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MicroRNA-409-3p/BTG2 Signaling Axis Improves Impaired Angiogenesis and Wound Healing in Obese Mice

ABSTRACT: MicroRNA-409-3p/BTG2 Signaling Axis Improves Impaired Angiogenesis and Wound Healing in Obese Mice

PROVIDER: PRJNA1062820 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27476167.fastq.gz	Fastqsanger.gz
	SRR27476168.fastq.gz	Fastqsanger.gz
	SRR27476169.fastq.gz	Fastqsanger.gz
	SRR27476170.fastq.gz	Fastqsanger.gz
	SRR27476171.fastq.gz	Fastqsanger.gz

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MicroRNA-409-3p/BTG2 Signaling Axis Improves Impaired Angiogenesis and Wound Healing in Obese Mice

Project description:Wound healing is facilitated by neoangiogenesis, a complex process that is essential to tissue repair in response to injury. MicroRNAs are small, non-coding RNAs that can regulate the wound healing process including stimulation of impaired angiogenesis that is associated with Type-2 diabetes (T2D). Expression of miR-409-3p was significantly increased in the non-healing skin wounds of patients with T2D compared to the non-wounded normal skin, and in the skin of a murine model with T2D. In response to high glucose, neutralization of miR-409-3p markedly improved EC growth and migration in human umbilical vein endothelial cells (HUVECs), promoted wound closure and angiogenesis as measured by increased CD31 in human skin organoids, while overexpression attenuated EC angiogenic responses. Bulk mRNA-Seq transcriptomic profiling revealed BTG2 as a target of miR-409-3p, where overexpression of miR-409-3p significantly decreased BTG2 mRNA and protein expression. A 3′ untranslated region (3′-UTR) luciferase assay of BTG2 revealed decreased luciferase activity with overexpression of miR-409-3p, while inhibition had opposite effects. Mechanistically, in response to high glucose, miR-409-3p deficiency in ECs resulted in increased mTOR phosphorylation meanwhile BTG2 silencing significantly decreased mTOR phosphorylation. Endothelial specific and tamoxifen-inducible miR-409-3p knock out mice (MiR-409IndECKO) with hyperglycemia that underwent dorsal skin wounding showed significant improvement of wound closure, increased blood flow, granulation tissue thickness (GTT), and CD31 that correlated with increased BTG2 expression. Taken together, our results show that miR-409-3p is a critical mediator of impaired angiogenesis in diabetic skin wound healing.

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Project description:Macrophages are progenitors of osteoclasts, but macrophages themselves also regulates bone metabolism. Macrophages mediate not only bone formation by osteoblasts in physiological conditions, but also regeneration after fracture. However, the mechanisms how macrophages control bone formation and regeneration remain unclear. Here we demonstrate that liposome-encapsulated Clodronate (Clod-lip) model with targeted depletion of phagocytic macrophages exhibits impaired angiogenesis of type H vessels, which couple angiogenesis and osteogenesis, in mouse cortical bone defect model by drill-hole injury. Additionaly, we identify Tgfbi (encoding TGF, beta-induced protein), Plau (encoding uPA), and Tgfb1 (encoding TGF-β1) as genes of macrophage-secreted factors mediating angiogenesis and wound healing by RNA-seq analysis. These mRNAs were highly expressed in bone marrow-derived macrophages among bone cells by qRT-PCR. Finally, we show that treatment with uPA inhibitor or TGF-β Receptor I, Receptor II inhibitor impaired bone regeneration after injury, confirming importance of uPA and TGF-β1 for bone repair. Therefore, we proposed that these factors may be potential for therapeutic targets for delayed union, or non-union patients. Our findings reveal a novel mechanism of bone regeneration mediated by macrophages.

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BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

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