miR-126-3p is essential for CXCL12-induced angiogenesis.

Area of Science:

• Cardiovascular Biology
• Molecular Biology
• Regenerative Medicine

Background:

• Atherosclerosis, a severe cardiovascular disease, necessitates angiogenesis for tissue repair.
• Chemokines and microRNAs (miRs) are investigated as potential pro-angiogenic agents.
• The miR-126/CXCL12 axis's role in angiogenesis requires further elucidation, particularly comparing miR-126-3p and miR-126-5p strands.

Purpose of the Study:

• To compare the pro-angiogenic effects of miR-126-3p and miR-126-5p strands in CXCL12-induced angiogenesis.
• To investigate the role of the miR-126/CXCL12 axis in regulating angiogenesis in vitro and ex vivo.
• To identify downstream targets of miR-126 involved in CXCL12-mediated angiogenesis.

Main Methods:

• Human Umbilical Vein Endothelial Cells (HUVEC) and rat aortic ring assays were used to study 2D-angiogenesis and migration.
• Transfection with premiR-126-3p/-5p or antimiR-126-3p/-5p strands was performed.
• Cells and tissues were stimulated with CXCL12, and miR-126 expression and SPRED-1 inhibition were analyzed.

Main Results:

• CXCL12 demonstrated pro-angiogenic effects, correlating with increased miR-126-3p expression in HUVEC and rat aortas.
• Inhibition of miR-126-3p abolished CXCL12-induced angiogenesis and migration.
• CXCL12 treatment led to SPRED-1 inhibition in HUVEC, enhancing CXCL12's pro-angiogenic potential.

Conclusions:

• CXCL12 modulates miR-126 expression, playing a key role in angiogenesis.
• miR-126 is critically involved in mediating the pro-angiogenic effects of CXCL12.
• SPRED-1 is identified as a crucial target in the miR-126/CXCL12-mediated angiogenesis pathway, offering therapeutic potential for vascular regeneration.