Details

Autor(en) / Beteiligte

• Cabral, Vladmir Lenine Ferreira
• Wang, Feng
• Peng, Xin
• Gao, Jiawei
• Zhou, Zhimin
• Sun, Rui
• Bao, Junping
• Wu, Xiaotao

Titel

Omentin-1 promoted proliferation and ameliorated inflammation, apoptosis, and degeneration in human nucleus pulposus cells

Ist Teil von

• Archives of gerontology and geriatrics, 2022-09, Vol.102, p.104748-104748, Article 104748

Ort / Verlag

Netherlands: Elsevier B.V

Erscheinungsjahr

2022

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• •Omentin-1 is downregulated by interleukin-1 in human nucleus pulposus cells.•Omentin-1 exerts a proliferative effect on nucleus pulposus cells.•Omentin-1 lessens nucleus pulposus cell degeneration via PI3K/Akt signaling pathway.•Omentin-1 reveals potential in treating intervertebral disc degeneration. Intervertebral disc degeneration is an abnormal, cell-mediated process of tissue remodeling, recognized as the principal cause of low back pain affecting 80% of the population worldwide. Inflammatory cytokine, Interleukin-1beta (IL-1β) is involved in the intervertebral disc degeneration (IDD) process, and it is upregulated in degenerated discs. Omentin-1, also known as intelectin-1, is an adipokine with anti-inflammatory, anti-apoptosis, pro-proliferation, and proangiogenic properties in various types of cells. However, little is known about the effects of omentin-1 on human nucleus pulposus cells (HNPCs). This study aims to investigate the effects of omentin-1 on healthy HNPCs regarding proliferation and further investigate the effects of omentin-1 on IL-1β-induced inflammation, apoptosis, and degeneration in HNPCs. Genes and proteins of interest were measured by qRT-PCR, immunoblotting, and immunofluorescence to conduct related experiments. Cell viability (CCK-8), EdU, and mitochondrial membrane potential (JC-1), flow cytometry assays were used to assess proliferation and apoptosis, respectively. Our study showed that omentin-1 promoted proliferation in normal HNPCs. Furthermore, omentin-1 expression was decreased in IL-1β-treated HNPCs. Omentin-1 protected against IL-1β-induced inflammation, apoptosis, and degeneration in HNPCs in vitro via the activation of the PI3K/Akt signaling pathway. These findings may contribute to understanding the role of omentin-1 in HNPCs and may be a potential therapeutic candidate for intervertebral disc degeneration.