Limits...
Rat Notochordal Cells Undergo Premature Stress-Induced Senescence by High Glucose.

Park JB, Byun CH, Park EY - Asian Spine J (2015)

Bottom Line: The telomerase activity declined at 1 and 3 days.Despite compensatory expression of antioxidants, high glucose-induced oxidative stress accelerates stress-induced senescence in rat notochordal cells.This may result in dysfunction of notochordal cells, leading to accelerated premature disc degeneration.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedic Surgery, Uijeongbu St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Uijeongbu, Korea.

ABSTRACT

Study design: In vitro cell culture.

Purpose: The purpose of the study was to investigate the effect of high glucose on premature stress-induced senescence of rat notochordal cells.

Overview of literature: Glucose-mediated increase of oxidative stress is a major causative factor for the development of diseases associated with diabetes mellitus such as senescence. However, no information is available for the effect of high glucose on premature stress-induced senescence of rat notochordal cells.

Methods: Notochordal cells were isolated from 4-week-old rats, cultured and placed in either 10% fetal bovine serum (FBS, normal control) or 10% FBS plus two high glucose concentrations (0.1 M and 0.2 M, experimental conditions) for 1 and 3 days. We identified and quantified the mitochondrial damage (mitochondrial transmembrane potential), reactive oxygen species (ROS) and antioxidants, such as manganese superoxide dismutase (MnSOD) and catalase, for each condition. We also identified and quantified senescence and telomerase activity. Finally, we determined the expression of proteins related to replicative senescence (p53-p21-pRB) and stress-induced senescence (p16-pRB) pathways.

Results: Two high glucose concentrations enhanced the disruption of mitochondrial transmembrane potential and excessive generation of ROS in notochordal cells for 1 and 3 days, respectively. The expressions of MnSOD and catalase were increased in notochordal cells treated with both high glucose concentrations at 1 and 3 days. The telomerase activity declined at 1 and 3 days. Two high glucose concentrations increased the occurrence of stress-induced senescence of notochordal cells by p16-pRB pathways at 1 and 3 days.

Conclusions: Despite compensatory expression of antioxidants, high glucose-induced oxidative stress accelerates stress-induced senescence in rat notochordal cells. This may result in dysfunction of notochordal cells, leading to accelerated premature disc degeneration. The prevention of excessive generation of oxidative stress by strict blood glucose control is important to prevent or to delay premature disc degeneration in young patients with diabetes mellitus.

No MeSH data available.


Related in: MedlinePlus

Immunofluorescence demonstrated that the two high glucose concentrations decreased the expression of p21 protein in rat notochordal cells at 1 and 3 days when compared with the control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4522436&req=5

Figure 7: Immunofluorescence demonstrated that the two high glucose concentrations decreased the expression of p21 protein in rat notochordal cells at 1 and 3 days when compared with the control.

Mentions: The mean percentage of SA-β-Gal-positive notochordal cells was significantly increased in notochordal cells treated with both high glucose concentrations for 1 and 3 days in a dose- and time-dependent manner, as compared with the control (Fig. 3). Immunofluorescence demonstrated that the two high glucose concentrations enhanced expression of p16 (Fig. 4) and pRB (Fig. 5) proteins in notochordal cells at 1 and 3 days when compared with the controls, respectively. However, immunofluorescence demonstrated that the two high glucose concentrations decreased the expression of p53 (Fig. 6) and p21 (Fig. 7) proteins in notochordal cells at 1 and 3 days when compared with the controls, respectively.


Rat Notochordal Cells Undergo Premature Stress-Induced Senescence by High Glucose.

Park JB, Byun CH, Park EY - Asian Spine J (2015)

Immunofluorescence demonstrated that the two high glucose concentrations decreased the expression of p21 protein in rat notochordal cells at 1 and 3 days when compared with the control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4522436&req=5

Figure 7: Immunofluorescence demonstrated that the two high glucose concentrations decreased the expression of p21 protein in rat notochordal cells at 1 and 3 days when compared with the control.
Mentions: The mean percentage of SA-β-Gal-positive notochordal cells was significantly increased in notochordal cells treated with both high glucose concentrations for 1 and 3 days in a dose- and time-dependent manner, as compared with the control (Fig. 3). Immunofluorescence demonstrated that the two high glucose concentrations enhanced expression of p16 (Fig. 4) and pRB (Fig. 5) proteins in notochordal cells at 1 and 3 days when compared with the controls, respectively. However, immunofluorescence demonstrated that the two high glucose concentrations decreased the expression of p53 (Fig. 6) and p21 (Fig. 7) proteins in notochordal cells at 1 and 3 days when compared with the controls, respectively.

Bottom Line: The telomerase activity declined at 1 and 3 days.Despite compensatory expression of antioxidants, high glucose-induced oxidative stress accelerates stress-induced senescence in rat notochordal cells.This may result in dysfunction of notochordal cells, leading to accelerated premature disc degeneration.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedic Surgery, Uijeongbu St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Uijeongbu, Korea.

ABSTRACT

Study design: In vitro cell culture.

Purpose: The purpose of the study was to investigate the effect of high glucose on premature stress-induced senescence of rat notochordal cells.

Overview of literature: Glucose-mediated increase of oxidative stress is a major causative factor for the development of diseases associated with diabetes mellitus such as senescence. However, no information is available for the effect of high glucose on premature stress-induced senescence of rat notochordal cells.

Methods: Notochordal cells were isolated from 4-week-old rats, cultured and placed in either 10% fetal bovine serum (FBS, normal control) or 10% FBS plus two high glucose concentrations (0.1 M and 0.2 M, experimental conditions) for 1 and 3 days. We identified and quantified the mitochondrial damage (mitochondrial transmembrane potential), reactive oxygen species (ROS) and antioxidants, such as manganese superoxide dismutase (MnSOD) and catalase, for each condition. We also identified and quantified senescence and telomerase activity. Finally, we determined the expression of proteins related to replicative senescence (p53-p21-pRB) and stress-induced senescence (p16-pRB) pathways.

Results: Two high glucose concentrations enhanced the disruption of mitochondrial transmembrane potential and excessive generation of ROS in notochordal cells for 1 and 3 days, respectively. The expressions of MnSOD and catalase were increased in notochordal cells treated with both high glucose concentrations at 1 and 3 days. The telomerase activity declined at 1 and 3 days. Two high glucose concentrations increased the occurrence of stress-induced senescence of notochordal cells by p16-pRB pathways at 1 and 3 days.

Conclusions: Despite compensatory expression of antioxidants, high glucose-induced oxidative stress accelerates stress-induced senescence in rat notochordal cells. This may result in dysfunction of notochordal cells, leading to accelerated premature disc degeneration. The prevention of excessive generation of oxidative stress by strict blood glucose control is important to prevent or to delay premature disc degeneration in young patients with diabetes mellitus.

No MeSH data available.


Related in: MedlinePlus