Research on the function and related mechanism of P27 gene in the intervertebral disc degeneration of mice.

Abstract:

:This study aims to investigate the function and related mechanism of P27 gene in intervertebral disc (IVD) degeneration of mice. X-ray, immunohistochemical staining, and alkaline phosphatase (ALP) histochemical staining were used to analyze the phenotypic difference of the intervertebral discs of 4-week-old mice with P27 gene knockout (P27-/-) and wild-type (WT) mice in the same brood. Protein in the intervertebral disc was extracted and western blot analysis was employed to detect the changes in the expression of related molecules in the Shh-signal pathways, including Shh, Patched, Smoothened and Gli2. As a result, the ALP histochemical staining revealed that the ALP-positive area of mice in the P27-/- group was obviously increased compared to the 4-week-old mice of the same brood in the WT group. In addition, the Col-I immunohistochemical staining showed that the Col-I-positive area of mice in the P27-/- group was significantly increased compared to mice in the WT group. Furthermore, Smo-positive cell rate of mice in the P27-/- group was apparently increased compared to mice in the WT group. Western blot analysis revealed that in terms of changes of protein expression levels of Shh, Patched, Smoothened and Gli2 in the intervertebral disc, protein expression levels of Shh, Patched, Smoothened and Gli2 of mice in the P27-/- group were significantly increased compared to those of mice in the WT group. The results show that P27 deficiency activates the expression of Shh-signal pathway and promotes the proliferation of osteoblast, thus, playing a role in promoting IVD degeneration, which provides a scientific and reliable experimental basis for the treatment of the IVD degeneration-related diseases in clinical practice.

journal_name

Exp Ther Med

authors

Liu X,Wang D,Zhang Z,Zhu F,Yao A,Tian J,Miao D

doi

10.3892/etm.2017.4584

subject

Has Abstract

pub_date

2017-08-01 00:00:00

pages

1141-1145

issue

2

eissn

1792-0981

issn

1792-1015

pii

ETM-0-0-4584

journal_volume

14

pub_type

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