Chi3l1 induction in Response to LPS Suppresses Osteoblast Apoptosis

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Huang Liying
Huang Liying
σ
Li Yishan
Li Yishan
ρ
Weng Xiquan
Weng Xiquan
α Guangzhou Sport University

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Chi3l1 induction in Response to LPS Suppresses Osteoblast Apoptosis

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Abstract

Upregulation of Chitinase-3-like protein 1(Chi3l1), a member of glycohydrolase family 18, is frequently seen in diseases associated with inflammatory responses, such as atherosclerosis, meningitis and asthma. However, little is known about either its regulation or its functions in the physiological and pathological processes in bone and related cells. In the mouse model of osteomyelitis used in this study, Chi3l1 was induced in the infected area. In vitro stimulation of osteoblasts and mesenchymal stem cells (MSCs) by lipopolysaccharide (LPS) resulted in elevated Chi3l1 expression. Overexpression of Chi3l1 attenuated TNFα-induced osteoblast apoptosis and promoted cell survival. Furthermore, Chi3l1 induced phosphorylation of AKT in a time-dependent fashion, while an inhibitor of the AKT signaling pathway abolished both the pro-survival and the anti-apoptotic effects of Chi3l1. Therefore, Chi3l1 might play a protective role in infected or inflammatory bone tissues by suppressing osteoblast apoptosis via an AKTdependent pathway.

References

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Funding

No external funding was declared for this work.

Conflict of Interest

The authors declare no conflict of interest.

Ethical Approval

No ethics committee approval was required for this article type.

Data Availability

Not applicable for this article.

How to Cite This Article

Huang Liying. 2017. \u201cChi3l1 induction in Response to LPS Suppresses Osteoblast Apoptosis\u201d. Global Journal of Science Frontier Research - I: Interdisciplinary GJSFR-I Volume 16 (GJSFR Volume 16 Issue I3): .

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GJSFR Volume 16 Issue I3
Pg. 13- 22
Journal Specifications

Crossref Journal DOI 10.17406/GJSFR

Print ISSN 0975-5896

e-ISSN 2249-4626

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GJSFR-I Classification: FOR Code: 060199
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v1.2

Issue date

January 25, 2017

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en
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Upregulation of Chitinase-3-like protein 1(Chi3l1), a member of glycohydrolase family 18, is frequently seen in diseases associated with inflammatory responses, such as atherosclerosis, meningitis and asthma. However, little is known about either its regulation or its functions in the physiological and pathological processes in bone and related cells. In the mouse model of osteomyelitis used in this study, Chi3l1 was induced in the infected area. In vitro stimulation of osteoblasts and mesenchymal stem cells (MSCs) by lipopolysaccharide (LPS) resulted in elevated Chi3l1 expression. Overexpression of Chi3l1 attenuated TNFα-induced osteoblast apoptosis and promoted cell survival. Furthermore, Chi3l1 induced phosphorylation of AKT in a time-dependent fashion, while an inhibitor of the AKT signaling pathway abolished both the pro-survival and the anti-apoptotic effects of Chi3l1. Therefore, Chi3l1 might play a protective role in infected or inflammatory bone tissues by suppressing osteoblast apoptosis via an AKTdependent pathway.

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Chi3l1 induction in Response to LPS Suppresses Osteoblast Apoptosis

Huang Liying
Huang Liying Guangzhou Sport University
Li Yishan
Li Yishan
Weng Xiquan
Weng Xiquan

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