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. 2019 Sep 20;39(9):BSR20191711.
doi: 10.1042/BSR20191711. Print 2019 Sep 30.

Hyper-osmolarity environment-induced oxidative stress injury promotes nucleus pulposus cell senescence in vitro

Jiawei Xu  1 , Haopeng Li  2 , Kai Yang  1 , Shuai Guo  1 , Jie Wang  1 , Chaoshuai Feng  1 , Huayou Chen  1
Affiliations

Hyper-osmolarity environment-induced oxidative stress injury promotes nucleus pulposus cell senescence in vitro

Jiawei Xu et al. Biosci Rep. .

Retraction in

Abstract

Nucleus pulposus (NP) cell senescence is involved in disc degeneration. The in situ osmolarity within the NP region is an important regulator of disc cell's biology. However, its effects on NP cell senescence remain unclear. The present study was aimed to investigate the effects and mechanism of hyper-osmolarity on NP cell senescence. Rat NP cells were cultured in the in situ-osmolarity medium and hyper-osmolarity medium. The reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) was added along with the medium to investigate the role of oxidative injury. Cell cycle, cell proliferation, senescence associated β-galactosidase (SA-β-Gal) activity, telomerase activity, expression of senescence markers (p16 and p53) and matrix molecules (aggrecan and collagen II) were tested to assess NP cell senescence. Compared with the in situ-osmolarity culture, hyper-osmolarity culture significantly decreased cell proliferation and telomerase activity, increased SA-β-Gal activity and cell fraction in the G0/G1 phase, up-regulated expression of senescence markers (p16 and p53) and down-regulated expression of matrix molecules (aggrecan and collagen II), and increased intracellular ROS accumulation. However, addition of NAC partly reversed these effects of hyper-osmolarity culture on cellular senescence and decreased ROS content in NP cells. In conclusion, a hyper-osmolarity culture promotes NP cell senescence through inducing oxidative stress injury. The present study provides new knowledge on NP cell senescence and helps us to better understand the mechanism of disc degeneration.

Keywords: intervertebral disc; nucleus pulposus; osmolarity; oxidative stress; senescence.

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Conflict of interest statement

The authors declare that there are no competing interests associated with the manuscript.

Figures

Figure 1
Figure 1. NP cell proliferation evaluated by CCK-8 assay
Data are expressed as mean ± SD (n=3). *: Means a statistical difference (P<0.05) between two groups.
Figure 2
Figure 2. SA-β-Gal activity of NP cells
Magnification: 200×; scale = 100 μM; n=3. Data are expressed as mean ± SD. *: Means a statistical difference (P<0.05) between two groups.
Figure 3
Figure 3. Telomerase activity of NP cells
Data are expressed as mean ± SD (n=3). *: Means a statistical difference (P<0.05) between two groups.
Figure 4
Figure 4. Cell-cycle analysis of NP cells
The cell fraction proportion of each cell cycle (G0/G1, S and G2/M) were calculated.
Figure 5
Figure 5. Measurement of the intracellular reactive oxygen species (ROS) in NP cells
Data are expressed as mean ± SD (n=3). *: Means a statistical difference (P<0.05) between two groups.
Figure 6
Figure 6. Expression of matrix molecules (aggrecan and collagen II) in NP cells
(A) Real-time PCR analysis. (B) Western blot analysis. Data are expressed as mean ± SD (n=3). *: Means a statistical difference (P<0.05) between two groups.
Figure 7
Figure 7. Expression of senescence-related molecules (p16 and p53) in NP cells
(A) Real-time PCR analysis. (B) Western blot analysis. Data are expressed as mean ± SD (n=3). *: Means a statistical difference (P<0.05) between two groups.
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