Mesenchymal stem cells regulate inflammatory milieu within degenerative nucleus pulposus cells via p38 MAPK pathway

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

It has been established that excessive apoptosis of nucleus pulposus cells (NPCs) are responsible for pathogenesis of human intervertebral disc degeneration (IDD). The present study aimed to shed light on the molecular mechanisms underlying the protective effects of mesenchymal stem cells (MSCs) on NPCs in an inflammatory environment. NPCs were treated with TNF-α to induce inflammation and then co-cultured with Wharton's Jelly-derived MSCs (WJ-MSCs)without direct interaction. The levels of inflammation markers (IL-1β, IL-6 and IL-8) in NPCs were detected by performing enzyme-linked immunosorbent assay (ELISA), and expression of metalloproteases and aggrecan, as well as the activity of p38 MAPK pathway were determined through immunoblotting. SB-203580 was used to inhibit p38 signaling, prior to evaluation of the effects of Wharton's Jelly-derived MSCs (WJ-MSCs) on inflammatory response within the co-cultured NPCs. After TNF-α treatment, the levels of inflammatory cytokines, MMP-3, and MMP-13 in NPCs were increased whereas aggrecan was decreased, which was then dramatically reversed by WJ-MSCs co-culture. Likewise, WJ-MSCs suppressed TNF-α-induced phosphorylation of p38 MAPK signaling components including p38, ASK-1, MKK-3 and MKK-6. Blocking p38 MAPK pathway enhanced the anti-inflammatory impact of WJ-MSCs, and there was no significant difference between NPCs co-cultured with WJ

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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