miR9 inhibits 6-mer HA-induced cytokine production and apoptosis in human chondrocytes by reducing NF-kB activation

Scuruchi, Michele; D’Ascola, Angela; Avenoso, Angela; Zappone, Annie; Mandraffino, Giuseppe; Campo, Salvatore; Campo, Giuseppe M.

doi:10.1016/j.abb.2022.109139

Cited by 6 publications

(4 citation statements)

References 49 publications

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“… 43 , 44 , 48 , 49 , 59 It became a molecule of interest during our investigation of miR-200b. Various studies have reported the role of miR-9 in regulating EndMT-adjacent processes such as proinflammatory signaling and TGF-β signaling, inhibiting, 45 – 47 , 59 – 61 but few have investigated miR-9 in the context of diabetic complications. MiR-9 has been reported to directly inhibit NFKB1, TGFBR2, and MALAT1 through complementarity-based silencing.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA 9 Is a Regulator of Endothelial to Mesenchymal Transition in Diabetic Retinopathy

Wang

Feng

Chakrabarti

2023

Invest. Ophthalmol. Vis. Sci.

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Purpose Diabetic retinopathy (DR) is a significant cause of blindness. Most research around DR focus on late-stage developments rather than early changes such as early endothelial dysfunction. Endothelial-to-mesenchymal transition (EndMT), an epigenetically regulated process whereby endothelial cells lose endothelial characteristics and adopt mesenchymal-like phenotypes, contributes to early endothelial changes in DR. The epigenetic regulator microRNA 9 (miR-9) is suppressed in the eyes during DR. MiR-9 plays a role in various diseases and regulates EndMT-related processes in other organs. We investigated the role miR-9 plays in glucose-induced EndMT in DR. Methods We examined the effects of glucose on miR-9 and EndMT using human retinal endothelial cells (HRECs). We then used HRECs and an endothelial-specific miR-9 transgenic mouse line to investigate the effect of miR-9 on glucose-induced EndMT. Finally, we used HRECs to probe the mechanisms through which miR-9 may regulate EndMT. Results We found that miR-9 inhibition was both necessary and sufficient for glucose-induced EndMT. Overexpression of miR-9 prevented glucose-induced EndMT, whereas suppressing miR-9 caused glucose-like EndMT changes. We also found that preventing EndMT with miR-9 overexpression improved retinal vascular leakage in DR. Finally, we showed that miR-9 regulates EndMT at an early stage by regulating EndMT-inducing signals such as proinflammatory and TGF-β pathways. Conclusions We have shown that miR-9 is an important regulator of EndMT in DR, potentially making it a good target for RNA-based therapy in early DR.

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Section: Discussionmentioning

confidence: 99%

“…MiR-9 has been reported to directly inhibit NFKB1, TGFBR2, and MALAT1 through complementarity-based silencing. 45 – 47 , 59 – 61 NFKB1 encodes the DNA binding subunit of the canonical NF-κB complex. Increased NF-κB activity is seen in the vasculature during hyperglycemia and is associated with the progression of EndMT.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA 9 Is a Regulator of Endothelial to Mesenchymal Transition in Diabetic Retinopathy

Wang

Feng

Chakrabarti

2023

Invest. Ophthalmol. Vis. Sci.

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“…The association of miRs with the NF-κB pathway in OA chondrocytes has been discussed ( 58 ). miR-9 has been reported to reduce the production of pro-inflammatory cytokines, MMPs, and pro-apoptotic factors by targeting NF-κB in human articular chondrocytes ( 59 ). Overexpression of miR-326 can inhibit the expression of HDAC3, leading to increased acetylation of p65 and enhanced activity of STAT1 in chondrocytes ( 60 ).…”

Section: Nf-κb Signaling In the Physiology And Pathogenesis Of Chondr...mentioning

confidence: 99%

The protective activity of natural flavonoids against osteoarthritis by targeting NF-κB signaling pathway

Zhou

2023

Front. Endocrinol.

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Osteoarthritis (OA) is a typical joint disease associated with chronic inflammation. The nuclear factor-kappaB (NF-κB) pathway plays an important role in inflammatory activity and inhibiting NF-κB-mediated inflammation can be a potential strategy for treating OA. Flavonoids are a class of naturally occurring polyphenols with anti-inflammatory properties. Structurally, natural flavonoids can be divided into several sub-groups, including flavonols, flavones, flavanols/catechins, flavanones, anthocyanins, and isoflavones. Increasing evidence demonstrates that natural flavonoids exhibit protective activity against the pathological changes of OA by inhibiting the NF-κB signaling pathway. Potentially, natural flavonoids may suppress NF-κB signaling-mediated inflammatory responses, ECM degradation, and chondrocyte apoptosis. The different biological actions of natural flavonoids against the NF-κB signaling pathway in OA chondrocytes might be associated with the differentially substituted groups on the structures. In this review, the efficacy and action mechanism of natural flavonoids against the development of OA are discussed by targeting the NF-κB signaling pathway. Potentially, flavonoids could become useful inhibitors of the NF-κB signaling pathway for the therapeutic management of OA.

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“…CircRNA plays an important regulatory role in disease by interacting with disease‐associated microRNA and have also been shown to mediate chondrocyte apoptosis 72 . Due to the close relationships and similar effects among the above three, we list them as regulating chondrocyte apoptosis in Table 1 instead of showing them one by one 73–97 …”

Section: Apoptosismentioning

confidence: 99%

Recent Therapeutic Strategies for Excessive Chondrocyte Death in Osteoarthritis: A Review

Xiang

Zheng

Liu

et al. 2023

Orthopaedic Surgery

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Osteoarthritis (OA) causes pain and disability in the elderly and has placed a severe burden on healthcare worldwide. Excessive death and decreased density of chondrocytes are recognized as the major pathological characteristic of OA. Chondrocytes have been shown to have multiple forms of death, including apoptosis, pyroptosis, necroptosis, and ferroptosis. The excessive death of chondrocytes often forms a vicious circle with imbalanced chondrocytes extracellular matrix (ECM) metabolism. Therefore, inhibiting chondrocytes excessive death has become a key point that cannot be ignored in the development of OA treatment strategies. We summarized recent studies on the functions and mechanisms of different modes of chondrocyte death and potential therapeutic strategies for OA and offered our views. This may provide direction and theoretical support for formulating OA treatment strategies in the future.

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miR9 inhibits 6-mer HA-induced cytokine production and apoptosis in human chondrocytes by reducing NF-kB activation

Cited by 6 publications

References 49 publications

MicroRNA 9 Is a Regulator of Endothelial to Mesenchymal Transition in Diabetic Retinopathy

MicroRNA 9 Is a Regulator of Endothelial to Mesenchymal Transition in Diabetic Retinopathy

The protective activity of natural flavonoids against osteoarthritis by targeting NF-κB signaling pathway

Recent Therapeutic Strategies for Excessive Chondrocyte Death in Osteoarthritis: A Review

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