/L group (P>0.05). Alkaline phosphatase (ALP) activity was significantly intensified in experiment group and control group (P<0.05). Meanwhile, it was found that this function of promotion was lessened after anti-PTHR antibody used.

CONCLUSIONIt can be seen that PTHrP, via its receptor, can promote proliferation and differentiation of chondrocytes of condyle, which resemble its modulation mechanism in epiphyseal growth plate cartilage intramembrane in mandibule.

OBJECTIVETo study parathyroid hormone-related protein (PTHrP) expression during forward mandibular positioning and compare it with the expression during natural growth in different seasons.

METHODSSixty-four SD rats were randomly divided into experimental and control groups. Each group were randomly divided into four groups according to seasons. Immunohistochemical (IHC) methods were used to test the protein expression of PTHrP. Macroscopic and microscopic approach were applied to analyze the results.

RESULTSPTHrP expressed in mandibular condylar cartilage (MCC), the expression was accelerated and enhanced when the mandible was positioned forward. Furthermore, there was a seasonal rhythm in the protein expression of PTHrP in both experimental and control groups. The protein expression in spring group rose more than other groups.

CONCLUSIONThe functional appliance therapy can enhance the protein expression of PTHrP. The enhancement has a seasonal rhythm, which indicates that for the functional treatment better results can be achieved in spring.

PTH-related peptide (PTHrP) improves the bone marrow micro-environment to activate the bone-remodelling, but the coordinated regulation of PTHrP and transforming growth factor-β (TGFβ) signalling in TMJ-OA remains incompletely understood. We used disordered occlusion to establish model animals that recapitulate the ordinary clinical aetiology of TMJ-OA. Immunohistochemical and histological analyses revealed condylar fibrocartilage degeneration in model animals following disordered occlusion. TMJ-OA model animals administered intermittent PTHrP (iPTH) exhibited significantly decreased condylar cartilage degeneration. Micro-CT, histomorphometry, and Western Blot analyses disclosed that iPTH promoted subchondral bone formation in the TMJ-OA model animals. In addition, iPTH increased the number of osterix (OSX)-positive cells and osteocalcin (OCN)-positive cells in the subchondral bone marrow cavity. However, the number of osteoclasts was also increased by iPTH, indicating that subchondral bone volume increase was mainly due to the iPTH-mediated increase in the bone-formation ability of condylar subchondral bone. In vitro, PTHrP treatment increased condylar subchondral bone marrow-derived mesenchymal stem cell (SMSC) osteoblastic differentiation potential and upregulated the gene and protein expression of key regulators of osteogenesis. Furthermore, we found that PTHrP-PTH1R signalling inhibits TGFβ signalling during osteoblastic differentiation. Collectively, these data suggested that iPTH improves OA lesions by enhancing osteoblastic differentiation in subchondral bone and suppressing aberrant active TGFβ signalling. These findings indicated that PTHrP, which targets the TGFβ signalling pathway, may be an effective biological reagent to prevent and treat TMJ-OA in the clinic.
Animals ; Osteoclasts ; Osteogenesis ; Parathyroid Hormone-Related Protein/pharmacology* ; Temporomandibular Joint ; Transforming Growth Factor beta/pharmacology*

Familial hypocalciuric hypercalcemia (FHH) is a genetic disorder characterized by mild asymptomatic hypercalcemia, hypocalciuria, a decreased urinary calcium-creatinine ratio, and normal or elevated parathyroid hormone levels. FHH is caused by an inactivating heterozygous mutation of the calcium-sensing receptor (CaSR) gene. A 62-year-old woman was referred to our center because of inadequate glucose control. Her son had hypercalcemia. Biochemical and endocrine studies showed hypercalcemia, hypocalciuria, a decreased urinary calcium-creatinine ratio, normal parathyroid hormone levels, normal PTH-related peptide levels, decreased free T4, increased TSH, and thyroid antibody positivity. Direct sequencing analyses revealed a heterozygous mutation of G21R at exon 2 and a single nucleotide polymorphism of R990G at exon 7 of the CaSR gene. Here, we report a case of FHH associated with a heterozygous mutation and a single nucleotide polymorphism of the CaSR gene, which coexisted with autoimmune thyroiditis and hypothyroidism. To our knowledge, this is the first such case reported.
Exons ; Female ; Glucose ; Humans ; Hypercalcemia ; Hypothyroidism ; Middle Aged ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein ; Polymorphism, Single Nucleotide ; Receptors, Calcium-Sensing ; Thyroid Gland ; Thyroiditis, Autoimmune