MALAT1 overexpression promotes the proliferation of human periodontal ligament stem cells by upregulating fibroblast growth factor 2
- Authors:
- Published online on: July 8, 2019 https://doi.org/10.3892/etm.2019.7748
- Pages: 1627-1632
-
Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
Fibroblast growth factor 2 (FGF2) has been revealed to promote human periodontal ligament stem cell (PDLSC) proliferation. The abnormal proliferation of PDLSCs has also been associated with the pathogenesis of periodontitis. The long non‑coding RNA, metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1), has been demonstrated to regulate FGF2 secretion. Therefore, MALAT1 may also be associated with periodontitis. The aim of the present study was to investigate the effect of MALAT1 overexpression on the proliferation of PDLSCs. In the current study, PDLSCs derived from healthy and periodontitis‑affected teeth were collected. MALAT1 and FGF2 mRNA expression in PDLSCs was detected using reverse transcription‑quantitative PCR. PDLSCs overexpressing MALAT1 were subsequently generated. PDLSC proliferation was analyzed using a Cell Counting kit‑8 assay. FGF2 protein expression was detected using western blot analysis. The results revealed that MALAT1 and FGF2 mRNA were significantly upregulated in PDLSCs derived from periodontitis‑affected teeth when compared with PDLSCs derived from healthy teeth. PDLSCs derived from periodontitis‑affected teeth also demonstrated a significantly higher proliferation rate than PDLSCs derived from healthy teeth. MALAT1 and FGF2 mRNA expression were positively correlated in both PDLSC groups. MALAT1 overexpression promoted the proliferation of healthy and periodontitis‑affected PDLSC groups and upregulated FGF2 protein expression. The present study concluded that MALAT1 overexpression promoted the proliferation of human PDLSC potentially via upregulating FGF2.