RGD Reference Report - Repression of microRNA-21 inhibits retinal vascular endothelial cell growth and angiogenesis via PTEN dependent-PI3K/Akt/VEGF signaling pathway in diabetic retinopathy. - Rat Genome Database

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Repression of microRNA-21 inhibits retinal vascular endothelial cell growth and angiogenesis via PTEN dependent-PI3K/Akt/VEGF signaling pathway in diabetic retinopathy.

Authors: Lu, Jian-Min  Zhang, Zhen-Zhen  Ma, Xiang  Fang, Shi-Feng  Qin, Xiu-Hong 
Citation: Lu JM, etal., Exp Eye Res. 2020 Jan;190:107886. doi: 10.1016/j.exer.2019.107886. Epub 2019 Nov 21.
RGD ID: 41410819
Pubmed: (View Article at PubMed) PMID:31759996
DOI: Full-text: DOI:10.1016/j.exer.2019.107886

Diabetic retinopathy (DR) is a microvascular complication of diabetes and one of the most common causes of blindness in active stage. This study is performed to explore the effects of microRNA-21 (miR-21) on retinal vascular endothelial cell (RVEC) viability and angiogenesis in rats with DR via the phosphatidylinositiol 3-kinase/protein kinase B (PI3K/Akt)/vascular endothelial growth factor (VEGF) signaling pathway by binding to phosphatase and tensin homolog (PTEN). Sprague Dawley (SD) rats were used for establishment of DR models. Target relationship between miR-21 and PTEN was assessed by bioinformatics prediction in combination with dual-luciferase reporter gene assay. Identification of expression of miR-21, PTEN and PI3K/Akt/VEGF signaling pathway-related genes in the retinal tissues was then conducted. In order to assess the contributory role of miR-21 in DR, the RVECs were transfected with mimic or inhibitor of miR-21, or siRNA-PTEN, followed by the detection of expression of PTEN and PI3K/Akt/VEGF-related genes, as well as the measurement of cell viability, cell cycle and apoptosis. Increased expression of miR-21 and PI3K/Akt/VEGF related genes, along with a reduced expression of PTEN was observed in the retinal tissues of DR rats. PTEN was targeted and negatively regulated by miR-21, while the PI3K/Akt/VEGF signaling pathway was activated by miR-21. RVECs transfected with miR-21 inhibitor exhibited promoted viability and angiogenesis, and inhibited apoptosis. To conclude, our results indicated that miR-21 overexpression could potentially stimulate RVEC viability and angiogenesis in rats with DR through activation of the PI3K/Akt/VEGF signaling pathway via repressing PTEN expression, highlighting the potential of miR-21 as a target for DR treatment.

Annotation

Disease Annotations    

Gene Ontology Annotations    

Objects Annotated

Genes (Rattus norvegicus)
Akt1  (AKT serine/threonine kinase 1)
Cd34  (CD34 molecule)
Mir21  (microRNA 21)
Pik3cg  (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma)
Pten  (phosphatase and tensin homolog)
Vegfa  (vascular endothelial growth factor A)

Genes (Mus musculus)
Akt1  (thymoma viral proto-oncogene 1)
Cd34  (CD34 antigen)
Mir21a  (microRNA 21a)
Pik3cg  (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma)
Pten  (phosphatase and tensin homolog)
Vegfa  (vascular endothelial growth factor A)

Genes (Homo sapiens)
AKT1  (AKT serine/threonine kinase 1)
CD34  (CD34 molecule)
MIR21  (microRNA 21)
PIK3CG  (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma)
PTEN  (phosphatase and tensin homolog)
VEGFA  (vascular endothelial growth factor A)


Additional Information