[Retracted] MicroRNA‑138 inhibits hypoxia‑induced proliferation of endothelial progenitor cells via inhibition of HIF‑1α‑mediated MAPK and AKT signaling

Zhou, Wei; Zhou, Weimin; Zeng, Qian; Xiong, Jixin

doi:10.3892/etm.2021.10428

Cited by 2 publications

(3 citation statements)

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“…[ 91 ] The angiogenic potential of antagomiR‐138 was also supported by previous research; which found that antagomiR‐138 was capable of modulating various signaling pathways and proteins, such as p‐STAT3 protein, [ 71 ] VEGFA, [ 72 ] mitogen‐activated protein kinase, AKT signaling, and HIF‐1α. [ 73 ] Overall, our study showed that the antagomiR‐138‐activated CuBG scaffold is a multifunctional biomaterial which catalyzes killing mechanisms in bacteria with no cytotoxicity to mammalian cells offering a compelling antibiotic‐free antimicrobial alternative while inducing bone regeneration through osteogenic and angiogenic coupling, which makes this system extremely advantageous for treating and regenerating infected bone tissue.…”

Section: Discussionmentioning

confidence: 92%

“…[ 72 ] Similarly, Zhou et al showed that miR‐138 inhibits endothelial progenitor cell proliferation and signaling by targeting mitogen‐activated protein kinase, AKT signaling, and HIF‐1 α . [ 73 ] Thus, the delivery of antagomiR‐138, which is an inhibitor of miR‐138, can potentially reverse these effects potentiating angiogenesis within the bone or other tissues. Overall, our results indicate the multifunctionality of the genetic cargo, showing that antagomiR‐138 regenerates bone through osteogenic‐angiogenic coupling.…”

Section: Discussionmentioning

confidence: 99%

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A Multifunctional Scaffold for Bone Infection Treatment by Delivery of microRNA Therapeutics Combined With Antimicrobial Nanoparticles

Sadowska,

Power,

Genoud

et al. 2023

Advanced Materials

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Treating bone infections and ensuring bone repair is one of the greatest global challenges of modern orthopedics, made complex by antimicrobial resistance (AMR) risks due to long‐term antibiotic treatment and debilitating large bone defects following infected tissue removal. An ideal multi‐faceted solution would will eradicate bacterial infection without long‐term antibiotic use, simultaneously stimulating osteogenesis and angiogenesis. Here, a multifunctional collagen‐based scaffold that addresses these needs by leveraging the potential of antibiotic‐free antimicrobial nanoparticles (copper‐doped bioactive glass, CuBG) to combat infection without contributing to AMR in conjunction with microRNA‐based gene therapy (utilizing an inhibitor of microRNA‐138) to stimulate both osteogenesis and angiogenesis, is developed. CuBG scaffolds reduce the attachment of gram‐positive bacteria by over 80%, showcasing antimicrobial functionality. The antagomiR‐138 nanoparticles induce osteogenesis of human mesenchymal stem cells in vitro and heal a large load‐bearing defect in a rat femur when delivered on the scaffold. Combining both promising technologies results in a multifunctional antagomiR‐138‐activated CuBG scaffold inducing hMSC‐mediated osteogenesis and stimulating vasculogenesis in an in vivo chick chorioallantoic membrane model. Overall, this multifunctional scaffold catalyzes killing mechanisms in bacteria while inducing bone repair through osteogenic and angiogenic coupling, making this platform a promising multi‐functional strategy for treating and repairing complex bone infections.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

A Multifunctional Scaffold for Bone Infection Treatment by Delivery of microRNA Therapeutics Combined With Antimicrobial Nanoparticles

Sadowska,

Power,

Genoud

et al. 2023

Advanced Materials

View full text Add to dashboard Cite

show abstract

“…It is composed of a subunit regulated by the oxygen content [i.e., hypoxia-induced factor 1 α (HIF1α)], and a subunit of sustained expression [i.e., hypoxia-induced factor 1 beta (HIF1β)], which play pivotal roles in bone formation ( 19 - 22 ). Other studies have shown that MAPKs and HIF1α influence each other ( 23 - 25 ); however, the effect of HIF1α on MAPKs in regulating osteoclast differentiation and activation is unknown. Prolyl hydroxylases (PHDs) act as cellular oxygen sensors ( 26 ), and HIF1α is degraded by PHDs under normoxia ( 27 - 29 ).…”

Section: Introductionmentioning

confidence: 96%

Hypoxia-inducible factor 1α enhances RANKL-induced osteoclast differentiation by upregulating the MAPK pathway

Wang¹,

Liu²,

Qu³

et al. 2022

Ann Transl Med

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Background: Hypoxia (low-oxygen tension) and excessive osteoclast activation are common conditions in many bone loss diseases, such as osteoporosis, rheumatoid arthritis (RA), and pathologic fractures. Hypoxiainducible factor 1 alpha (HIF1α) regulates cellular responses to hypoxic conditions. However, it is not yet known how HIF1α directly affects osteoclast differentiation and activation. This study sought to. explore the effects of HIF1α on osteoclast differentiation and it's molecular mechanisms.Methods: L-mimosine, a prolyl hydroxylase (PHDs) domain inhibitor, was used to stabilize HIF1α in normoxia. In the presence of receptor activator of nuclear factor-kB (NF-kB) ligand (RANKL), RAW264.7 cells were cultured and stimulated by treatment with L-mimosine at several doses to maintain various levels of intracellular HIF1α. The multi-nucleated cells were assessed by a tartrate-resistant acid phosphatase (TRAP) and F-actin ring staining assays. The osteoclast-specific genes, such as Cathepsin K, β3-Integrin, TRAP, c-Fos, nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), and matrix metallo-proteinase 9 (MMP9), were analyzed by real time-polymerase chain reaction (RT-PCR). The expression of relevant proteins was analyzed by Western blot.Results: L-mimosine increased the content of intracellular HIF1α in a dose-dependent manner, which in turn promoted RANKL-induced osteoclast formation and relevant protein expression by upregulating the mitogen-activated protein kinase (MAPK) pathways.Conclusions: Our findings suggest that HIF1α directly increases the osteoclast differentiation of RANKLmediated RAW264.7 cells in vitro by upregulating the MAPK pathways.

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[Retracted] MicroRNA‑138 inhibits hypoxia‑induced proliferation of endothelial progenitor cells via inhibition of HIF‑1α‑mediated MAPK and AKT signaling

Cited by 2 publications

References 0 publications

A Multifunctional Scaffold for Bone Infection Treatment by Delivery of microRNA Therapeutics Combined With Antimicrobial Nanoparticles

A Multifunctional Scaffold for Bone Infection Treatment by Delivery of microRNA Therapeutics Combined With Antimicrobial Nanoparticles

Hypoxia-inducible factor 1α enhances RANKL-induced osteoclast differentiation by upregulating the MAPK pathway

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