MIR-107/HMGB1/FGF-2 axis responds to excessive mechanical stretch to promote rapid repair of vascular endothelial cells

Wang, Li; Sun, Haoyu; Q, Yu; Yang, Tianen; Wang, Yajing; Ning, Bin; Jia, Yaru; Liu, Yang; Liang, Ziwei; An, Maozhu; Guo, Jun

doi:10.1016/j.abb.2023.109686

Cited by 3 publications

(1 citation statement)

References 52 publications

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“…Unfortunately, we could not clarify the mechanisms and/or the triggers of the expressional changes in miRs by intravitreal NMDA in the present study. Recently, the high-mobility group box-1 (HMGB1)-receptor of advanced glycation end-products (RAGE) axis has been found to be involved in the regulation of miR expression [26,27]. We previously reported that the HMGB1-RAGE axis was involved in neurodegeneration induced by intravitreal NMDA in the retina [28].…”

Section: Discussionmentioning

confidence: 99%

The Role of microRNAs Related to Apoptosis for N-Methyl-d-Aspartic Acid-Induced Neuronal Cell Death in the Murine Retina

Sone,

Mori,

Sakamoto

et al. 2024

IJMS

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Glaucoma is one of the leading causes of acquired blindness and characterized by retinal ganglion cell (RGC) death. MicroRNAs are small noncoding RNAs that degrade their target mRNAs. Apoptosis is one of the common mechanisms leading to neuronal death in many neurodegenerative diseases, including glaucoma. In the present study, we identified microRNAs that modulate RGC death caused by the intravitreal injection of N-methyl-d-aspartic acid (NMDA). We found an upregulation of miR-29b and downregulation of miR-124 in the retina of the NMDA-injected eyes. The intravitreal injection of an miR-29b inhibitor 18 h before NMDA injection reduced RGC death and the downregulation of myeloid cell leukemia 1 (MCL-1), an anti-apoptotic factor, induced by intravitreal NMDA. The intravitreal injection of an miR-124 mimic 18 h before NMDA injection also reduced RGC death and the upregulation of B-cell/chronic lymphocytic leukemia lymphoma 2 (bcl-2)-associated X protein (Bax) and bcl-2 interacting protein (Bim), pro-apoptotic factors, induced by intravitreal NMDA. These data suggest that expressional changes in microRNA are involved in the excitotoxicity of RGCs, and that complement and/or inhibition of microRNA may be a potential therapeutic approach for the diseases related to the excitotoxicity of RGCs, such as glaucoma and retinal central artery occlusion.

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Section: Discussionmentioning

confidence: 99%

The Role of microRNAs Related to Apoptosis for N-Methyl-d-Aspartic Acid-Induced Neuronal Cell Death in the Murine Retina

Sone,

Mori,

Sakamoto

et al. 2024

IJMS

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Role of LRP5/6/GSK‐3β/β‐catenin in the differences in exenatide‐ and insulin‐promoted T2D osteogenesis and osteomodulation

Chen,

Wang,

Zhang

et al. 2024

British J Pharmacology

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Background and PurposeInsulin and exenatide are two hypoglycaemic agents that exhibit different osteogenic effects. This study compared the differences between exenatide and insulin in osseointegration in a rat model of Type 2 diabetes (T2D) and explored the mechanisms promoting osteogenesis in this model of T2D.Experimental ApproachIn vivo, micro‐CT was used to detect differences in the peri‐implant bone microstructure in vivo. Histology, dual‐fluorescent labelling, immunofluorescence and immunohistochemistry were used to detect differences in tissue, cell and protein expression around the implants. In vitro, RT‐PCR and western blotting were used to measure the expression of osteogenesis‐ and Wnt signalling‐related genes and proteins in bone marrow mesenchymal stromal cells (BMSCs) from rats with T2D (TBMSCs) after PBS, insulin and exenatide treatment. RT‐PCR was used to detect the expression of Wnt bypass cascade reactions under Wnt inactivation.Key ResultsMicro‐CT and section staining showed exenatide extensively promoted peri‐implant osseointegration. Both in vivo and in vitro experiments showed exenatide substantially increased the expression of osteogenesis‐related and activated the LRP5/6/GSK‐3β/β‐catenin‐related Wnt pathway. Furthermore, exenatide suppressed expression of Bmpr1a to inhibit lipogenesis and promoted expression of Btrc to suppress inflammation.Conclusion and ImplicationsCompared to insulin, exenatide significantly improved osteogenesis in T2D rats and TBMSCs. In addition to its dependence on LRP5/6/GSK‐3β/β‐catenin signalling for osteogenic differentiation, exenatide‐mediated osteomodulation also involves inhibition of inflammation and adipogenesis by BMPR1A and β‐TrCP, respectively.

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Mechanical force regulates the paracrine functions of ADSCs to assist skin expansion in rats

Xue,

Hu,

Tang

et al. 2024

Stem Cell Res Ther

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Background In the repair of massive tissue defects using expanded large skin flaps, the incidence of complications increases with the size of the expanded area. Currently, stem cell therapy has limitations to solve this problem. We hypothesized that conditioned medium of adipose-derived stem cells (ADSC-CM) collected following mechanical pretreatment can assist skin expansion. Methods Rat aortic endothelial cells and fibroblasts were cultured with ADSC-CM collected under 0%, 10%, 12%, and 15% stretching force. Ten-milliliter cylindrical soft tissue expanders were subcutaneously implanted into the backs of 36 Sprague-Dawley rats. The 0% and 10% stretch groups were injected with ADSC-CM collected under 0% and 10% stretching force, respectively, while the control group was not injected. After 3, 7, 14, and 30 days of expansion, expanded skin tissue was harvested for staining and qPCR analyses. Results Endothelial cells had the best lumen formation and highest migration rate, and fibroblasts secreted the most collagen upon culture with ADSC-CM collected under 10% stretching force. The skin expansion rate was significantly increased in the 10% stretch group. After 7 days of expansion, the number of blood vessels in the expanded area, expression of the angiogenesis-associated proteins vascular endothelial growth factor, basic fibroblast growth factor, and hepatocyte growth factor, and collagen deposition were significantly increased in the 10% stretch group. Conclusions The optimal mechanical force upregulates specific paracrine proteins in ADSCs to increase angiogenesis and collagen secretion, and thereby promote skin regeneration and expansion. This study provides a new auxiliary method to expand large skin flaps. Supplementary Information The online version contains supplementary material available at 10.1186/s13287-024-03822-0.

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MIR-107/HMGB1/FGF-2 axis responds to excessive mechanical stretch to promote rapid repair of vascular endothelial cells

Cited by 3 publications

References 52 publications

The Role of microRNAs Related to Apoptosis for N-Methyl-d-Aspartic Acid-Induced Neuronal Cell Death in the Murine Retina

The Role of microRNAs Related to Apoptosis for N-Methyl-d-Aspartic Acid-Induced Neuronal Cell Death in the Murine Retina

Role of LRP5/6/GSK‐3β/β‐catenin in the differences in exenatide‐ and insulin‐promoted T2D osteogenesis and osteomodulation

Mechanical force regulates the paracrine functions of ADSCs to assist skin expansion in rats

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