Effects of CCN3 on rat cartilage endplate chondrocytes cultured under serum deprivation in vitro

Ding, Lei; Wu, Jingsong; Li, Defang; Wang, Houlei; Zhu, Bin; Lu, Wenjing; Xu, Guoxiong

doi:10.3892/mmr.2016.4803

Cited by 5 publications

(4 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PCR products were subjected to amplification curve analysis and quantified using SYBR Green (Invitrogen; Thermo Fisher Scientific, Inc.). The data were normalized to GAPDH and quantified using the 2 −ΔΔCq method ( 27 , 28 ).…”

Section: Methodsmentioning

confidence: 99%

Caveolin-1 regulates oxidative stress-induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro

Ding¹,

Zeng²,

Wu³

et al. 2017

Molecular Medicine Reports

Self Cite

View full text Add to dashboard Cite

Previous studies have indicated that cellular senescence is a critical underlying mechanism of intervertebral disc degeneration. However, the precise mechanism by which cellular senescence accelerates disc degeneration has not been fully elucidated. Caveolin-1 has recently emerged as an important regulator of cellular senescence. Therefore, the aim of the present study was to investigate whether caveolin-1 is involved in nucleus pulposus (NP) cellular senescence during oxidative stress. PCR was used to detect caveolin-1 mRNA expression and protein expression was detected by western blotting. Caveolin-1 expression at the mRNA and protein levels was markedly increased following treatment with tert-butyl hydroperoxide, and an increase in premature senescence was observed, as determined by senescence-associated β-galactosidase staining and the decline of cellular proliferative ability. In addition, caveolin-1 gene expression was successfully knocked down by lentivirus-mediated RNA interference, which exerted a protective effect against the cellular senescence induced by oxidative stress. Notably, p53 and p21 protein expression, though not p16 protein expression, decreased with caveolin-1 silencing. The results suggested that caveolin-1 may be involved in NP cellular senescence during oxidative stress in vitro, mainly via the p53/p21 signaling pathway. Thus, caveolin-1 may represent a novel therapeutic target for the prevention of intervertebral disc degeneration.

show abstract

Section: Methodsmentioning

confidence: 99%

Caveolin-1 regulates oxidative stress-induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro

Ding¹,

Zeng²,

Wu³

et al. 2017

Molecular Medicine Reports

Self Cite

View full text Add to dashboard Cite

show abstract

“…CCN3 may regulate apoptosis under conditions of serum deprivation. The presence of this CCN decreased levels of both proteoglycan and collagen, which may mimic the cartilage environment in which no vascularization occurs and thus conditions are somewhat hypoxic [291]. Bone regeneration in mice that lack CCN3 is enhanced [292].…”

Section: Ccns In Cartilage and Bone Pathophysiologymentioning

confidence: 97%

Composition and Function of the Extracellular Matrix in the Human Body

Travascio¹

2016

View full text Add to dashboard Cite

The moral rights of the editor(s) and the author(s) have been asserted. All rights to the book as a whole are reserved by InTech. The book as a whole (compilation) cannot be reproduced, distributed or used for commercial or non-commercial purposes without InTech's written permission. Enquiries concerning the use of the book should be directed to InTech's rights and permissions department (permissions@intechopen.com). Violations are liable to prosecution under the governing Copyright Law.Individual chapters of this publication are distributed under the terms of the Creative Commons Attribution 3.0 Unported License which permits commercial use, distribution and reproduction of the individual chapters, provided the original author(s) and source publication are appropriately acknowledged. More details and guidelines concerning content reuse and adaptation can be found at http://www.intechopen.com/copyright-policy.html. NoticeStatements and opinions expressed in the chapters are these of the individual contributors and not necessarily those of the editors or publisher. No responsibility is accepted for the accuracy of information contained in the published chapters. The publisher assumes no responsibility for any damage or injury to persons or property arising out of the use of any materials, instructions, methods or ideas contained in the book.

show abstract

“… 168 Other conditions/scenarios, such as high-glucose environments and serum deprivation, also promote apoptosis of cartilage endplate cells via mitochondrial mechanisms. 169 Serum deprivation increased apoptosis of cartilage endplate cells, 170 and this process has been shown to be induced by the mitochondrial intrinsic pathway. 171 However, research on the role of estrogen in these processes warrants further exploration.…”

Section: Molecular Mechanisms By Which Estrogen Alleviates Ivd Degene...mentioning

confidence: 99%

Low back pain and osteoarthritis pain: a perspective of estrogen

et al. 2023

View full text Add to dashboard Cite

Low back pain (LBP) is the world’s leading cause of disability and is increasing in prevalence more rapidly than any other pain condition. Intervertebral disc (IVD) degeneration and facet joint osteoarthritis (FJOA) are two common causes of LBP, and both occur more frequently in elderly women than in other populations. Moreover, osteoarthritis (OA) and OA pain, regardless of the joint, are experienced by up to twice as many women as men, and this difference is amplified during menopause. Changes in estrogen may be an important contributor to these pain states. Receptors for estrogen have been found within IVD tissue and nearby joints, highlighting the potential roles of estrogen within and surrounding the IVDs and joints. In addition, estrogen supplementation has been shown to be effective at ameliorating IVD degeneration and OA progression, indicating its potential use as a therapeutic agent for people with LBP and OA pain. This review comprehensively examines the relationship between estrogen and these pain conditions by summarizing recent preclinical and clinical findings. The potential molecular mechanisms by which estrogen may relieve LBP associated with IVD degeneration and FJOA and OA pain are discussed.

show abstract

Effects of CCN3 on rat cartilage endplate chondrocytes cultured under serum deprivation in vitro

Cited by 5 publications

References 28 publications

Caveolin-1 regulates oxidative stress-induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro

Caveolin-1 regulates oxidative stress-induced senescence in nucleus pulposus cells primarily via the p53/p21 signaling pathway in vitro

Composition and Function of the Extracellular Matrix in the Human Body

Low back pain and osteoarthritis pain: a perspective of estrogen

Contact Info

Product

Resources

About