The lncRNA PILA promotes NF-κB signaling in osteoarthritis by stimulating the activity of the protein arginine methyltransferase PRMT1

Tang, Simin; Cao, Yumei; Cai, Zhaopeng; Nie, Xiaoyu; Ruan, Jianzhao; Zhou, Zhilai; Ruan, Guangfeng; Zhu, Zhaohua; Han, Weiyu; Ding, Changhai

doi:10.1126/scisignal.abm6265

Cited by 25 publications

(8 citation statements)

References 58 publications

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“…Protein arginine methyltransferase PRMT1 regulated AKT/FOXO1 pathway and enhanced ECM degradation and apoptosis of chondrocytes in joint osteoarthritis (165). The activity of PRMT1 was elevated and controlled osteoarthritis via induction of DHX9 arginine methylation and activation of NF-kB signaling pathway (166). Suppression of PRMT5 reduced MAPK and NF-kB signaling pathway and blocked cartilage degradation in osteoarthritis (167).…”

Section: Conclusion and Discussionmentioning

confidence: 99%

Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression

Zheng

Chen

et al. 2023

Front. Immunol.

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Osteoarthritis is non-inflammatory degenerative joint arthritis, which exacerbates disability in elder persons. The molecular mechanisms of osteoarthritis are elusive. Ubiquitination, one type of post-translational modifications, has been demonstrated to accelerate or ameliorate the development and progression of osteoarthritis via targeting specific proteins for ubiquitination and determining protein stability and localization. Ubiquitination process can be reversed by a class of deubiquitinases via deubiquitination. In this review, we summarize the current knowledge regarding the multifaceted role of E3 ubiquitin ligases in the pathogenesis of osteoarthritis. We also describe the molecular insight of deubiquitinases into osteoarthritis processes. Moreover, we highlight the multiple compounds that target E3 ubiquitin ligases or deubiquitinases to influence osteoarthritis progression. We discuss the challenge and future perspectives via modulation of E3 ubiquitin ligases and deubiquitinases expression for enhancement of the therapeutic efficacy in osteoarthritis patients. We conclude that modulating ubiquitination and deubiquitination could alleviate the osteoarthritis pathogenesis to achieve the better treatment outcomes in osteoarthritis patients.

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Section: Conclusion and Discussionmentioning

confidence: 99%

Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression

Zheng

Chen

et al. 2023

Front. Immunol.

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“…Conversely, miR-17-5p agomiR had a better protective effect on the surface layer of cartilage and surface erosion was reduced ( Hu et al, 2018 ). Adenovirus-mediated expression of PILA Long non-coding RNA PILA stimulated NF-κB signaling in OA, induing spontaneous cartilage degradation by regulating MMP3, MMP13, and ADAMTS4 in knee joints of DMM-induced mice, thus leading to the degradation of articular cartilage and exacerbating inflammation in osteoarthritis ( Tang et al, 2022b ). Mao et al reported that miR-455-3p expression was decreased while lncRNA HOTTIP and CCL3 were significantly upregulated in OA cartilage tissue and chondrocytes.…”

Section: Regulation Of the Ecm By Lncrnas In Osteoarthritismentioning

confidence: 99%

Biological functions and applications of LncRNAs in the regulation of the extracellular matrix in osteoarthritis

Shi,

Mei,

Hao

et al. 2024

Front. Cell Dev. Biol.

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Osteoarthritis (OA) is a major cause of disability, characterized by chronic pain, irreversible destruction, and loss of function of the articular cartilage. The integrity and arrangement of the composition and structure of the extracellular matrix (ECM) are essential for maintaining the elasticity, integrity, and mechanical support function of the cartilage tissue. Osteoarthritis causes substantial changes in the ECM, driving the progression of the disease. Recent studies have shown that the ECM plays a critical role in the development of cartilage tissue as well as the occurrence and development of osteoarthritis by directly or indirectly regulating chondrocyte proliferation, apoptosis, differentiation, and gene expression. Long non-coding RNAs (lncRNAs) are a class of non-coding RNAs derived from large transcripts. Mutations and disorders of lncRNAs are closely related to the development of osteoarthritis. Abnormal expression of lncRNAs in osteoarthritic cartilage regulates the synthesis and decomposition of the cartilaginous ECM. Therefore, the use of lncRNAs as nucleic acid drugs that regulate their targets may reduce ECM degradation, thereby delaying the pathological progression of osteoarthritis. In this review, the regulatory effects of lncRNAs on ECM in different cell behaviors related to OA are summarized. The roles of lncRNAs in the proliferation, apoptosis, differentiation, and ECM-related gene activity of chondrocytes, as well as the application of lncRNAs as potential gene therapy drugs for the repair and regeneration of osteoarthritic tissue, are also reviewed. A better understanding of the roles of lncRNAs in guiding chondrocyte behavior and ECM metabolism is critical for their future applications in osteoarthritis therapy and regenerative medicine.

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“…This PDF file includes: Supplementary Materials and Methods Figs. S1 to S12 Tables S1 to S4 references (65)(66)(67)(68)(69)(70)(71)(72)(73) Other Supplementary Material for this manuscript includes the following: data file S1 Mdar reproducibility checklist…”

Section: Supplementary Materialsmentioning

confidence: 99%

Single-cell atlas of human infrapatellar fat pad and synovium implicates APOE signaling in osteoarthritis pathology

Tang,

Yao,

Ruan

et al. 2024

Sci. Transl. Med.

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The infrapatellar fat pad (IPFP) and synovium play essential roles in maintaining knee joint homeostasis and in the progression of osteoarthritis (OA). The cellular and transcriptional mechanisms regulating the function of these specialized tissues under healthy and diseased conditions are largely unknown. Here, single-cell and single-nuclei RNA sequencing of human IPFP and synovial tissues were performed to elucidate the cellular composition and transcriptional profile. Computational trajectory analysis revealed that dipeptidyl peptidase 4 + mesenchymal cells function as a common progenitor for IPFP adipocytes and synovial lining layer fibroblasts, suggesting that IPFP and synovium represent an integrated tissue unit. OA induced a profibrotic and inflammatory phenotype in mesenchymal lineage cells with biglycan + intermediate fibroblasts as a major contributor to OA fibrosis. Apolipoprotein E (APOE) signaling from intermediate fibroblasts and macrophages was identified as a critical regulatory factor. Ex vivo incubation of human cartilage with soluble APOE accelerated proteoglycan degeneration. Inhibition of APOE signaling by intra-articular injection of an anti-APOE neutralizing antibody attenuated the progression of collagenase-induced OA in mice, demonstrating a detrimental effect of APOE on cartilage. Our studies provide a framework for designing further therapeutic strategies for OA by describing the cellular and transcriptional landscape of human IPFP and synovium in healthy versus OA joints.

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The lncRNA PILA promotes NF-κB signaling in osteoarthritis by stimulating the activity of the protein arginine methyltransferase PRMT1

Cited by 25 publications

References 58 publications

Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression

Elucidating the role of ubiquitination and deubiquitination in osteoarthritis progression

Biological functions and applications of LncRNAs in the regulation of the extracellular matrix in osteoarthritis

Single-cell atlas of human infrapatellar fat pad and synovium implicates APOE signaling in osteoarthritis pathology

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