HO‐1 overexpression alleviates senescence by inducing autophagy via the mitochondrial route in human nucleus pulposus cells. Issue 11 (2nd April 2020)

• Record Type: Journal Article
• Authors: Yi, Weiwei; Lan, Haiyang; Wen, Yafeng; Wang, Yiyang; He, Danshuang; Bai, Zhibiao; Zhang, Ye; Jiang, Wei; Liu, Bo; Shen, Jieliang; Hu, Zhenming
• Is Part Of: Journal of cellular physiology. Volume 235:Issue 11(2020:Nov.)
• Page Start: 8402
• Page End: 8415
• Publication Date: 2020-04-02
• Subjects: autophagy -- HO‐1 -- mitochondrial -- nucleus pulposus cells -- senescence; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.29684
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Intervertebral disc degeneration (IDD) is closely associated with aging. Our previous studies have confirmed that heme oxygenase‐1 (HO‐1) can inhibit nucleus pulposus (NP) cell apoptosis. However, whether or not HO‐1 is involved in NP cell senescence and autophagy is unclear. Our results indicated that HO‐1 expression was reduced in IDD tissues and replicative senescent NP cells. HO‐1 overexpression using a lentiviral vector reduced the NP cell senescence level, protected mitochondrial function, and promoted NP cell autophagy through the mitochondrial pathway. Autophagy inhibitor 3‐MA pretreatment reversed the anti‐senescent and protective effects on the mitochondrial function of HO‐1, which promoted the degradation of the extracellular matrix (ECM) in the intervertebral disc. In vivo, HO‐1 overexpression inhibited IDD and enhanced autophagy. In summary, these results suggested that HO‐1 overexpression alleviates NP cell senescence by inducing autophagy via the mitochondrial route. Abstract : Heme oxygenase‐1 (HO‐1) expression was reduced in intervertebral disc degeneration (IDD) tissues and replicative senescent nucleus pulposus (NP) cells. HO‐1 overexpression using a lentiviral vector reduced the NP cell senescence level, protected mitochondrial function, and promoted NP cell autophagy through the mitochondrial pathway, and inhibited IDD.