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Endogenous parathyroid hormone (PTH) signals through osteoblasts via RANKL during fracture healing to affect osteoclasts.

Abstract：

AIM:To investigate the effect of endogenous PTH deficiency on osteoclasts during fracture healing and its mechanism. METHODS:A femoral fracture model was used to determine the role of endogenous PTH in fracture healing. Immunohistochemistry, qPCR, and Western blot were used to determine the potential functions and mechanisms of endogenous PTH. RESULT:In this study, we found that expression of RANKL and CK was lower in PTH knockout (KO) mice than in wild type (WT) mice. In vitro culture of osteoclasts showed that under the same stimulation, there was no statistical difference in the number of osteoclasts and the area of bone resorption areas in PTH WT mice and PTH KO mice. We found that a high concentration of RANKL could promote the number and activity of osteoclasts. Upon induction of osteoblasts in vitro, those from the PTH WT group expressed higher RANKL protein and mRNA than those from the PTH KO group. Lastly, we confirmed that the PI3K/AKT/STAT5 pathway promotes RANKL increase from osteoblasts. CONCLUSION:During fracture healing, endogenous PTH deficiency can affect osteoclast activity by reducing RANKL expression in osteoblasts.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Sun P,Wang M,Yin GY

doi

10.1016/j.bbrc.2020.02.177

subject

Has Abstract

pub_date

2020-05-14 00:00:00

pages

850-856

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)30501-5

journal_volume

525

pub_type

杂志文章

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