ELAV-like RNA binding protein 1 regulates osteogenesis in diabetic osteoporosis: Involvement of divalent metal transporter 1

Ren, Yuanfei; Yang, Mon-Yuan; Wang, Xindong; Xu, Buxuan; Xu, Zerong; Su, Bo

doi:10.1016/j.mce.2022.111559

Cited by 10 publications

(5 citation statements)

References 44 publications

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“…Indeed, literatures indicated that ELAVL1 played a role part in diabetes. For example, ELAVL1 depletion induced osteogensis in a mouse model of diabetes mellitus [25]. In addition, ELAVL1 was involved in renal tubular epithelial pyroptosis in diabetic nephropathy [26].…”

Section: Discussionmentioning

confidence: 99%

“…an example, ELAVL1 depletion induced osteogenesis in a diabetic mouse model. 25 In addition, ELAVL1 was involved in renal tubular epithelial pyroptosis in diabetic nephropathy. 26 We further demonstrated that after overexpressing ELAVL1, the effects of miR-192-5p on HG-regulated endothelial cell proliferation, migration and angiogenesis were attenuated.…”

Section: Overexpressed Pi3kδ Overturned the Inhibitory Effects Of Mir...mentioning

confidence: 99%

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Up‐regulation of miR‐192‐5p inhibits the ELAVL1/PI3Kδ axis and attenuates microvascular endothelial cell proliferation, migration and angiogenesis in diabetic retinopathy

et al. 2023

Diabet Med

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Background: Diabetic retinopathy (DR) is a common complication of diabetes and a sight threaten among adults. MicroRNAs (miRNAs) serve a key role in DR progression. However, the role and mechanism of miR-192-5p in DR remain unclear. We aim to investigate the effect of miR-192-5p on cell proliferation, migration and angiogenesis in DR. Methods: The expressions of miR-192-5p, ELAVL1 and PI3Kδ in DR samples and human retinal microvascular endothelial cells (HRMECs) were assessed using RT-qPCR. ELAVL1 and PI3Kδ protein levels were evaluated by Western blot. RIP and dual luciferase reporter assays were performed to con rm the miR-192-5p/ELAVL1/PI3Kδ regulatory network. Cell proliferation, migration and angiogenesis were evaluated by CCK8, transwell and tube formation assays. Results: MiR-192-5p was decreased in DR patients and high glucose (HG)-treated HRMECs. In function, overexpressed miR-192-5p suppressed cell proliferation, migration and angiogenesis in HG-treated HRMECs. Mechanically, miR-192-5p directly target ELAVL1 and decreased its expression. We further veri ed that ELAVL1 bound to PI3Kδ and maintained PI3Kδ mRNA stability. Rescue assays demonstrated that the inhibitive effects of HG-treated HRMECs caused by miR-192-5p upregulation were overturned by overexpressed ELAVL1 or PI3Kδ. Conclusion: MiR-192-5p alleviated DR progression via targeting ELAVL1 and reducing PI3Kδ expression, indicating a biomarker for therapy in DR.

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Section: Discussionmentioning

confidence: 99%

Section: Overexpressed Pi3kδ Overturned the Inhibitory Effects Of Mir...mentioning

confidence: 99%

Up‐regulation of miR‐192‐5p inhibits the ELAVL1/PI3Kδ axis and attenuates microvascular endothelial cell proliferation, migration and angiogenesis in diabetic retinopathy

et al. 2023

Diabet Med

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“…HuR binds the 3′UTR of LPR6 mRNA, thus promoting its stability and stimulating its translation. In this manner, LPR6 can induce the activation of the Wnt pathway, promoting osteogenic differentiation ( Maeda et al, 2013 ; Li et al, 2014 ; Liu et al, 2022 ; Ren et al, 2022 ).…”

Section: Role Of Rbps In the Bone Pathologiesmentioning

confidence: 99%

RNA-binding proteins in bone pathophysiology

Maroni,

Pesce,

Lombardi

2024

Front. Cell Dev. Biol.

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Bone remodelling is a highly regulated process that maintains mineral homeostasis and preserves bone integrity. During this process, intricate communication among all bone cells is required. Indeed, adapt to changing functional situations in the bone, the resorption activity of osteoclasts is tightly balanced with the bone formation activity of osteoblasts. Recent studies have reported that RNA Binding Proteins (RBPs) are involved in bone cell activity regulation. RBPs are critical effectors of gene expression and essential regulators of cell fate decision, due to their ability to bind and regulate the activity of cellular RNAs. Thus, a better understanding of these regulation mechanisms at molecular and cellular levels could generate new knowledge on the pathophysiologic conditions of bone. In this Review, we provide an overview of the basic properties and functions of selected RBPs, focusing on their physiological and pathological roles in the bone.

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“…Divalent metal transporter 1 (DMT1) is a transmembrane ferroprotein that is responsible for the transport of the ferrous iron, and its regulation of iron overload has been shown to promote autophagy and apoptosis in osteoblasts [ 35 ]. Based on whether the 3′ untranslated region (UTR) contains the iron responsive element (IRE), DMT1 is defined as IRE(-)DMT1 or IRE(+)DMT1 [ 36 ].…”

Section: Molecules Involved In Cfp and Their Mechanisms Of Actionmentioning

confidence: 99%

Chronic Pain after Bone Fracture: Current Insights into Molecular Mechanisms and Therapeutic Strategies

Zhao

Zhang

et al. 2022

Brain Sciences

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Bone fracture following traumatic injury or due to osteoporosis is characterized by severe pain and motor impairment and is a major cause of global mortality and disability. Fracture pain often originates from mechanical distortion of somatosensory nerve terminals innervating bones and muscles and is maintained by central sensitization. Chronic fracture pain (CFP) after orthopedic repairs is considered one of the most critical contributors to interference with the physical rehabilitation and musculoskeletal functional recovery. Analgesics available for CFP in clinics not only have poor curative potency but also have considerable side effects; therefore, it is important to further explore the pathogenesis of CFP and identify safe and effective therapies. The typical physiopathological characteristics of CFP are a neuroinflammatory response and excitatory synaptic plasticity, but the specific molecular mechanisms involved remain poorly elucidated. Recent progress has deepened our understanding of the emerging properties of chemokine production, proinflammatory mediator secretion, caspase activation, neurotransmitter release, and neuron-glia interaction in initiating and sustaining synaptogenesis, synaptic strength, and signal transduction in central pain sensitization, indicating the possibility of targeting neuroinflammation to prevent and treat CFP. This review summarizes current literature on the excitatory synaptic plasticity, microgliosis, and microglial activation-associated signaling molecules and discusses the unconventional modulation of caspases and stimulator of interferon genes (STING) in the pathophysiology of CFP. We also review the mechanisms of action of analgesics in the clinic and their side effects as well as promising therapeutic candidates (e.g., specialized pro-resolving mediators, a caspase-6 inhibitor, and a STING agonist) for pain relief by the attenuation of neuroinflammation with the aim of better managing patients undergoing CFP in the clinical setting.

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ELAV-like RNA binding protein 1 regulates osteogenesis in diabetic osteoporosis: Involvement of divalent metal transporter 1

Cited by 10 publications

References 44 publications

Up‐regulation of miR‐192‐5p inhibits the ELAVL1/PI3Kδ axis and attenuates microvascular endothelial cell proliferation, migration and angiogenesis in diabetic retinopathy

Up‐regulation of miR‐192‐5p inhibits the ELAVL1/PI3Kδ axis and attenuates microvascular endothelial cell proliferation, migration and angiogenesis in diabetic retinopathy

RNA-binding proteins in bone pathophysiology

Chronic Pain after Bone Fracture: Current Insights into Molecular Mechanisms and Therapeutic Strategies

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