Mechano growth factor attenuates mechanical overload-induced nucleus pulposus cell apoptosis through inhibiting the p38 MAPK pathway.
Xu. Qing Q; Fang. Haolin H; Zhao. Liang L; Zhang. Cunxin C; Zhang. Luo L; Tian. Baofang B
Key Findings
- Mechanical overload makes nucleus pulposus (NP) cells more likely to undergo apoptosis (cell death).
- Adding MGF to the culture partially reverses the increase in apoptosis markers (Bax, caspase‑3, cleaved PARP) and restores anti‑apoptosis Bcl‑2 levels.
- MGF treatment reduces activity of the p38 MAPK signaling pathway, which is linked to the protective effect.
Practical Outcomes
- For biohackers interested in spine health, the study hints that MGF could be a candidate for protecting disc cells from overload‑induced damage. However, the evidence is limited to rat cells in a dish, with no human dosing or safety data, so any supplementation would be experimental and should be approached with caution.
Summary
A lab study in rats showed that a peptide called Mechano Growth Factor (MGF) can protect the soft inner part of spinal discs from dying when they’re stressed by too much mechanical load. It does this by lowering the activity of a stress‑related pathway (p38 MAPK) and reducing cell‑death signals. The work is early‑stage and done in cell cultures, not people.
Abstract
Mechanical overload is a risk factor of disc degeneration. It can induce disc degeneration through mediating cell apoptosis. Mechano growth factor (MGF) has been reported to inhibit mechanical overload-induced apoptosis of chondrocytes. The present study is aimed to investigate whether MGF can attenuate mechanical overload-induced nucleus pulposus (NP) cell apoptosis and the possible signaling transduction pathway. Rat NP cells were cultured and subjected to mechanical overload for 7 days. The control NP cells did not experience mechanical load. The exogenous MGF peptide was added into the culture medium to investigate its protective effects. NP cell apoptosis ratio, caspase-3 activity, gene expression of Bcl-2, Bax and caspase-3, protein expression of cleaved caspase-3, cleaved PARP, Bax and Bcl-2 were analyzed to evaluate NP cell apoptosis. In addition, activity of the p38 MAPK pathway was also detected. Compared with the control NP cells, mechanical overload significantly increased NP cell apoptosis and caspase-3 activity, up-regulated gene/protein expression of pro-apoptosis molecules (i.e. Bax, caspase-3, cleaved caspase-3 and cleaved PARP) whereas down-regulated gene/protein expression of anti-apoptosis molecule (i.e. Bcl-2). However, exogenous MGF partly reversed these effects of mechanical overload on NP cell apoptosis. Further results showed that activity of the p38 MAPK pathway of NP cells cultured under mechanical overload was decreased by addition of MGF peptide. In conclusion, MGF is able to attenuate mechanical overload-induced NP cell apoptosis, and the p38 MAPK signaling pathway may be involved in this process. The present study provides that MGF supplementation may be a promising strategy to retard mechanical overload-induced disc degeneration.
Study Information
pubmed
2019
2019-03-28T00:00:00.000Z
10.1042/bsr20182462