Cartilage endplate stem cells inhibit intervertebral disc degeneration by releasing exosomes to nucleus pulposus cells to activate Akt/autophagy

Jan 18, 2021Stem cells (Dayton, Ohio)

Stem cells from cartilage layers may slow disc wear by sending tiny packages that activate cell repair in disc center cells

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Longevity & Aging on OpenScience ↗PubMed ↗DOI ↗OA ↗

Abstract

N-Exos treatment significantly reduced NPC apoptosis compared to D-Exos.

Degeneration of the cartilage endplate is linked to intervertebral disc degeneration.
N-Exos promote activation more effectively than D-Exos.
The apoptotic rate of nucleus pulposus cells decreased after N-Exos treatment.
N-Exos inhibited apoptosis and attenuated intervertebral disc degeneration through activation of the AKT and autophagy signaling pathways.
The findings suggest that the cartilage endplate may delay the progression of intervertebral disc degeneration via .

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Degeneration of the cartilage endplate (CEP) induces intervertebral disc degeneration (IVDD). Nucleus pulposus cell (NPC) apoptosis is also an important exacerbating factor in IVDD, but the cascade mechanism in IVDD is not clear. We investigated the apoptosis of NPCs and IVDD when stimulated by normal cartilage endplate stem cell (CESC)-derived (N-Exos) and degenerated CESC-derived exosomes (D-Exos) in vitro and in vivo. Tert-butyl hydroperoxide (TBHP) was used to induce inflammation of CESCs. The bioinformatics differences between N-Exos and D-Exos were analyzed using mass spectrometry, heat map, and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. NPC apoptosis was examined using TUNEL staining. The involvement of the AKT and signaling pathways was investigated using the signaling inhibitor LY294002. Magnetic resonance imaging, Western blotting, and immunofluorescence staining were used to evaluate the therapeutic effects of N-Exos in rats with IVDD. TBHP effectively induced inflammation and the degeneration of CEP in rat. N-Exos were more conducive to autophagy activation than D-Exos. The apoptotic rate of NPCs decreased obviously after treatment with N-Exos compared to D-Exos. N-Exos inhibited NPCs apoptosis and attenuated IVDD in rat via activation of the AKT and autophagy pathways. These results are the first findings to confirm that CEP delayed the progression of IVDD via exosomes. The therapeutic effects of N-Exos on NPC apoptosis inhibition and the slowing of IVDD progression were more effective than D-Exos due to activation of the PI3K/AKT/autophagy pathway, which explained the increase in the incidence of IVDD after inflammation of the CEP.

Key numbers

11.66%

Recurrence Rate Increase

Recurrence rate of 243 patients with lumbar disc herniation with CEP degeneration.

2.5%

Recurrence Rate Without CEP Inflammation

Recurrence rate of IVDD patients without CEP degeneration.

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Cartilage endplate stem cells inhibit intervertebral disc degeneration by releasing exosomes to nucleus pulposus cells to activate Akt/autophagy

Abstract

Key numbers

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