IADR Abstract Archives
3D TECA Hydrogel Modulates Cellular Senescence and Reduces Telomere Dysfunction
Objectives: This study is designed to investigate the effect of 3D TECA hydrogel on the inflammatory induced senescence marker, to measure the gel effect on fibroblast telomere length associated with DNA damage response (DDR) and to assess the impact of the gel on the human periodontal ligament fibroblasts (HPDLFs) migration.
Methods: Nuclear factor Kappa B (NF-KB) of HPDLFs was induced with 10 ng TNF-α in the presence or absence of 50 µM of 3D TECA gel for 24 hours. The gel effect on the Secretory associated-β- galactosidase (SA-β-gal) activity was measured by a histochemical staining. Fibroblast telomeres length was determined by chemiluminescent assay to ascertain the DDR. For assessing fibroblasts migration, the scratch wound healing assay and Pro-Plus Imaging software were used.
Results: The activity of senescence marker, SA-β-gal, was positive in the TNF-α- induced NFKB cells. SA-β-gal percentage is suppressed (> 30%) in the treated cells as compared to the non-treated cells (P > 0.05). Telomeres were significantly longer in TECA treated cells (20.1 kbp) than the control cells (15.2 kbp). Scratch wound test indicated that the cells migration rate was significantly higher (14.9 µm/hr) in the treated versus (11 µm/hr) for control HPDLFs.
Conclusions: Inflammatory induced NFKB results in premature irreversible cell cycle arrest (cellular senescence) of HPDLFs. The new formula of 3D TECA suppressed the inflammatory mediated cellular senescence and reduced DNA damage response. It may preserve the telomere function and rescue tissues regeneration potential during wound closure. The 3D TECA may play a role in restoration of gingival and periodontal structures.
Methods: Nuclear factor Kappa B (NF-KB) of HPDLFs was induced with 10 ng TNF-α in the presence or absence of 50 µM of 3D TECA gel for 24 hours. The gel effect on the Secretory associated-β- galactosidase (SA-β-gal) activity was measured by a histochemical staining. Fibroblast telomeres length was determined by chemiluminescent assay to ascertain the DDR. For assessing fibroblasts migration, the scratch wound healing assay and Pro-Plus Imaging software were used.
Results: The activity of senescence marker, SA-β-gal, was positive in the TNF-α- induced NFKB cells. SA-β-gal percentage is suppressed (> 30%) in the treated cells as compared to the non-treated cells (P > 0.05). Telomeres were significantly longer in TECA treated cells (20.1 kbp) than the control cells (15.2 kbp). Scratch wound test indicated that the cells migration rate was significantly higher (14.9 µm/hr) in the treated versus (11 µm/hr) for control HPDLFs.
Conclusions: Inflammatory induced NFKB results in premature irreversible cell cycle arrest (cellular senescence) of HPDLFs. The new formula of 3D TECA suppressed the inflammatory mediated cellular senescence and reduced DNA damage response. It may preserve the telomere function and rescue tissues regeneration potential during wound closure. The 3D TECA may play a role in restoration of gingival and periodontal structures.