Journal Info

Journal Info

副标题

For Authors

For Authors

副标题

For Reviewers

For Reviewers

副标题

2024, Vol. 28 ›› Issue (28): 4565-4571

Effects of long intergenic non-protein coding RNA 00707 on chondrocyte injury and inflammatory factor secretion in osteoarthritis

Chu Kai, Sun Jianhua   

  1. Orthopedic Center, The First Affiliated Hospital of Shihezi University School of Medicine, Shihezi 832000, Xinjiang Uygur Autonomous Region, China

  • Received:2022-11-10 Accepted:2023-09-02 Online:2024-10-08 Published:2023-11-27

  • Contact: Sun Jianhua, MD, Chief physician, Orthopedic Center, The First Affiliated Hospital of Shihezi University School of Medicine, Shihezi 832000, Xinjiang Uygur Autonomous Region, China

  • About author:Chu Kai, Master, Orthopedic Center, The First Affiliated Hospital of Shihezi University School of Medicine, Shihezi 832000, Xinjiang Uygur Autonomous Region, China

Abstract: BACKGROUND: Long intergenic non-protein coding RNA 00707 (LINC00707) and microRNA-423-5p (miR-423-5p) are both involved in the occurrence and development of osteoarthritis. Starbase predicts that LINC00707 and miR-423-5p have complementary sequences, but whether LINC00707 and miR-423-5p interact to regulate the progress of osteoarthritis still needs further research.
OBJECTIVE: To investigate whether LINC00707 targets miR-423-5p to affect chondrocyte injury and inflammatory factor secretion in osteoarthritis.
METHODS: Articular chondrocytes were divided into eight groups: (1) blank control group was given no treatment; (2) interleukin (IL)-1β group was cultured with 10 ng/mL IL-1β for 48 hours; (3) IL-1β+si-NC group was transfected with si-NC and then treated with 10 ng/mL IL-1β for 48 hours; (4) IL-1β+si-LINC00707 group was transfected with si-LINC00707 and then treated with 10 ng/mL IL-1β for 48 hours; (5) IL-1β+miR-NC group was transfected with miR-NC and then treated with 10 ng/mL IL-1β for 48 hours; (6) IL-1β+miR-423-5p group was transfected with miR-423-5p mimic and then treated with 10 ng/mL IL-1β for 48 hours; (7) IL-1β+si-LINC00707+anti-miR-NC group was co-transfected with si-LINC00707 and anti-miR-NC and then treated with 10 ng/mL IL-1β for 48 hours; (8) IL-1β+si-LINC00707+anti-miR-423-5p group was co-transfected with si-LINC00707 and anti-miR-423-5p and then treated with 10 ng/mL IL-1β for 48 hours. Relevant tests were performed at the end of the intervention.
RESULTS AND CONCLUSION: Compared with the blank control group, the mRNA expression of LINC00707, apoptosis rate, protein expression of C-caspase3 and C-caspase9, and levels of tumor necrosis factor-α and IL-6 in articular chondrocytes were increased in the IL-1β group, while there was a decrease in miR-423-5p expression and IL-10 level (P < 0.05). Compared with the IL-1β group, the mRNA expression of LINC00707, apoptosis rate, protein expression of C-caspase3 and C-caspase9, and levels of tumor necrosis factor-α and IL-6 in articular chondrocytes were decreased in the IL-1β+si-LINC00707 group, while miR-423-5p expression and IL-10 level increased (P < 0.05). Compared with the IL-1β+miR-NC group, the protein expression of C-caspase3 and C-caspase9 and levels of tumor necrosis factor-α and IL-6 in articular chondrocytes were decreased in the IL-1β+miR-423-5p group, while miR-423-5p expression and IL-10 level increased (P < 0.05). Compared with the IL-1β+si-LINC00707+anti-miR-NC group, apoptosis rate, protein expression of C-caspase3 and C-caspase9, and levels of tumor necrosis factor-α and IL-6 in articular chondrocytes were increased in the IL-1β+si-LINC00707+anti-miR-423-5p group, while miR-423-5p expression and IL-10 level decreased (P < 0.05). To conclude, inhibiting LINC00707 by targeting miR-423-5p can reduce IL-1β-induced apoptosis and inflammation in articular chondrocytes.

Key words: osteoarthritis, LINC00707, miR-423-5p, interleukin-1β, chondrocyte, apoptosis, inflammatory factor


分享到:

Publishing Information

Publishing House of Chinese Journal of Tissue Engineering Research


The Official Publication of

Chinese Association of Rehabilitation Medicine

Contact Us

General editorial enquiries:

Email: bwb01@crter.org

Copyright related contact:

Email: crter@crter.org

Commercial Sales contact (Reprints, advertising, etc.):

Email: bwb@crter.org