Abstract
Although nervous and vascular systems are functionally different, they usually share similar mechanisms for function maintenance. Neurovascular dysfunction has became the pathogenesis of several vascular and nervous disorders. Here we show that long non-coding RNA-MIAT is aberrantly expressed under neurovascular dysfunction condition. MIAT is shown as a regulator of vascular dysfunction, including retinal angiogenesis, corneal angiogenesis, and vascular permeability. MIAT is also shown as a regulator of retinal neurodegeneration under diabetic condition. Mechanistically, MIAT regulates neural and vascular cell function via MIAT/miR-150-5p/VEGF network. The eye is a valuable model to study central nervous system (CNS) disorders. We show that MIAT knockdown leads to cerebral microvascular degeneration, progressive neuronal loss and neurodegeneration, and behavioral deficits in a CNS neurovascular disorder, Alzheimer's disease. MIAT may represent a pharmacological target for treating neurovascular-related disorders.
Highlights
Nervous and vascular systems are anatomically closely tied to each other
We show that MIAT knockdown leads to cerebral microvascular degeneration, progressive neuronal loss and neurodegeneration, and behavioral deficits in a central nervous system (CNS) neurovascular disorder, Alzheimer's disease
In the mouse model of oxygen-induced retinopathy (OIR), MIAT expression was significantly reduced at the vaso-obliteration stage (P7-P12), whereas MIAT expression was increased at the neovascularization stage (P12-P17) (Figure 1A)
Summary
Nervous and vascular systems are anatomically closely tied to each other. The nerves are often vascularized by vasa nervorum to supply oxygen and nutriment, whereas the vascular is often innervated by nerve fibers that regulate vascular tone. Nerves and blood vessels usually share similar mechanisms and regulators for function maintenance [1, 2]. Abnormal neurovascular interactions have been reported in several human diseases, such as stroke, brain injury, and retinopathy, and cancer [3]. Clarifying the potential mechanism of neurovascular interaction would provide novel strategies for treating neurovascular dysfunction. LncRNAs participate in numerous biological processes to regulate gene expression through mRNA splicing, transcription regulation, translation regulation, and genomic imprinting [4]. Abnormal lncRNA expression has been found in many human disorders ranging from neurodegeneration to cancer [5, 6]. The homeostasis and plasticity of neurovascular interaction is required for exquisite gene regulatory mechanism. Given the crucial role of lncRNAs in gene regulation, it is not surprised that lncRNAs are potential regulators of neurovascular interaction
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