Keloid Core Factor CTRP3 Overexpression Significantly Controlled TGF-β1-Induced Propagation and Migration in Keloid Fibroblasts

Purpose. Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid...

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Bibliographic Details
Published in:Disease markers 2023-04, Vol.2023, p.1-12
Main Authors: He, Lin, Zhu, Chan, Dou, Huicong, Yu, Xueyuan, Jia, Jing, Shu, Maoguo
Format: Article
Language:English
Subjects:
Antibodies
Cell adhesion & migration
Cell growth
Cytokines
Extracellular matrix
Fibroblasts
Fibronectin
Growth factors
Localization
Metabolism
mRNA
Nuclear transport
Propagation
Proteins
Reagents
Scars
Scleroderma
Signal paths
siRNA
Smad protein
Smad2 protein
Smad3 protein
Smooth muscle
Stimulation
Tissues
Transfection
Transforming growth factor-b
Transforming growth factor-b1
Translocation
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Summary:Purpose. Keloid is a type of benign fibrous proliferative tumor characterized by excessive scarring. C1q/TNF-related protein 3 (CTRP3) has been proven to possess antifibrotic effect. Here, we explored the role of CTRP3 in keloid. In the current research, we examined the influence of CTRP3 on keloid fibroblasts (KFs) and investigated the potential molecular mechanism. Methods. KF tissue specimens and adjacent normal fibroblast (NF) tissues were collected cultured from 10 keloid participants. For the TGF-β1 stimulation group, KFs were processed with human recombinant TGF-β1. Cell transfection of pcDNA3.1-CTRP3 or pcDNA3.1 was performed. The siRNA of CTRP3 (si-CTRP3) or negative control siRNA (si-scramble) was transfected into KFs. Results. CTRP3 was downregulated in keloid tissues and KFs. CTRP3 overexpression significantly controlled TGF-β1-induced propagation and migration in KFs. Col I, α-SMA, and fibronectin mRNA and protein levels were enhanced by TGF-β1 stimulation, whereas they were inhibited by CTRP3 overexpression. In contrast, CTRP3 knockdown exhibited the opposite effect. In addition, CTRP3 attenuated TGF-β receptors TRI and TRII in TGF-β1-induced KFs. Furthermore, CTRP3 prevented TGF-β1-stimulated nuclear translocation of smad2 and smad3 and suppressed the expression levels of p-smad2 and p-smad3 in KFs. Conclusion. CTRP3 exerted an antifibrotic role through inhibiting proliferation, migration, and ECM accumulation of KFs via regulating TGF-β1/Smad signal path.
ISSN:0278-0240
1875-8630
DOI:10.1155/2023/9638322