Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways

Chang, Ting‐Kuo; Wang, Yuhan; Kuo, Sheng‐Fong; Wang, Shih‐Wei; Tsai, Cheng-Han; Fong, Yi‐Chin; Wu, Nan-Lin; Liu, Shan‐Chi; Tang, Chih‐Hsin

doi:10.18632/aging.103195

Cited by 22 publications

(20 citation statements)

References 45 publications

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“…RNA isolation and RT‐qPCR assays followed the methodology described in our previous study (Chang et al, 2020).…”

Section: Methodsmentioning

confidence: 99%

“…Wt‐IL‐1β and mut‐IL‐1β‐3ʹ‐UTRs were purchased from Invitrogen. Luciferase activity was quantified using the methodology described in our previous studies (Chang et al, 2020; Chen, Lu, et al, 2020).…”

Section: Methodsmentioning

confidence: 99%

“…For histological analysis, rat knee specimens were fixed in 10% neutral formalin for more than 72 h, then decalcified using 10% ethylenediaminetetraacetic acid (EDTA) in PBS for 14 days, and dehydrated for 1 day in increasing concentrations of ethanol (50%–100%). The specimens were then embedded in paraffin and the sagittal plane section slides were prepared with hematoxylin and eosin (H&E), Safranin‐O/Fast‐green, or IL‐1β antibody, following our previously published procedures (Chang et al, 2020; Wang et al, 2020). Images were captured by a light microscope (DM500, Leica Inc.) at ×40 magnification for H&E and Safranin‐O/Fast‐green staining and at ×200 magnification for IL‐1β staining.…”

Section: Methodsmentioning

confidence: 99%

“…Moreover, pro‐inflammatory mediators including IL‐1β, IL‐6, TNF‐α, and MMPs are responsible for histological changes in OA (Guan et al, 2018; Huang et al, 2019; Malemud, 2018). Notably, IL‐1β stimulation effectively downregulates miR‐144‐3p expression in the human lung cancer cell line A549 (Wu et al, 2016) and we have previously demonstrated that the adipokine apelin enhances IL‐1β expression by inhibiting miR‐144‐3p in human OA synovial fibroblasts (Chang et al, 2020). However, the role of endogenous miR‐144‐3p in OA is unclear.…”

Section: Introductionmentioning

confidence: 99%

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miR‐144‐3p ameliorates the progression of osteoarthritis by targeting IL‐1β: Potential therapeutic implications

Lin

Liu

et al. 2021

Journal Cellular Physiology

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The pro‐inflammatory cytokine interleukin 1 beta (IL‐1β) plays a critical role in osteoarthritis (OA) disease pathogenesis. MicroRNA (miRNA) activity is related to inflammation in OA and some miRNAs specifically regulate IL‐mediated degradation of cartilage type II collagen. Previous studies have indicated that miR‐144‐3p is a useful target in the regulation of pro‐inflammatory cytokines in different diseases. However, the role of miR‐144‐3p in OA is unclear. In this study, we observed a negative correlation between miR‐144‐3p and IL‐1β expression in OA. miR‐144‐3p mimic transfection of OA synovial fibroblasts downregulated levels of IL‐1β expression, while blocking the MAPK, PI3K/Akt, and NF‐κB signaling pathways relating to IL‐1β production, and effectively increased miR‐144‐3p expression in OASFs. Findings from an anterior cruciate ligament transection rat model revealed that administration of miR‐144‐3p mimic effectively ameliorated OA progression and reduced the numbers of IL‐1β‐positive cells in synovial tissue. This study suggests that miR‐144‐3p is a useful therapeutic target in OA disease.

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“…RNA isolation and RT‐qPCR assays followed the methodology described in our previous study (Chang et al, 2020).…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

miR‐144‐3p ameliorates the progression of osteoarthritis by targeting IL‐1β: Potential therapeutic implications

Lin

Liu

et al. 2021

Journal Cellular Physiology

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“…The major pathological abnormalities in OA include cartilage degeneration, remodeling of subchondral bone, and synovial membrane inflammation (synovitis). Although the degree of inflammation in OA is remarkably less than that in rheumatoid arthritis, synovitis is now considered an important feature of OA that adversely affects whole joint function (21)(22)(23). Evidence-based medicine has demonstrated that acute or chronic synovitis in varying degrees was observed in OA patients (24).…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone-loaded thermo-sensitive hydrogel attenuates osteoarthritis by protecting cartilage and providing effective pain relief

Wang¹,

Xu²,

Fan³

et al. 2021

Ann Transl Med

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Background: We utilized the destabilization of medial meniscus (DMM)-induced mice to illustrate the osteoarthritis (OA) suppressing and pain-relieving effects of a novel prolonged-release intra-articular (IA)dexamethasone-loaded thermo-sensitive hydrogel (DLTH).Methods: The effects of temperature and pH on DLTH formation and in vitro DLTH release profile were assessed. C57BL/6J mice were randomly divided into three groups: Ctrl group Model group and DLTH group. The DLTH group received joint injections of 10 μL DLTH (1 mg/kg) into the right knee once a week from week 2 to week 11. We performed micro-computed tomography (Micro-CT) and histological analyses of safranin O-fast green, hematoxylin and eosin, and tartrate-resistant acid phosphatase in knee joints. We also carried out immunohistochemical (IHC) staining for matrix metalloproteinase-9 (MMP-9), MMP-13, and a disintegrin and metalloproteinase with thrombospondin motifs-5 in cartilage and Ki-67 in synovia. Pain behavioral testing was carried out in all mice. The serum content of prostaglandin E2 (PGE2) and real-time polymerase chain reaction (PCR) of inflammatory cytokines and pain-related factors in dorsal root ganglia (DRGs) were evaluated. Results: It took 20 minutes to form DLTH at pH 7.0 and 37 ℃. The cumulative release profiles of dexamethasone (Dex) from DLTH at 37 ℃ revealed a rapid release in the first 24 h and a sustained slow release for 7 days. In vivo study illustrated that DLTH attenuated OA bone destruction and ameliorated synovitis and progression of OA in DMM-induced mice. The chondroprotective effects of DLTH were mediated by decreased expressions of MMP-9, MMP-13, and ADAMTS-5. The results showed that IA-DLTH exerted pain-relieving effects in OA mice. Upregulation of nociceptive response time (NRT) and downregulations of serum PGE2, inflammatory factors, and pain-related mediators in DRGs of mice in the DLTH group were recorded. Conclusions: Data presented in this study elucidated that DLTH exhibited a long and lasting Dex release and it is a potential sustainable drug delivery system (DDS) to treat OA locally. IA-DLTH injection exerted chondroprotective and pain-relieving effects in DMM-induced arthritis. The involvement of MMP-9, MMP-13, ADAMTS-5, and inflammatory and pain-related factors, may account for the suppression of OA progression and pain.

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Reciprocal Interactions Between Apelin and Noncoding RNAs in Cancer Progression

Jafarzadeh,

Naseri,

Khorramdelazad

et al. 2024

Cell Biochemistry & Function

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Apelin, a bioactive peptide that serves as an endogenous ligand for the apelin receptor (APJ), is overexpressed in various types of cancers and contributes to cancer cell proliferation, viability, migration, angiogenesis, and metastasis, as well as immune deviation. Noncoding RNAs (ncRNAs) regulate gene expression, and there is growing evidence suggesting a bidirectional crosstalk between ncRNAs (including long noncoding RNAs [lncRNAs], circular RNAs [circRNAs], and microRNAs [miRNAs]) and apelin in cancers. Certain miRNAs can directly target the apelin and inhibit its expression, thereby suppressing tumor growth. It has been indicated that miR‐224, miR‐195/miR‐195‐5p, miR‐204‐5p, miR‐631, miR‐4286, miR‐637, miR‐4493, and miR‐214‐3p target apelin mRNA and influence its expression in prostate cancer, lung cancer, esophageal cancer, chondrosarcoma, melanoma, gastric cancer, glioma, and hepatocellular carcinoma (HCC), respectively. Moreover, circ‐NOTCH1, circ‐ZNF264, and lncRNA BACE1‐AS upregulate apelin expression in gastric cancer, glioma, and HCC, respectively. On the other hand, apelin has been shown to regulate the expression of certain ncRNAs to affect tumorigenesis. It was revealed that apelin affects the expression of circ_0000004/miR‐1303, miR‐15a‐5p, and miR‐106a‐5p in osteosarcoma, lung cancer, and prostate cancer, respectively. This review explains a bidirectional interplay between ncRNAs and apelin in cancers to provide insights concerning the molecular mechanisms underlying this crosstalk and potential implications for cancer therapy.

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Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways

Cited by 22 publications

References 45 publications

miR‐144‐3p ameliorates the progression of osteoarthritis by targeting IL‐1β: Potential therapeutic implications

miR‐144‐3p ameliorates the progression of osteoarthritis by targeting IL‐1β: Potential therapeutic implications

Dexamethasone-loaded thermo-sensitive hydrogel attenuates osteoarthritis by protecting cartilage and providing effective pain relief

Reciprocal Interactions Between Apelin and Noncoding RNAs in Cancer Progression

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