MicroRNA-145 overexpression attenuates apoptosis and increases matrix synthesis in nucleus pulposus cells

Life Sciences
Jie ZhouWei Ye

Abstract

Lower back pain is often associated with intervertebral disc degeneration (IDD), which results from a decrease in nucleus pulposus (NP) cells and an imbalance between the degradation and synthesis of extracellular matrix (ECM) components. Multiple microRNAs play crucial roles in the modulation of NP cell apoptosis and matrix degradation. miR-145 is an important microRNA related to degenerative diseases such as osteoarthritis. Here, the effect of miR-145 in IDD was elucidated. The aim of this study was to explore the role and mechanism of miR-145 in the apoptosis of NP cells and in matrix metabolism in NP cells. Real-time PCR, western blotting and flow cytometry analysis were used to observe the effect of miR-145 on NP cell apoptosis in the absence or presence of oxidative stress. Cell transfection, loss-of-function experiments using an ADAM17 inhibitor or lentiviral shADAM17, immunofluorescence, real-time PCR and western blotting were performed to demonstrate the role and mechanism of miR-145 in NP cell matrix metabolism. miR-145 attenuated NP cell apoptosis in the absence and presence of oxidative stress. Moreover, miR-145 overexpression increased and miR-145 suppression decreased matrix synthesis. ADAM17, which is expressed i...Continue Reading

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Citations

Nov 22, 2019·Current Pharmaceutical Biotechnology·Songfeng ChenHongjian Liu
Nov 27, 2019·Spine·Srikanth N DiviChristopher K Kepler
May 24, 2020·International Journal of Molecular Sciences·Petra Cazzanelli, Karin Wuertz-Kozak
Jan 18, 2021·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Nader Akbari DilmaghnaiSoudeh Ghafouri-Fard
Mar 3, 2021·Inflammation·Milad AshrafizadehSaeed Samarghandian

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis