IL1β inhibits differentiation of cementoblasts via microRNA‐325‐3p

Wang, Yuzhuo; Li, Ying; Shao, Pu; Wang, Liuyi; Bao, Xingfu; Hu, Min

doi:10.1002/jcb.29482

Cited by 12 publications

(3 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-325-3p has been shown to contribute to tumor progression and development [ 38 ]. Although in the skeletal-muscular system, miR-325-3p had a negative effect on osteoblast differentiation, myogenic differentiation, and osteoclastogenesis; however, whether miR-325-3p could affect chondrocytes has never been reported [ 39 – 41 ]. Our study indicated that chondrocytes treated with mechanical overloading had low expression of miR-325-3p.…”

Section: Discussionmentioning

confidence: 99%

Mechanical overloading-induced miR-325-3p reduction promoted chondrocyte senescence and exacerbated facet joint degeneration

et al. 2023

View full text Add to dashboard Cite

Objective Lumbar facet joint (LFJ) degeneration is one of the main causes of low back pain (LBP). Mechanical stress leads to the exacerbation of LFJ degeneration, but the underlying mechanism remains unknown. This study was intended to investigate the mechanism of LFJ degeneration induced by mechanical stress. Methods Here, mice primary chondrocytes were used to screen for key microRNAs induced by mechanical overloading. SA-β-gal staining, qRT-PCR, western blot, and histochemical staining were applied to detect chondrocyte senescence in vitro and in vivo. We also used a dual-luciferase report assay to examine the targeting relationship of miRNA-325-3p (miR-325-3p) and Trp53. By using NSC-207895, a p53 activator, we investigated whether miR-325-3p down-regulated trp53 expression to reduce chondrocyte senescence. A mice bipedal standing model was performed to induce LFJ osteoarthritis. Adeno-associated virus (AAV) was intraarticularly injected to evaluate the effect of miR-325-3p on facet joint degeneration. Results We observed chondrocyte senescence both in human LFJ osteoarthritis tissues and mice LFJ after bipedally standing for 10 weeks. Mechanical overloading could promote chondrocyte senescence and senescence-associated secretory phenotype (SASP) expression. MicroRNA-array analysis identified that miR-325-3p was obviously decreased after mechanical overloading, which was further validated by fluorescence in situ hybridization (FISH) in vivo. Dual-luciferase report assay showed that miR-325-3p directly targeted Trp53 to down-regulated its expression. MiR-325-3p rescued chondrocyte senescence in vitro, however, NSC-207895 reduced this effect by activating the p53/p21 pathway. Intraarticular injection of AAV expressing miR-325-3p decreased chondrocyte senescence and alleviated LFJ degeneration in vivo. Conclusion Our findings suggested that mechanical overloading could reduce the expression of miR-325-3p, which in turn activated the p53/p21 pathway to promote chondrocyte senescence and deteriorated LFJ degeneration, which may provide a promising therapeutic strategy for LFJ degeneration.

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanical overloading-induced miR-325-3p reduction promoted chondrocyte senescence and exacerbated facet joint degeneration

et al. 2023

View full text Add to dashboard Cite

show abstract

“…The expression of miR‐3064‐3p decreases during cementoblast differentiation and its overexpression inhibits cementoblast differentiation via targeting of DKK1 24 . miR‐155‐3p 25 and miR‐325‐3p 26 mediate inflammatory cytokine‐related cementoblast differentiation. Considering our results of these miRNAs, the expression of miR‐155‐3p significantly increased and the expression of miR‐361‐3p and miR‐3064‐3p tended to decrease after cementogenesis, basically in line with previous studies.…”

Section: Discussionmentioning

confidence: 99%

The long non‐coding RNA, miRNA and mRNA landscapes of cementoblasts during cementogenesis

Zhang

Huang

2023

Orthod Craniofacial Res

View full text Add to dashboard Cite

ObjectiveStimulation of cementogenesis is essential to cementum regeneration and root restoration. Long non‐coding RNAs (lncRNAs) participate in the regulatory networks of periodontal regeneration processes. We identified and analysed differentially expressed lncRNAs, miRNAs and mRNAs associated with cementogenic differentiation of cementoblasts.Materials and MethodsOCCM‐30 immortalized mouse cementoblast cells were induced in cementogenic medium for 7 and 14 days. Total RNA was extracted and subjected to RNA sequencing to screen for differentially expressed lncRNAs, miRNAs and mRNAs. Quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR) was performed to determine the expression levels of RNAs. Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were used to clarify the potential functions of differentially expressed genes in biological processes and pathways. lncRNA‐miRNA‐mRNA networks were constructed based on correlation and algorithmic analyses.ResultsIn all, 461 lncRNAs, 89 miRNAs and 2157 mRNAs showed differential expression in OCCM‐30 cells after cementoblast differentiation. At day 7, upregulation of 248 lncRNAs, 30 miRNAs and 905 mRNAs was observed, along with downregulation of 127 lncRNAs, 34 miRNAs and 960 mRNAs. At day 14, 197 lncRNAs, 13 miRNAs and 847 mRNAs were upregulated, while 74 lncRNAs, 12 miRNAs and 760 mRNAs were downregulated. The results of qRT‐PCR showed that four candidate lncRNAs, H19, Gdap10, Foxo6os and Ipw, were significantly upregulated after 7 and 14 days of cementogenic induction. The lncRNA‐miRNA‐mRNA network illustrated a possible competitive endogenous RNA regulatory mechanism. GO analysis showed that consistently differentially expressed mRNAs were involved in blood vessel morphogenesis, cell‐substrate adhesion, cell adhesion, ossification and extracellular matrix organization. KEGG analysis indicated that extracellular matrix‐receptor interaction, focal adhesion, and the PI3K‐Akt, Rap1, mitogen‐activated protein kinase, and Ras signalling pathways varied significantly during cementogenesis.ConclusionThe expressions of lncRNA, miRNA and mRNA were significantly altered in cementoblasts after cementogenesis. This study highlighted the effect of lncRNAs in the process of cementogenesis and revealed their potential for the discovery of novel biomarkers and therapeutic targets for cementum regeneration.

show abstract

“…To our best knowledge, limited studies focused on the effect of miR-325-3p on bone remodeling. It was reported that miR-325-3p in cementoblasts can be induced by IL-1β and prevent the cementum regeneration in inflammatory microenvironment through targeting Runx2 (Wang et al 2020), indicating miR-325-3p may have a "double-edged sword" effect on bone remodeling. In microenvironment of CRC, bone resorption was predominant, and the abnormal a.…”

Section: Discussionmentioning

confidence: 99%

miR-325-3p, a novel regulator of osteoclastogenesis in osteolysis of colorectal cancer through targeting S100A4

Chengling

Zhang

Xie

et al. 2021

Mol Med

View full text Add to dashboard Cite

Background To investigate effect of microRNA-325-3p (miR-325-3p) on bone metastasis of colorectal cancer (CRC) and the precise role on osteoclastogenesis. Methods CT-26 cells were injected into tibias to establish bone metastatic model of CRC in vivo. AgomiR-325-3p or antagomir-325-3p were injected in tail-veins of Balb/c mice to interfere the osteoclastogenesis and bone metastasis of CRC. Safranin O and Fast Green staining examined the changes of trabecular area and TRAP staining examined the osteoclast number in bone metastasis of CRC. Real-time PCR was conducted to test the RNA level of miR-325-3p and mRNA levels of TRAP and Cathepsin K in osteoclast precursors (OCPs). Dual-luciferase reporter system was utilized to identify the direct target of miR-325-3p. Conditioned medium from CT-26 cells was collected to stimulate the OCPs during osteoclastogenesis induced by RANKL and M-CSF in vitro. Western blot analysis was performed to examine the protein level of S100A4 in OCPs after interfered by agomiR-325-3p or antagomir-325-3p cultured in CM or not. Results miR-325-3p downregulated in OCPs in CRC microenvironment both in vivo and in vitro. By luciferase activity assay, S100A4 was the target gene of miR-325-3p and the protein level of S100A4 in OCPs upregulated in CRC microenvironment. Overexpression of miR-325-3p inhibited the osteoclastogenesis of OCPs and it can be reversed after transfection with plasmid containing S100A4. Treatment with miR-325-3p can preserve trabecular area in bone metastasis of CRC. Conclusion miR-325-3p can prevent osteoclast formation through targeting S100A4 in OCPs. Overexpression of miR-325-3p efficiently decreased the osteoclast number and attenuated bone resorption in bone metastasis of CRC.

show abstract

IL1β inhibits differentiation of cementoblasts via microRNA‐325‐3p

Cited by 12 publications

References 34 publications

Mechanical overloading-induced miR-325-3p reduction promoted chondrocyte senescence and exacerbated facet joint degeneration

Mechanical overloading-induced miR-325-3p reduction promoted chondrocyte senescence and exacerbated facet joint degeneration

The long non‐coding RNA, miRNA and mRNA landscapes of cementoblasts during cementogenesis

miR-325-3p, a novel regulator of osteoclastogenesis in osteolysis of colorectal cancer through targeting S100A4

Contact Info

Product

Resources

About