CTHRC1 expressed in periodontitis and human periodontal fibroblasts exposed to inflammatory stimuli
Objectives Collagen triple helix repeat containing‐1 (CTHRC1) is a glycoprotein that can be secreted extracellularly and is involved in the regulation of collagen matrix in a variety of diseases. The expression level of CTHRC1 in periodontitis was detected in this study. Materials and Methods The gi...
Saved in:
Published in | Oral diseases Vol. 29; no. 4; pp. 1738 - 1746 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Denmark
Wiley Subscription Services, Inc
01.05.2023
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Objectives
Collagen triple helix repeat containing‐1 (CTHRC1) is a glycoprotein that can be secreted extracellularly and is involved in the regulation of collagen matrix in a variety of diseases. The expression level of CTHRC1 in periodontitis was detected in this study.
Materials and Methods
The gingival tissues from clinically healthy subjects (15 cases) and those with periodontitis (30 cases) were taken for immunohistochemical staining. Lipopolysaccharide of the Porphyromonas gingivalis was added in the periodontal ligament fibroblast culture in vitro. Cells were collected, and the mRNA levels of the intracellular CTHRC1 and protein expression of the extracellular CTHRC1 were detected.
Results
The protein expression of CTHRC1 in the periodontitis group was higher than that of the clinically healthy group. The in vitro cell experiments showed that 10 μg/ml of P.g LPS could induce a significant increase in protein secretion of CTHRC1, and 5 μg/ml P.g LPS had a significant effect on promoting the mRNA expression of CTHRC1.
Conclusions
Collagen triple helix repeat containing‐1 might be involved in the development of periodontitis, and the expression level might be significantly correlated with the stimulation of P.g LPS on fibroblasts. Different stimulation intensities of P.g LPS might result in different expression patterns of CTHRC1. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1354-523X 1601-0825 1601-0825 |
DOI: | 10.1111/odi.14151 |