2019
DOI: 10.1002/jor.24425
|View full text |Cite
|
Sign up to set email alerts
|

CCN5 Reduces Ligamentum Flavum Hypertrophy by Modulating the TGF‐β Pathway

Abstract: Ligamentum flavum hypertrophy (LFH) is the most important component of lumbar spinal canal stenosis. Although the pathophysiology of LFH has been extensively studied, no method has been proposed to prevent or treat it. Since the transforming growth factor‐β (TGF‐β) pathway is known to be critical in LFH pathology, we investigated whether LFH could be prevented by blocking or modulating the TGF‐β mechanism. Human LF cells were used for the experiments. First, we created TGF‐β receptor 1 (TGFBR1) knock out (KO) … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
23
0

Year Published

2020
2020
2024
2024

Publication Types

Select...
7

Relationship

0
7

Authors

Journals

citations
Cited by 20 publications
(25 citation statements)
references
References 26 publications
1
23
0
Order By: Relevance
“…[105][106][107] As previously reported, CCN4 and CCN5 is abundantly expressed in hypertrophied LF specimens. 108,109 Furthermore, CCN5 modulates the TGF-β1 pathway when acting on fibroblasts via inhibiting TGF-β1induced transdifferentiation of fibroblast to myofibroblast by activating Smad2/3 complex via TGF-β1/2 receptors. 109 Moreover, microRNA transcriptome analysis showed that Aryl hydrocarbon receptor and Wnt/β-catenin signaling may also be involved in TGF-β1-induced LF fibrosis ( Figure 2).…”
Section: Tgf-βmentioning
confidence: 99%
See 1 more Smart Citation
“…[105][106][107] As previously reported, CCN4 and CCN5 is abundantly expressed in hypertrophied LF specimens. 108,109 Furthermore, CCN5 modulates the TGF-β1 pathway when acting on fibroblasts via inhibiting TGF-β1induced transdifferentiation of fibroblast to myofibroblast by activating Smad2/3 complex via TGF-β1/2 receptors. 109 Moreover, microRNA transcriptome analysis showed that Aryl hydrocarbon receptor and Wnt/β-catenin signaling may also be involved in TGF-β1-induced LF fibrosis ( Figure 2).…”
Section: Tgf-βmentioning
confidence: 99%
“…108,109 Furthermore, CCN5 modulates the TGF-β1 pathway when acting on fibroblasts via inhibiting TGF-β1induced transdifferentiation of fibroblast to myofibroblast by activating Smad2/3 complex via TGF-β1/2 receptors. 109 Moreover, microRNA transcriptome analysis showed that Aryl hydrocarbon receptor and Wnt/β-catenin signaling may also be involved in TGF-β1-induced LF fibrosis ( Figure 2). 110 Together, TGF-β1 not only activates the formation of ECM in fibroblast cells, it also increases the differentiation of fibroblast to myofibroblast by promoting or triggering the processes of producing ECM.…”
Section: Tgf-βmentioning
confidence: 99%
“…Unlike the other CCN family proteins, CCN5 specially lacks a cysteine-rich carboxyl-terminal repeat domain, suggesting that it may be an alternative regulator of other CCN family proteins. Comparison studies of CCN2 with prominent pro-fibrotic activity in cardiac remodeling, in which CCN5 is best characterized, reported anti-hypertrophic and anti-fibrotic effects in the heart ( Jeong et al., 2016 ; Ye et al., 2019 ). Besides cardiac tissue, lung and adipose tissue show high CCN5 expression ( Hammarstedt et al., 2013 ; Fiaturi et al., 2018 ; Grunberg et al., 2018 ).…”
Section: Discussionmentioning
confidence: 99%
“…Several members of the CCN family play essential roles in the development of pressure overload-induced myocardial fibrosis. CCN2 (cellular communication network 2), also called as connective tissue growth factor, is a pro-fibrotic mediator in the development of CF, which can be induced by TGF-β 1 in cardiac fibroblasts and cardiomyocytes ( Ye et al., 2019 ). Besides these pro-fibrotic effects of CCN2, the anti-fibrotic potential of cellular communication network 5 (CCN5, Wisp-2) ( Grunberg et al., 2018 ).…”
Section: Introductionmentioning
confidence: 99%
“…| 4201 (Ye et al, 2019). Recently, it is found that elevated Angiotensin II levels decreased CCN5 expression, subsequently promoting the direct deposition of the ECM and fibroblast-to-myofibroblast transition via Smad-3 activation, which accelerated cardiac fibrosis during the development of hypertensive heart failure (Huang et al, 2020).…”
Section: Role Of Ccn5 In Fibrosismentioning
confidence: 99%