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In vitro analysis of the role of tumor necrosis factor?stimulated gene?6 in keloid.

ABSTRACT: An increasing number of studies have demonstrated that tumor necrosis factor?stimulated gene?6 (TSG?6) has a key role in the progression of fibrosis; however, the exact effects of TSG?6 in keloid fibroblasts (KFs) remain unknown. The aim of the current study was to investigate the role of TSG?6 in the pathogenesis of keloids. Primary fibroblasts from 10 patients with keloid were cultured and transfected with pLVX?Puro or pLVX?Puro?TSG?6. Alterations of TSG?6 expression were then determined by reverse transcription?polymerase chain reaction (RT?PCR) and regulation was observed in KFs transfected with pLVX?Puro?TSG?6. Compared with the control group, transfection with pLVX?Puro?TSG?6 induced growth suppression, cell apoptosis and G2/M arrest in KFs. In addition, the mitochondrial apoptosis pathway was activated in KFs transfected with pLVX?Puro?TSG?6. These findings indicate that TSG?6 is a novel regulator of keloid fibrogenesis, and thus could be used/targeted TSG?6 as a promising treatment for keloid.

SUBMITTER: Li X

PROVIDER: S-EPMC6323212 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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In vitro analysis of the role of tumor necrosis factor‑stimulated gene‑6 in keloid.

Li Xinyi X Chen Zhao Z Li Xiaojing X Wang Hui H

Molecular medicine reports 20181214 2

An increasing number of studies have demonstrated that tumor necrosis factor‑stimulated gene‑6 (TSG‑6) has a key role in the progression of fibrosis; however, the exact effects of TSG‑6 in keloid fibroblasts (KFs) remain unknown. The aim of the current study was to investigate the role of TSG‑6 in the pathogenesis of keloids. Primary fibroblasts from 10 patients with keloid were cultured and transfected with pLVX‑Puro or pLVX‑Puro‑TSG‑6. Alterations of TSG‑6 expression were then determined by re ...[more]

PMID: 30569148

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Project description:Immediately before parturition the cervix undergoes striking changes in structure (ripening) that facilitate dilatation and effacement. Cervical ripening shares many features in common with inflammation-associated tissue remodeling, making it a valuable process to explore with respect to the biochemical events in extracellular matrix restructuring. Cervical ripening can be pharmacologically induced with prostaglandin E(2) (PGE(2)). Among the biochemical changes in the cervix at parturition is a marked increase in the hyaluronic acid (HA) content. HA and HA-binding proteins have been implicated in tissue hydration, release of collagenase, and leukocyte migration, but their roles in cervical ripening have not been explored. In the present study we examined the ability of PGE(2) to induce expression of the HA-binding protein, tumor necrosis factor-stimulated gene (TSG)-6, in human cervical smooth muscle cells (hCSMCs) and compared the PGE(2) response to that of tumor necrosis factor-alpha (TNF-alpha), an established inducer of TSG-6. TNF-alpha stimulated TSG-6 mRNA accumulation in a dose- and time-dependent manner, with the maximal response observed at 10 ng/ml after 6 hours of incubation. PGE(2) stimulated TSG-6 mRNA expression, but the magnitude of response was substantially less than that produced by TNF-alpha, and it was maximal only after 24 hours of incubation. Quantitative real-time polymerase chain reaction was performed to assess the induction of TSG-6 mRNA and nascent transcripts at 24 hours of treatment. Induction of TSG-6 mRNA and nascent transcripts in response to 10 micromol/L of PGE(2) was 5.7-fold and 6.3-fold greater than control values, respectively, whereas TNF-alpha (10 ng/ml) induced TSG-6 mRNA and nascent transcripts by 80-fold and 134-fold, respectively. TNF-alpha and PGE(2) stimulated secretion of TSG-6 into the culture medium as detected by Western blotting. The effects of PGE(2) on secretion of TSG-6 were delayed compared to TNF-alpha. A 1.3-kb fragment of the human TSG-6 proximal promoter drove luciferase expression in transfected hCSMCs. PGE(2) increased TSG-6 promoter activity 1.75-fold. Paradoxically, TNF-alpha reduced TSG-6 promoter activity by 50%. We conclude that hCSMCs express the hyaladherin TSG-6; that TSG-6 expression in these cells is regulated by PGE(2) as well as proinflammatory cytokines; responses of hCSMCs to TNF-alpha and PGE(2) are distinct in terms of magnitude and the time course; and PGE(2) and TNF-alpha exert different effects on the TSG-6 proximal promoter.

Dataset Information

In vitro analysis of the role of tumor necrosis factor?stimulated gene?6 in keloid.

Publications

In vitro analysis of the role of tumor necrosis factor‑stimulated gene‑6 in keloid.

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