Background: Inflammation plays an important role in intervertebral disc degeneration (IDD). The protein follistatin-like 1 (FSTL1) plays a proinflammatory role in a variety of inflammatory diseases.
Objectives: The purpose of this study was to investigate whether IDD could be delayed by inhibiting FSTL-1 expression.
Methods: We established a puncture-induced IDD model in wild-type and FSTL-1+/- mice and collected intervertebral discs (IVDs) from the mice. Safranin O staining was used to detect cartilage loss of IVD tissue, and HE staining was used to detect morphological changes of IVD tissue. We measured the expression of FSTL-1 and related inflammatory indicators in IVD tissues by immunohistochemical staining, real-time PCR, and Western blotting.
Results: In the age-induced model of IDD, the level of FSTL-1 increased with the exacerbation of degeneration. In the puncture-induced IDD model, FSTL-1-knockdown mice showed a reduced degree of degeneration compared with that of wild-type mice. Further experiments showed that FSTL-1 knockdown also significantly reduced the level of related inflammatory factors in IVD. In vitro experiments showed that FSTL-1 knockdown significantly reduced TNF--induced inflammation. Specifically, the expression levels of the inflammatory factors COX-2, iNOS, MMP-13, and ADAMTS-5 were reduced. Knockdown of FSTL-1 attenuated inflammation by inhibiting the expression of P-Smad1/5/8, P-Erk1/2, and P-P65.
Conclusion: Knockdown of FSTL-1 attenuated inflammation by inhibiting the TNF- response and Smad pathway activity and ultimately delayed IDD.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8055391 | PMC |
| http://dx.doi.org/10.1155/2021/6640751 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Ferristatin II protects nucleus pulposus against degeneration through inhibiting ferroptosis and activating HIF-1α pathway mediated mitophagy.
Int Immunopharmacol
January 2025
Department of Spine Surgery, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, Shandong 250000, China; Department of Spine Surgery, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250000, China. Electronic address:
Background: Nucleus pulposus (NP) degeneration represents a significant contributing factor in the pathogenesis of intervertebral disc (IVD) degeneration (IVDD), and is a key underlying mechanism in several lumbar spine pathologies. Nevertheless, the precise mechanisms that govern NP degeneration remain unclear. A significant contributing factor to IVDD has been identified as ferroptosis.
View Article and Find Full Text PDFThe influence of workload on muscle fatigue, tissue properties, and postural stability in older and younger workers.
PLoS One
January 2025
Department of Human Kinetics, Université du Québec à Trois-Rivières, Trois-Rivières, Québec, Canada.
Demographic aging and extended working lives have prompted interest in the physiological changes that occur with age, particularly in the lumbar spine. Age-related declines in muscle quality and intervertebral disc alterations may reduce muscular endurance, strength, and postural stability, potentially increasing the risk of musculoskeletal injuries in older workers. As experienced workers play an important role in addressing labor shortages, understanding the impact of age-related physiological changes on the biomechanical properties of the lumbar spine is key to ensure safe and sustainable employment for aging individuals.
View Article and Find Full Text PDFMARCHF8-mediated ubiquitination via TGFBI regulates NF-κB dependent inflammatory responses and ECM degradation in intervertebral disc degeneration.
PLoS One
January 2025
Department of Orthopedics, Shanghai Pudong New Area People's Hospital, Shanghai, China.
Article Synopsis
- The study investigates the role of TGFBI as a key gene in the development of intervertebral disc degeneration (IDD) and how it is regulated by MARCHF8.
- The researchers used advanced gene analysis techniques to identify significant gene modules related to IDD and found that changes in TGFBI levels affect cell behavior, inflammation, and extracellular matrix breakdown.
- Results indicated that MARCHF8 plays a crucial role in regulating TGFBI expression, which impacts NP cell apoptosis and inflammatory responses through the NF-κB signaling pathway.
'Disc degeneration in distal unfused segments: cause or consequence of adding-on after posterior fusion of lenke 3c, 5c, 6c adolescent idiopathic scoliosis?'.
Acta Neurochir (Wien)
January 2025
Department of Orthopaedics & Traumatology, Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey.
Background: The aim of this study is to examine the association between adding-on (AO) and disc degeneration(DD) of distal unfused levels in Lenke 3 C, 5 C, 6 C adolescent idiopathic scoliosis (AIS) patients with a follow-up of at least two years by comparing preoperative and postoperative magnetic resonance imaging (MRI).
Methods: 47 AIS patients (32 females and 15 males) with structural thoracolumbar/lumbar (TL/L) curves treated with long segment thoracolumbar fusion were retrospectively evaluated. Patients were divided into two groups according to the occurrence of the AO (AO and Non-AO groups).
Automatic detection, classification, and segmentation of sagittal MR images for diagnosing prolapsed lumbar intervertebral disc.
Sci Rep
January 2025
Khulna University of Engineering and Technology, Khulna, 9203, Bangladesh.
Magnetic resonance (MR) images are commonly used to diagnose prolapsed lumbar intervertebral disc (PLID). However, for a computer-aided diagnostic (CAD) system, distinguishing between pathological abnormalities of PLID in MR images is a challenging and intricate task. Here, we propose a comprehensive model for the automatic detection and cropping of regions of interest (ROI) from sagittal MR images using the YOLOv8 framework to solve this challenge.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!