ALX1-transcribed LncRNA AC132217.4 promotes osteogenesis and bone healing via IGF-AKT signaling in mesenchymal stem cells

Zhang, Cui; Wu, Shali; Chen, Erman; Yu, Luyang; Wang, Jinfu; Wu, Mengrui

doi:10.1007/s00018-022-04338-7

Cited by 13 publications

(10 citation statements)

References 71 publications

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“…Long non-coding RNAs (lncRNAs), which are transcripts longer than 200 nucleotides without protein-coding potential, have been found to regulate gene expression at multiple levels, including chromatin modi cation, transcription, and post-transcriptional processing [30,31]. LncRNAs represent a rapidly evolving area of research with signi cant potential to improve our understanding and treatment of fracture healing [13,32,33]. For example, lncRNA KCNQ1OT1 as a competing endogenous RNA of miR-701-3p to promote osteoblast proliferation, migration, and inhibit apoptosis in vitro and in vivo [34].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Previous studies have hinted at the involvement of non-coding RNAs (ncRNAs) in the cellular response to hypoxic conditions [13][14][15]. Among these, long non-coding RNAs (lncRNAs) have emerged as key regulators of gene expression, capable of modulating diverse biological processes including osteogenesis [13]. Recent studies suggest that LINC00323 regulate the expression of speci c genes by interacting with chromatin or other RNA molecules and involved in the progression of cancer by affecting tumor cell proliferation, migration, and invasion [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

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LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

黄,

Wang,

Sun

et al. 2024

Preprint

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Intermittent hypoxia has been reported to contribute beneficial effects on fracture healing depending on various factors like duration, frequency, and severity. Yet, little is known about the underlying molecular mechanism. Our previous study found that LINC00323 was up-regulated under hypoxic conditions, suggesting that it might play a final role in hypoxia-induced fracture repair. The present study is to investigate the osteogenic effect of LINC00323 in vitro and in vivo. Upregulation of LINC00323 enhanced the mineralization and activity ALP and increased the expression of osteogenic markers. Further analysis revealed that LINC00323 promoted PDGFB expression by binding FUS to regulate the growth and osteogenic differentiation of MC3T3-E1. Lentivirus mediated LINC00323 particles were injected into the fracture site of the tibia of mice, and fracture healing was evaluated by X-rays, micro-CT examination, biomechanical test and histological staining. Local injection of Lentivirus-LINC00323 increased bone mass, biomechanical strength and cartilage callus formation. These findings indicated that LINC00323 induced the differentiation of osteoblast-like cells via regulation of the expression of PDGFB, represents a theoretical basis to accelerate fracture healing.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

黄,

Wang,

Sun

et al. 2024

Preprint

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“…Though ALX4 was not differentially expressed between cases and controls in our study, ALX1 was significantly increased in metopic craniosynostosis in our primary and male-stratified models. ALX1 has not previously been associated with craniosynostosis, however, it is involved in osteogenesis and regulates a lncRNA transcript that is involved in bone marrow mesenchymal cell osteogenesis [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Signatures of Single-Suture Craniosynostosis Phenotypes

Lapehn

Gustafson

Timms

et al. 2023

IJMS

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Craniosynostosis is a birth defect where calvarial sutures close prematurely, as part of a genetic syndrome or independently, with unknown cause. This study aimed to identify differences in gene expression in primary calvarial cell lines derived from patients with four phenotypes of single-suture craniosynostosis, compared to controls. Calvarial bone samples (N = 388 cases/85 controls) were collected from clinical sites during reconstructive skull surgery. Primary cell lines were then derived from the tissue and used for RNA sequencing. Linear models were fit to estimate covariate adjusted associations between gene expression and four phenotypes of single-suture craniosynostosis (lambdoid, metopic, sagittal, and coronal), compared to controls. Sex-stratified analysis was also performed for each phenotype. Differentially expressed genes (DEGs) included 72 genes associated with coronal, 90 genes associated with sagittal, 103 genes associated with metopic, and 33 genes associated with lambdoid craniosynostosis. The sex-stratified analysis revealed more DEGs in males (98) than females (4). There were 16 DEGs that were homeobox (HOX) genes. Three TFs (SUZ12, EZH2, AR) significantly regulated expression of DEGs in one or more phenotypes. Pathway analysis identified four KEGG pathways associated with at least one phenotype of craniosynostosis. Together, this work suggests unique molecular mechanisms related to craniosynostosis phenotype and fetal sex.

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“…37 According to Jeffery et al, distinct osseous injuries are repaired by particular skeletal stem/progenitor cells (SSCs), with periosteal cells regenerating bone and marrow stroma following non-stabilized fractures. 38 [39][40][41][42][43][44][45][46][47] BONE FORMATION -OSTEOBLASTS AND CHONDROCYTES Following the fibrovascular stage of healing, many of the MSCs that formed the fibrovascular callus experience differentiation to either osteoblasts or chondrocytes to start the bone formation stage of healing. Differentiation of MSCs into bi-potential osteochondral progenitor cells is initially regulated by Sox9.…”

Section: Recent Advances In Mscsmentioning

confidence: 99%

Recent developments on cells involved in bone repair and their potential clinical applications

Rodriguez-Merchan

2024

SurgiColl

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This review of the literature has summarized recent developments on cells implicated in the different phases of bone healing and their potential clinical applications including inflammatory phase (neutrophils, macrophages, mast cells), fibrovascular phase (endothelial cells and mesenchymal stem cells - MSCs), bone formation (osteoblasts, chondrocytes), and callus remodeling (osteoclasts). Some studies have confirmed the two well-known facts that alcohol intake and dexamethasone negatively affect bone healing. Other studies have shown that Aucubin, Bortezomib, and human umbilical cord MSCs (HUCMSCs)Wnt10b promote bone healing of bone fractures. However, more research is needed to confirm their actual utility in the clinical practice of bone fracture treatment.

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ALX1-transcribed LncRNA AC132217.4 promotes osteogenesis and bone healing via IGF-AKT signaling in mesenchymal stem cells

Cited by 13 publications

References 71 publications

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

Transcriptomic Signatures of Single-Suture Craniosynostosis Phenotypes

Recent developments on cells involved in bone repair and their potential clinical applications

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