Dataset Information

Proteomic Profiling of PTEN Inhibition on Periodontal Ligament Stem Cells

ABSTRACT: : Phosphatase and tensin homolog (PTEN) is a critical regulator of cell proliferation, differentiation, and inflammatory balance. However, its downstream proteomic effects in periodontal ligament stem cells (PDLSCs) remain poorly understood. This study aimed to elucidate the proteomic alterations induced by PTEN inhibition and identify potential molecular pathways underlying periodontal regeneration.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Stem Cell, Cell Culture

SUBMITTER: Suphalak Phothichailert

LAB HEAD: Suphalak Phothichailert

PROVIDER: PXD074161 | Pride | 2026-03-30

REPOSITORIES: Pride

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Proteomic Profiling of PTEN Inhibition on Periodontal Ligament Stem Cells.

Phothichailert Suphalak S Nowwarote Nunthawan N Kornsuthisopon Chatvadee C Murakami Shinya S Srithanyarat Supreda Suphanantachat SS Osathanon Thanaphum T

International dental journal 20260320 3

<h4>Objective</h4>Phosphatase and tensin homolog (PTEN) is a critical regulator of cell proliferation, differentiation, and inflammatory balance. However, its downstream proteomic effects in periodontal ligament stem cells (PDLSCs) remain poorly understood. This study aimed to elucidate the proteomic alterations induced by PTEN inhibition and identify potential molecular pathways underlying periodontal regeneration.<h4>Materials and methods</h4>PDLSCs were treated with 5 μM VO-OHpic for 24 hours ...[more]

PMID: 41863976

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Project description:<p><strong>BACKGROUND:</strong> Periodontal ligament mesenchymal stem cells (PDLSCs) are a promising cell resource for cell-based regenerative medicine in dentistry. PDLSCs inevitably acquire a senescent phenotype after prolonged in vitro expansion, and the key regulators of cells during replicative senescence remain unclear.</p><p><strong>METHODS:</strong> We cultured periodontal ligament stem cells to passages 4, 10 and 20 (P4, P10, P20). The senescent phenotypes, proliferation and migration ability of PDLSCs (P4, P10, P20) were detected, and non-targeted metabonomic sequencing was performed. We treated PDLSCs with AICAR and detected the expression of FOXO1, FOXO3a, FOXO6 and AMPK phosphorylation (p-AMPK) levels of replicating senescent PDLSCs to explore the correlation between the metabolic changes and the AMPK pathway.</p><p><strong>RESULTS:</strong> Immunofluorescence staining of γ-H2AX, β-galactosidase staining, cell scratch test and qPCR were performed to confirm the occurrence of replicative senescence in PDLSCs during passaging. Three groups of cells at passage 4 (P4), passage 10 (P10) and passage 20 (P20) were collected for non-targeted metabolomics analysis. Metabonomic sequencing showed that the metabolism of replicative senescence in PDLSCs varied significantly. In particular, the content of fatty acid metabolites decreased with senescence, including capric acid, stearic acid, myristic acid and dodecanoic acid. KEGG pathway analysis showed that the AMPK signaling pathway was closely related to AMP levels. The AMP:ATP ratio increased in senescent PDLSCs; however, the levels of p-AMPK and the profile of FOXO1 and FOXO3a, which are downstream of the AMPK signaling pathway, decreased with senescence. We treated PDLSCs with AICAR, an activator of the AMPK pathway, and the phosphorylated AMPK level at P20 PDLSCs was partially restored. </p><p><strong>CONCLUSION:</strong> In summary, our study suggests that the metabolic process of PDLSCs is active in the early stage of senescence, prefers to consume fatty acids, and is attenuated in the later stages of senescence. AMP accumulates in replicative senescent PDLSCs; however, the sensitivity of AMPK phosphorylation sites is impaired, causing senescent PDLSCs to fail to respond to changes in energy metabolism. Our findings provide a new basis for the clinical application of periodontal ligament stem cells.</p>

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	B.zip	Other
	OV-OHpic-1-1.dat	Other
	OV-OHpic-1-2.dat	Other
	OV-OHpic-1-3.dat	Other
	OV-OHpic-2-1.dat	Other