Downregulation of miRNA‑328 promotes the angiogenesis of HUVECs by regulating the PIM1 and AKT/mTOR signaling pathway under high glucose and low serum condition

Zou, Yan; Wu, Fei; Liu, Qi; Deng, Xian; Hai, Rui; He, Xuemei; Zhou, Xiangyu

doi:10.3892/mmr.2020.11141

Cited by 10 publications

(7 citation statements)

References 44 publications

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“…Under high-glucose and low-serum conditions, the migration and tube-like structure formation of HUVECs were decreased, while the expression of miR-328 was increased. Transfection of high-glucose and low-serum-cultured HUVECs with miR-328 inhibitor stimulated cell migration and angiogenesis ( 14 ). Another study suggested that miR-328-3p promoted HUVEC migration and invasion and protected HUVECs against oxidized low-density lipoprotein-induced injury ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

“…miR-328 has been involved in numerous biological activities, such as cellular apoptosis ( 14 ), brown adipose tissue differentiation ( 15 ) and glucose uptake ( 16 ). Emerging studies have associated miR-328 with numerous diseases, including leukemic blasts ( 17 ), atrial fibrillation ( 18 , 19 ), intervertebral disc degeneration ( 20 ) and hepatocellular carcinoma ( 21 ).…”

Section: Introductionmentioning

confidence: 99%

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miR‑328a‑3p stimulates endothelial cell migration and tubulogenesis

et al. 2021

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Endothelial cells have important biological roles after peripheral nerve injury by forming blood vessels within the nerve gap and guiding Schwann cell migration. MicroRNAs (miRNAs/miRs) affect cellular behavior and regulate a wide variety of physiological and pathological activities, including peripheral nerve regeneration. Emerging studies have identified the essential roles of miRNAs in the phenotype modulation of Schwann cells, while the effects of miRNAs on endothelial cells have remained to be thoroughly investigated. miR-328a-3p was differentially expressed in peripheral nerve stumps after nerve injury. In the present study, the effects of miR-328a-3p on biological functions of endothelial cells were determined by transfecting cultured human umbilical vein endothelial cells (HUVECs) with miR-328a-3p mimics or inhibitor. Transfection with miR-328a-3p mimics led to slightly decreased HUVEC proliferation and robustly increased HUVEC migration and tubulogenesis, while transfection with miR-328a-3p inhibitor led to opposite results. Using bioinformatics analysis, potential regulators and effectors of miR-328a-3p were further discovered and a miR-328a-3p-centered competing endogenous RNA network was constructed. Collectively, the present study demonstrated that dysregulated miR-328a-3p after peripheral nerve injury may affect the migration and angiogenesis of endothelial cells and contribute to peripheral nerve regeneration.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR‑328a‑3p stimulates endothelial cell migration and tubulogenesis

et al. 2021

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“…Under high glucose and low serum condition, the migration and tube-like structure formation of HUVECs were decreased while the expression of miR-328 was increased. Transfection high glucose and low serum-cultured HUVECs with miR-328 inhibitor would stimulate cell migration and angiogenesis (14). Another study showed that miR-328-3p would promote HUVEC migration and invasion and protect HUVECs against oxidized low-density lipoprotein induced injury (31).…”

Section: Discussionmentioning

confidence: 99%

“…However, in spite of the essential roles of endothelial cells during peripheral nerve regeneration, the regulatory effects of miRNAs on endothelial cells, as compared with Schwann cells, remain largely unknown. miR-328 has been involved in numerous biological activities, such as cellular apoptosis (14), brown adipose tissue differentiation (15), and glucose uptake (16). Emerging studies have associated miR-328 with numerous diseases, including leukemic blasts (17), atrial brillation (18,19), intervertebral disc degeneration (20), and hepatocellular carcinoma (21).…”

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confidence: 99%

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

Chen

zhang

Cai

et al. 2021

Preprint

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Background Endothelial 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). Methods Here, 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. Results Transfection 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. Conclusions Collectively, 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. Trial registration: The rats were obtained from the Experimental Animal Center of Nantong University (Animal licenses No. SCXK [Su] 2014-0001 and SYXK [Su] 2012-0031).

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“…Draw a straight line through the cells along a ruler, and the plates were washed with PBS three times for removing debris. To minimize effects of cell proliferation [ 26 , 27 ], the cells were then cultured in RPMI-1640 medium enriched with 2% FBS and were photographed with a light microscope (Olympus, Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

ROS-Responsive miR-150-5p Downregulation Contributes to Cigarette Smoke-Induced COPD via Targeting IRE1α

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

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MicroRNAs (miRNAs) have been reported in human diseases, in which chronic obstructive pulmonary disease (COPD) is included. Herein, we assessed the role along with the possible mechanisms of miR-150-5p in cigarette smoke- (CS-) induced COPD. The plasma miR-150-5p expression was lower in patients with COPD and acute exacerbation of COPD (AECOPD) and was related to disease diagnosis, disease severity, and lung function. Consistently, exposure to CS for 3 months or 3 days reduced miR-150-5p in the plasma and lung tissues of mice, and CS extract (CSE) inhibited miR-150-5p in human bronchial epithelial cells (HBECs) in a concentration along with time-dependent approach. In vitro, miR-150-5p overexpression decreased the contents of inflammatory factors interleukin- (IL-) 6, IL-8 along with cyclooxygenase-2 (COX-2), and endoplasmic reticulum (ER) stress markers glucose-regulated protein (GRP) 78 and C/-EBP homologous protein (CHOP) and promoted cell migrate. Mechanistically, miR-150-5p could bind with the 3 ′ -untranslated region (UTR) of inositol requiring enzyme 1α (IRE1α), while IRE1α overexpression obliterated the impacts of miR-150-5p. Besides, N-acetyl-cysteine (NAC) reversed CSE-induced miR-150-5p downregulation and its downstream effects. In vivo, miR-150-5p overexpression counteracted CS-triggered IRE1α upregulation, inflammation, and ER stress in the lung tissues of mice. In conclusion, our findings illustrated that ROS-mediated downregulation of miR-150-5p led to CS-induced COPD by inhibiting IRE1α expression, suggesting to serve as a useful biomarker for diagnosing and treating COPD.

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Downregulation of miRNA‑328 promotes the angiogenesis of HUVECs by regulating the PIM1 and AKT/mTOR signaling pathway under high glucose and low serum condition

Cited by 10 publications

References 44 publications

miR‑328a‑3p stimulates endothelial cell migration and tubulogenesis

miR‑328a‑3p stimulates endothelial cell migration and tubulogenesis

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

ROS-Responsive miR-150-5p Downregulation Contributes to Cigarette Smoke-Induced COPD via Targeting IRE1α

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