Bone marrow mesenchymal stem cells-derived exosomes suppress miRNA-5189-3p to increase fibroblast-like synoviocyte apoptosis via the BATF2/JAK2/STAT3 signaling pathway

Zhang, Yiqun; Tu, Bizhi; Sha, Qi; Qian, Jun

doi:10.1080/21655979.2022.2045844

Cited by 11 publications

(5 citation statements)

References 45 publications

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“…Mice were randomly classified into 10 groups (n = 10): the normal group (mice without treatment), the model group (the modeled mice were injected with 1 × PBS), the si-NC group (the modeled mice were injected with 5 μL adenovirus silencing HOTTIP NC (5 × 10 9 viral particles/μL)) [ 30 ], the si-HOTTIP group (the modeled mice were injected with adenovirus silencing HOTTIP (5 × 10 9 viral particles/μL)), the agomir NC group (the modeled mice were injected with adenovirus overexpressing miR-30b-3p NC (5 × 10 9 viral particles/μL)), the miR-30b-3p agomir group (the modeled mice were injected with adenovirus overexpressing miR-30b-3p (5 × 10 9 viral particles/μL)), the si-HOTTIP + antagomir NC group (the modeled mice were injected with adenovirus silencing HOTTIP and adenovirus inhibiting miR-30b-3p NC (both 5 × 10 9 viral particles/μL)), the si-HOTTIP + miR-30b-3p antagomir group (the modeled mice were injected with adenovirus silencing HOTTIP and adenovirus inhibiting miR-30b-3p (both 5 × 10 9 viral particles/μL)), the miR-30b-3p agomir + oe-NC group (the modeled mice were injected with adenovirus overexpressing miR-30b-3p and adenovirus overexpressing PGK1 NC (both 5 × 10 9 viral particles/μL)) and the miR-30b-3p agomir + oe-PGK1 group (the modeled mice were injected with adenovirus overexpressing miR-30b-3p and adenovirus overexpressing PGK1 (both 5 × 10 9 viral particles/μL)). All of the adenoviruses were obtained from RiboBio Co., Ltd. (Guangdong, China), and were performed intra-articular injection into mice, once weekly after the first immunization for a total of 6 weeks.…”

Section: Methodsmentioning

confidence: 99%

LncRNA HOTTIP impacts the proliferation and differentiation of fibroblast-like synoviocytes in ankylosing spondylitis through the microRNA-30b-3p/PGK1 axis

Zhang

Yao

et al. 2023

J Orthop Surg Res

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Objective Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been reported to exert regulatory effects on biological processes. This study intended to assess the role of the lncRNA HOXA transcript at the distal tip (HOTTIP)/miR-30b-3p/phosphoglycerate kinase 1 (PGK1) axis in ankylosing spondylitis (AS). Methods Levels of HOTTIP, miR-30b-3p and PGK1 in AS synovial tissues and cultured AS fibroblast-like synoviocytes (ASFLSs) were assessed. The ASFLSs were identified and, respectively, treated with altered expression of HOTTIP and miR-30b-3p, and then, the proliferation and differentiation of the ASFLSs were assessed. The AS mouse models were established by injection of proteoglycan and Freund’s complete adjuvant and then were treated with altered expression of HOTTIP and miR-30b-3p, and the pathological changes and apoptosis of synoviocytes in mice’ synovial tissues were measured. The relationship of HOTTIP, miR-30b-3p and PGK1 was verified. Results HOTTIP and PGK1 were elevated, while miR-30b-3p was reduced in AS synovial tissues and ASFLSs. Elevated miR-30b-3p or inhibited HOTTIP restrained proliferation and differentiation of ASFLSs and also improved the pathological changes and promoted apoptosis of synoviocytes in mice’s synovial tissues. PGK1 was a target of miR-30b-3p, and miR-30b-3p could directly bind to HOTTIP. Silencing miR-30b-3p or overexpressing PGK1 reversed the improvement of AS by knocking down HOTTIP or up-regulating miR-30b-3p. Conclusion Our study suggests that reduced HOTTIP ameliorates AS progression by suppressing the proliferation and differentiation of ASFLSs through the interaction of miR-30b-3p and PGK1.

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Section: Methodsmentioning

confidence: 99%

LncRNA HOTTIP impacts the proliferation and differentiation of fibroblast-like synoviocytes in ankylosing spondylitis through the microRNA-30b-3p/PGK1 axis

Zhang

Yao

et al. 2023

J Orthop Surg Res

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“…Interestingly, BAF2 can inactivate Jak2/stat3 pathway, whereas BMSCS-EXOs can inhibit miR-5189-3p to promote apoptosis of FLS through BAF2/Jak2/stat3 pathway. This observation could form the foundation for using BMSCs in the treatment of ankylosing spondylitis (AS) ( 85 86 ). Despite these findings, there are limited reports on AS, posing a significant challenge in identifying other potential therapeutic targets.…”

Section: Application Prospect Of Exos Treatmentmentioning

confidence: 99%

Exosomes in Action: Unraveling Their Role in Autoimmune Diseases and Exploring Potential Therapeutic Applications

Zhou,

Huang,

Zhang

et al. 2024

Immune Netw

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Exosomes are double phospholipid membrane vesicles that are synthesized and secreted by a variety of cells, including T cells, B cells, dendritic cells, immune cells, are extracellular vesicles. Recent studies have revealed that exosomes can play a significant role in under both physiological and pathological conditions. They have been implicated in regulation of inflammatory responses, immune response, angiogenesis, tissue repair, and antioxidant activities, particularly in modulating immunity in autoimmune diseases (AIDs). Moreover, variations in the expression of exosome-related substances, such as miRNA and proteins, may not only offer valuable perspectives for the early warning, and prognostic assessment of various AIDs, but may also serve as novel markers for disease diagnosis. This article examines the impact of exosomes on the development of AIDs and explores their potential for therapeutic application.

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“…Many ncRNAs are also involved in the remission of autoimmune diseases. MSCs-derived exosomes suppress miR-5189-3p to facilitate the apoptosis of fibroblast-like synoviocytes via the basic leucine zipper ATF-like transcription factor 2/JAK2/STAT3 signaling pathway, which facilitate relieve ankylosing spondylitis (AS) [ 136 ]. The MSCs-secreted miR-26a inhibit the proliferation of high glucose-induced human skin fibroblasts cells and promote cell apoptosis, which may be related to the TLR4/NF-κB signaling pathway [ 137 ].…”

Section: Mscs Enhance Apoptosis Of Target Cellsmentioning

confidence: 99%

“…Promote hepatic stellate cells apoptosis [134,135] Via the BATF2/JAK2/STAT3 signaling pathway Facilitate relieve ankylosing spondylitis [136] miR-26a Related to the TLR4/NF-κB signaling pathway Inhibit the proliferation of high glucose-induced human skin fibroblasts cells, and promote cell apoptosis [137] MSCs mesenchymal stem cells, TRIM14 tripartite motif containing 14, PI3K phosphatidylinositol 3-kinase, TRAIL TNF-related apoptosis inducing ligand, MDA MDA-MB-231 cells, Fas-L Fas ligand, MM multiple myeloma, EMT Epithelial-mesenchymal transition, MMP7 matrilysin; matrix metalloproteinase 7, TGF-β transforming growth factor-beta, BATF2 basic leucine zipper transcriptional factor ATF like 2, JAK Janus kinase, STAT signal transducer and activator of transcription, TLR4 Toll-like receptor 4.…”

Section: Insights Into the Dual Regulatory Effects Of Mscs On Apoptosismentioning

confidence: 99%

The dual role of mesenchymal stem cells in apoptosis regulation

Chen,

Xia,

Yao

et al. 2024

Cell Death Dis

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Mesenchymal stem cells (MSCs) are widely distributed pluripotent stem cells with powerful immunomodulatory capacity. MSCs transplantation therapy (MSCT) is widely used in the fields of tissue regeneration and repair, and treatment of inflammatory diseases. Apoptosis is an important way for tissues to maintain cell renewal, but it also plays an important role in various diseases. And many studies have shown that MSCs improves the diseases by regulating cell apoptosis. The regulation of MSCs on apoptosis is double-sided. On the one hand, MSCs significantly inhibit the apoptosis of diseased cells. On the other hand, MSCs also promote the apoptosis of tumor cells and excessive immune cells. Furthermore, MSCs regulate apoptosis through multiple molecules and pathways, including three classical apoptotic signaling pathways and other pathways. In this review, we summarize the current evidence on the regulation of apoptosis by MSCs.

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Bone marrow mesenchymal stem cells-derived exosomes suppress miRNA-5189-3p to increase fibroblast-like synoviocyte apoptosis via the BATF2/JAK2/STAT3 signaling pathway

Cited by 11 publications

References 45 publications

LncRNA HOTTIP impacts the proliferation and differentiation of fibroblast-like synoviocytes in ankylosing spondylitis through the microRNA-30b-3p/PGK1 axis

LncRNA HOTTIP impacts the proliferation and differentiation of fibroblast-like synoviocytes in ankylosing spondylitis through the microRNA-30b-3p/PGK1 axis

Exosomes in Action: Unraveling Their Role in Autoimmune Diseases and Exploring Potential Therapeutic Applications

The dual role of mesenchymal stem cells in apoptosis regulation

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