Abstract
CCN family proteins 2 and 3 (CCN2 and CCN3) belong to the CCN family of proteins, all having a high level of structural similarity. It is widely known that CCN2 is a profibrotic molecule that mediates the development of fibrotic disorders in many different tissues and organs. In contrast, CCN3 has been recently suggested to act as an anti-fibrotic factor in several tissues. This CCN3 action was shown earlier to be exerted by the repression of the CCN2 gene expression in kidney tissue, whereas different findings were obtained for liver cells. Thus, the molecular action of CCN3 yielding its anti-fibrotic effect is still controversial. Here, using a general model of fibrosis, we evaluated the effect of CCN3 overexpression on the gene expression of all of the CCN family members, as well as on that of fibrotic marker genes. As a result, repression of CCN2 gene expression was modest, while type I collagen and α-smooth muscle actin gene expression was prominently repressed. Interestingly, not only CCN2, but also CCN4 gene expression showed a decrease upon CCN3 overexpression. These findings indicate that fibrotic gene induction is under the control of a complex molecular network conducted by CCN family members functioning together.
| Original language | English |
|---|---|
| Pages (from-to) | 11-18 |
| Number of pages | 8 |
| Journal | Journal of Cell Communication and Signaling |
| Volume | 7 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Mar 2013 |
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Keywords
- CCN family
- CCN2
- CCN3
- CCN4
- Fibrosis
- NOV
ASJC Scopus subject areas
- Biochemistry
- Cell Biology
- Molecular Biology
Cite this
Anti-fibrotic effect of CCN3 accompanied by altered gene expression profile of the CCN family. / Abd El Kader, Tarek; Kubota, Satoshi; Janune, Danilo; Nishida, Takashi; Hattori, Takako; Aoyama, Eriko; Perbal, Bernard; Kuboki, Takuo; Takigawa, Masaharu.
In: Journal of Cell Communication and Signaling, Vol. 7, No. 1, 03.2013, p. 11-18.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Anti-fibrotic effect of CCN3 accompanied by altered gene expression profile of the CCN family
AU - Abd El Kader, Tarek
AU - Kubota, Satoshi
AU - Janune, Danilo
AU - Nishida, Takashi
AU - Hattori, Takako
AU - Aoyama, Eriko
AU - Perbal, Bernard
AU - Kuboki, Takuo
AU - Takigawa, Masaharu
PY - 2013/3
Y1 - 2013/3
N2 - CCN family proteins 2 and 3 (CCN2 and CCN3) belong to the CCN family of proteins, all having a high level of structural similarity. It is widely known that CCN2 is a profibrotic molecule that mediates the development of fibrotic disorders in many different tissues and organs. In contrast, CCN3 has been recently suggested to act as an anti-fibrotic factor in several tissues. This CCN3 action was shown earlier to be exerted by the repression of the CCN2 gene expression in kidney tissue, whereas different findings were obtained for liver cells. Thus, the molecular action of CCN3 yielding its anti-fibrotic effect is still controversial. Here, using a general model of fibrosis, we evaluated the effect of CCN3 overexpression on the gene expression of all of the CCN family members, as well as on that of fibrotic marker genes. As a result, repression of CCN2 gene expression was modest, while type I collagen and α-smooth muscle actin gene expression was prominently repressed. Interestingly, not only CCN2, but also CCN4 gene expression showed a decrease upon CCN3 overexpression. These findings indicate that fibrotic gene induction is under the control of a complex molecular network conducted by CCN family members functioning together.
AB - CCN family proteins 2 and 3 (CCN2 and CCN3) belong to the CCN family of proteins, all having a high level of structural similarity. It is widely known that CCN2 is a profibrotic molecule that mediates the development of fibrotic disorders in many different tissues and organs. In contrast, CCN3 has been recently suggested to act as an anti-fibrotic factor in several tissues. This CCN3 action was shown earlier to be exerted by the repression of the CCN2 gene expression in kidney tissue, whereas different findings were obtained for liver cells. Thus, the molecular action of CCN3 yielding its anti-fibrotic effect is still controversial. Here, using a general model of fibrosis, we evaluated the effect of CCN3 overexpression on the gene expression of all of the CCN family members, as well as on that of fibrotic marker genes. As a result, repression of CCN2 gene expression was modest, while type I collagen and α-smooth muscle actin gene expression was prominently repressed. Interestingly, not only CCN2, but also CCN4 gene expression showed a decrease upon CCN3 overexpression. These findings indicate that fibrotic gene induction is under the control of a complex molecular network conducted by CCN family members functioning together.
KW - CCN family
KW - CCN2
KW - CCN3
KW - CCN4
KW - Fibrosis
KW - NOV
UR - http://www.scopus.com/inward/record.url?scp=84874935003&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84874935003&partnerID=8YFLogxK
U2 - 10.1007/s12079-012-0180-4
DO - 10.1007/s12079-012-0180-4
M3 - Article
C2 - 23065484
AN - SCOPUS:84874935003
VL - 7
SP - 11
EP - 18
JO - Journal of Cell Communication and Signaling
JF - Journal of Cell Communication and Signaling
SN - 1873-9601
IS - 1
ER -