Role of Long Intergenic Nonprotein-Coding RNA 00511 in Nod-Like Receptor Protein Pyrin Domain 3-Induced Chondrocyte Pyroptosis via the MicroRNA-9-5p/FUT1 Axis

Aug 24, 2026

This study investigated the function of LINC00511 in Nod-like receptor pyrin domain 3 (NLRP3) inflammasome-mediated chondrocyte pyroptosis through a miR-9-5p/FUT1 regulatory pathway. Chondrocytes and ATDC5 cells were stimulated with LPS to induce inflammatory injury, characterized by increased IL-1β and IL-18, elevated NLRP3, ASC, caspase-1, and GSDMD, reduced viability, and increased LDH. LINC00511 silencing suppressed NLRP3 inflammasome activation and limited LPS-driven pyroptosis by sponging miR-9-5p, which targeted FUT1. Moreover, modulating miR-9-5p or overexpressing FUT1 reversed the anti-pyroptotic effects of LINC00511 knockdown.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages11

Reading Time28 min

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Introduction

Osteoarthritis background and inflammatory injury

LINC00511 and ceRNA mechanisms in OA

Experimental design and cellular outcomes

LPS-induced pyroptosis and inflammasome markers

LINC00511 knockdown and mechanistic validation

Proposed miRNA axis

LINC00511–miR-9-5p interaction

miR-9-5p targeting FUT1 and rescue experiments

J. Microbiol. Biotechnol. 2024. 34(7): 1511–1521 [https://doi.org/10.4014/jmb.2312.12014](https://doi.org/10.4014/jmb.2312.12014) Received: December 12, 2023 Accepted: March 29, 2024 First published online: April 15, 2024 *Corresponding author Phone: +13162096637 Fax: +13162096637 E-mail: [fwei1129@163.com](fwei1129@163.com) [pISSN 1017-7825](pISSN 1017-7825)[ ](pISSN 1017-7825)[eISSN 1738-8872](eISSN 1738-8872) Copyright © 2024 by the authors. Licensee KMB. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. Role of Long Intergenic Nonprotein-Coding RNA 00511 in Nod-Like Receptor Protein Pyrin Domain 3-Induced Chondrocyte Pyroptosis via the MicroRNA-9-5p/FUT1 Axis Tianjun Zhai1,2, Zengqiao Zhang3, Xiaoshen Hu4, Dongyi He5, and Wei Feng1,2,6* 1School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China 2Shanghai University of Traditional Chinese Medicine Rehabilitation Institute, Shanghai 201203, P.R. China 3Tuina Department of Yueyang Hospital of Integrated Traditional Chinese and Western Medicine Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200083, P.R. China 4School of Health Preservation and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu 610075, P.R. China 5Rheumatoid Internal Medicine in Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Me6ThicSeo,SnhdangRehaibil2it0tiH, Po.Rsp. CitilnoafShanghai, Shanghai 200441, P.R. China This study aimed to determine the function of LINC00511 in Nod-Like Receptor Pyrin Domain 3 inflammasome-mediated chondrocyte pyroptosis via the regulation of miR-9-5p and FUT 1. Chondrocyte inflammatory injury was induced by treating chondrocytes with LPS. Afterwards, the levels of IL-1β and IL-18, the expression of NLRP3, ASC, Caspase-1, and GSDMD, cell viability, and LDH activity inchondrocytes were assessed. LINC00511 expression in LPS-treated chondrocytes was detected, and LINC00511 was subsequently silenced to analyse its role in chondrocyte pyroptosis. The subcellular localization of LINC00511 was predicted and verified. Furthermore, the binding relationships between LINC00511 and miR-9-5p and between miR-9-5p and FUT1 were validated. LINC00511 regulated NLRP3 inflammasome-mediated chondrocyte pyroptosis through the miR-9- 5p/FUT1 axis. LPS-treated ATDC5 cells exhibited elevated levels of inflammatory injury; increased levels of NLRP3, ASC, Caspase-1, and GSDMD; reduced cell viability; increased LDH activity; and increased LINC00511 expression, while LINC00511 silencing inhibited the NLRP3 inflammasome to restrict LPS-induced chondrocyte pyroptosis. Next, LINC00511 sponged miR-9-5p, which targeted FUT1. Silencing LINC00511 suppressed FUT1 by upregulating miR-9-5p. Additionally, downregulation of miR-9-5p or overexpression of FUT1 neutralized the suppressive effect of LINC00511 knockdown on LPS-induced chondrocyte pyroptosis. Silencing LINC00511 inhibited the NLRP3 inflammasome to quench Caspase-1-dependent chondrocyte pyroptosis in OA by promoting miR-9-5p and downregulating FUT1 . Keywords: Osteoarthritis, chondrocyte, inflammatory injury, long intergenic nonprotein coding RNA 00511, microRNA-9-5p, FUT1 Introduction As one of the most common types of arthritis, osteoarthritis (OA) is characterized by the proliferation of subchondral bones and degeneration of articular cartilage [1]. OA is a serious and complicated disorder resulting from a series of factors, such as uric acid, heredity, smoking, body weight, and cardiovascular disease [2, 3] . Currently, the occurrence and disability rates of chronic OA are increasing, which could lead to debilitating living standards, deficient functions, medical expenditures, and social burdens [4] . Currently, feasible management strategies for OA include physical exercise, intra-articular treatment, and th

FAQs

What role does LINC00511 play in LPS-induced chondrocyte pyroptosis?

LINC00511 levels increase after LPS treatment, and silencing LINC00511 suppresses NLRP3 inflammasome activation, thereby restricting chondrocyte pyroptosis.

Which pathway connects LINC00511 to NLRP3 inflammasome activation?

The study links LINC00511 to pyroptosis via the miR-9-5p/FUT1 axis, where LINC00511 sponges miR-9-5p and miR-9-5p targets FUT1.

How were miR-9-5p and FUT1 involved in the functional rescue?

Downregulating miR-9-5p or overexpressing FUT1 neutralized the inhibitory effect of LINC00511 knockdown on LPS-induced chondrocyte pyroptosis.

Aug 24, 2026

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