Archive | 2021

miR-328a-3p stimulates endothelial cell migration and angiogenesis

 
 
 
 
 

Abstract


\n Background\n\nEndothelial cells play important biological roles after peripheral nerve injury by forming blood vessels within the nerve gap after peripheral nerve injury and guiding Schwann cell migration. microRNAs (miRNAs) affect cellular behavior and regulate a wide variety of physiological and pathological activities, including peripheral nerve regeneration. Emerging studies identified the essential roles of miRNAs on the phenotype modulation of Schwann cells while the effects of miRNAs on endothelial cells were not well investigated. miR-328a-3p was differentially expressed in peripheral nerve stumps after nerve injury. This study aimed to identify the biological effects of miR-328a-3p on human umbilical vein endothelial cells (HUVECs).\nMethods\n\nHere, the biological functions of miR-328a-3p on endothelial cells were determined by transfecting cultured human umbilical vein endothelial cells (HUVECs) with miR-328a-3p mimic or inhibitor. Heatmaps of lncRNAs and mRNAs were generated using meV software according to previous obtained sequencing data of sciatic nerve stumps at 0, 1, 4, 7, and 14 days after nerve crush injury.\nResults\n\nTransfection with miR-328a-3p mimic led to slightly decreased HUVEC proliferation and robustly increased HUVEC migration and tubulogenesis while transfection with miR-328a-3p mimic led to opposite observations. Bioinformatic analysis further discovered potential regulators and effectors of miR-328a-3p and constructed a miR-328a-3p-centered competing endogenous RNA (ceRNA) network.\nConclusions\n\nCollectively, our present study demonstrated that dysregulated miR-328a-3p after peripheral nerve injury might affect the migration and angiogenesis of endothelial cells and contribute to peripheral nerve regeneration.\nTrial registration:\n\nThe rats were obtained from the Experimental Animal Center of Nantong University (Animal licenses No. SCXK [Su] 2014-0001 and SYXK [Su] 2012-0031).

Volume None
Pages None
DOI 10.21203/RS.3.RS-142878/V1
Language English
Journal None

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