Abstract
Mechanical stimuli obviously affect disc nucleus pulposus (NP) biology. Previous studies have indicated that static compression exhibits detrimental effects on disc biology compared with dynamic compression. To study disc NP cell senescence under static compression and dynamic compression in a disc organ culture, porcine discs were cultured and subjected to compression (static compression: 0.4 MPa for 4 h once per day; dynamic compression: 0.4 MPa at a frequency of 1.0 Hz for 4 h once per day) for 7 days using a self-developed mechanically active bioreactor. The non-compressed discs were used as controls. Compared with the dynamic compression, static compression significantly promoted disc NP cell senescence, reflected by the increased senescence-associated β-galactosidase (SA-β-Gal) activity, senescence-associated heterochromatic foci (SAHF) formation and senescence markers expression, and the decreased telomerase (TE) activity and NP matrix biosynthesis. Static compression accelerates disc NP cell senescence compared with the dynamic compression in a disc organ culture. The present study provides that acceleration of NP cell senescence may be involved in previously reported static compression-mediated disc NP degenerative changes.
Highlights
Low back pain (LBP) is a common and severe public health problem worldwide, which produces heavy economic burden and causes distress to patients [1]
Results showed that the percentage of senescence-associated heterochromatic foci (SAHF)-positive nucleus pulposus (NP) cells in the static compression group was higher whereas it was lower in the dynamic compression group than that in the control group
Results showed that gene expression of NP matrix macromolecules was down-regulated in the static compression group and up-regulated in the dynamic compression group compared with the control group, but they were significantly decreased in the static compression group compared with the dynamic compression group (Figure 5A)
Summary
Low back pain (LBP) is a common and severe public health problem worldwide, which produces heavy economic burden and causes distress to patients [1]. LBP is closely correlated with intervertebral disc degeneration (IDD) [2]. Current treatments for IDD aim to relieve pain symptoms but not to interdict its pathogenesis [3]. Apart from cell number, cellular morphology, and cell apoptosis, cellular senescence has been studied in the human disc recently [6-9]. These studies have reached a consensus that cellular senescence is positively correlated with the progressive degree of disc degeneration. Acceleration of disc cell senescence may be a potential approach for certain pathological risk factors aggravated disc degeneration
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