scholarly journals Immunohistochemical analysis of low-grade and high-grade prostate carcinoma: relative changes of parathyroid hormone-related protein and its parathyroid hormone 1 receptor, osteoprotegerin and receptor activator of nuclear factor-kB ligand

2006 ◽  
Vol 60 (3) ◽  
pp. 290-284 ◽  
Author(s):  
F. C Perez-Martinez ◽  
V. Alonso ◽  
J. L Sarasa ◽  
S.-G. Nam-Cha ◽  
R. Vela-Navarrete ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Immunohistochemical Analysis ◽  
Low Grade ◽  
Nuclear Factor ◽  
High Grade ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Parathyroid Hormone 1 Receptor ◽  
Receptor Activator ◽  
Nuclear Factor Kb

scholarly journals Parathyroid Hormone-Related Protein (PTHrP) Accelerates Soluble RANKL Signals for Downregulation of Osteogenesis of Bone Mesenchymal Stem Cells

2019 ◽  
Vol 8 (6) ◽  
pp. 836 ◽  
Author(s):  
Jeevithan Elango ◽  
Saeed Ur Rahman ◽  
Yves Henrotin ◽  
José Eduardo Maté Sánchez de Val ◽  
Bin Bao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Parathyroid Hormone ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Related Protein ◽  
Bone Mesenchymal Stem Cells ◽  
Parathyroid Hormone Related Protein ◽  
Receptor Activator

A recent study reported the expression of receptor activator of nuclear factor-κB (RANK) in mesenchymal stem cells (MSCs) surface that negatively regulates osteogenesis of MSCs. Empirical evidence from the previous study confirmed the role of parathyroid hormone-related protein (PTHrP) in osteoblastogenesis. However, it is necessary to understand the paracrine role of PTHrP and RANKL for osteogenesis in order to explore the hidden secrets in bone biology. Considering the above concept, paracrine cues of soluble-receptor activator of nuclear factor-κB ligand (sRANKL) and PTHrP in osteogenic differentiation of MSCs were investigated. Our results confirmed that sRANKL increased the expression of surface-RANK in MSCs at the earlier stage of osteogenesis, which was downregulated later in differentiated MSCs. In contrast, RANKL expression was low at the earlier stage of MSCs proliferation and high at the differentiation stage of MSCs, which may play a fundamental role in osteoclast formation. sRANKL downregulated osteogenesis of MSCs by decreasing progressive ankylosis (ANK) protein expression while PTHrP upregulated the osteogenic exploitive effect of sRANKL. Interestingly, when they were co-cultured with MSCs, T-lymphocytes expressed high membrane-RANKL levels that contribute to osteogenesis inhibition during MSC differentiation. Thus, our results disclose that sRANKL treatment downregulates osteogenesis of MSCs by increasing RANK expression at the earlier stage of differentiation and by inhibiting ANK. Further, we demonstrated that PTHrP accelerated the downregulating osteogenic effect of sRANKL.

Zahneruption und Zahnbewegung bei kongenitaler Retention mit Mutation des PTH1-Rezeptor-Gens

2018 ◽  
Vol 50 (03) ◽  
pp. 169-175
Author(s):  
Jan Danz
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Receptor ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Soluble Receptor ◽  
Related Protein ◽  
Parathyroid Hormone Receptor ◽  
Parathyroid Hormone Related Protein ◽  
Receptor Activator

ZusammenfassungDie primäre kongenitale Retention von Zähnen des Typs heterozygote Mutation von Parathyroid hormone receptor type 1 (PTH1R) mit autosomal dominanter Vererbung ist eine Regulationsstörung des Knochenumbaus, welche die Zahneruption und die Zahnbewegungen stark behindert oder verhindert. Bei beginnender Zahneruption und bei Zahnbewegung wird PTHrP (Parathyroid hormone-related protein) ausgeschüttet, welches durch Osteozyten den Knochenumbau Richtung Knochenresorption entkoppelt. Bei PTH1R-Mutation mit Funktionsverlust dieses Rezeptors fehlt einerseits die Verringerung der Osteoprotegerin (OPG)- und der Sclerostin-Ausschüttung durch Osteozyten und andererseits die erhöhte Expression und Ausschüttung von Soluble receptor activator of nuclear factor κB (sRANKL) durch Osteozyten und Osteoblasten, was zu einer ausbleibenden Osteoklastenaktivierung führt. Ohne Knochenresorption durch Osteoklasten sind sowohl die Zahneruption als auch die Zahnbewegung gestört. Durch das als kompetitiver Antagonist des wnt-Rezeptor-Komplexes (kanonischer-wnt-Signalweg) und der BMP-I/BMP-II-Rezeptoren wirkende Sclerostin modulieren Osteozyten auch die Osteoblastenaktivität. Bei Verdacht auf kongenitale Retention ist eine humangenetische Abklärung zum Test einer PTH1-Rezeptor-Mutation ein wichtiges diagnostisches Mittel, um nicht erfolgsversprechende kieferorthopädische Therapien zu vermeiden und Behandlungsalternativen planen zu können.

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