Apelin-13/APJ system delays intervertebral disc degeneration by activating the PI3K/AKT signaling pathway.

Abstract

OBJECTIVE:

To study the effect of Apelin-13/APJ system on intervertebral disc degeneration and its mechanism.

PATIENTS AND METHODS:

This study detected the expression of APJ in human intervertebral disc tissue with varying degrees of degeneration. IL-1β is used to stimulate the degeneration of nucleus pulposus cells. We used recombinant human Apelin-13 and Ala13 to activate and inhibit the APJ receptor, respectively. The inhibitor LY294002 was used to inhibit the PI3K/AKT signaling pathway. We studied the effects of Apelin-13/APJ system on nucleus pulposus cells and its mechanism by Western blot, RT-PCR, and so on.

RESULTS:

APJ is lowly expressed in the nucleus pulposus of patients with a high degree of degeneration. IL-1β stimulates the nucleus pulposus cells and reduces the expression of APJ in nucleus pulposus cells. Recombinant human Apelin-13 reduces the degradation of nucleus pulposus extracellular matrix, promotes proliferation, and reduces the levels of apoptosis and inflammation. In addition, the Apelin-13/APJ system increases the expression of PI3K and AKT and activates the PI3K/AKT signaling pathway.

CONCLUSIONS:

Apelin-13/APJ system activates PI3K/AKT signaling pathway activity, reduces the degradation of nucleus pulposus extracellular matrix, promotes proliferation, and reduces the level of apoptosis and inflammation, thus delaying the degeneration of the intervertebral disc.

• Authors: W Liu, F Niu, H Sha, L-D Liu, Z-S Lv, W-Q Gong, M Yan
• Journal: European review for medical and pharmacological sciences (Eur Rev Med Pharmacol Sci) Vol. 24 Issue 6 Pg. 2820-2828 (03 2020) ISSN: 2284-0729 [Electronic] Italy
• PMID: 32271399 (Publication Type: Journal Article)

Chemical References

• APLN protein, human
• APLNR protein, human
• Apelin
• Apelin Receptors
• Proto-Oncogene Proteins c-akt

Topics

• Apelin (genetics, metabolism)
• Apelin Receptors (genetics, metabolism)
• Cells, Cultured
• Humans
• Intervertebral Disc Degeneration (metabolism, pathology)
• Nucleus Pulposus (metabolism, pathology)
• Phosphatidylinositol 3-Kinases (metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• Signal Transduction