Angiotensin II induces the exocytosis of galectin-3 via integrin αv/AKT/NF-κB signaling pathway

L. Tian, D. Coletti, Z.-L. Li

Sorbonne Universités, UPMC Univ Paris 06, INSERM ERL U1164, Institut Biologie Paris-Seine, Paris, CNRS, France. tgydtl@163.com

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• Cardiology

OBJECTIVE: To explore the role of integrin αv in Angiotensin II (Ang II)-induced exocytosis and endocytosis of galectin-3 (gal-3) in vascular smooth muscle cells (VSMCs).

MATERIALS AND METHODS: A primary culture of mouse VSMCs was established by the enzymatic digestion of aorta. Adeno-Cre was used to specifically knockdown integrin αv. VSMCs were treated with Ang II, LY294002 (inhibitor of AKT signaling pathway), and Bay11-7082 (inhibitor of nuclear factor-kappa B, NF-κB), respectively. Endocytosis of His-tagged gal-3 was analyzed by immunofluorescence. The Western blot was performed to detect the protein level in cell supernatant and lysate.

RESULTS: Ang II increased the exocytosis of gal-3 and activated AKT and NF-κB signaling pathways. The knockdown integrin αv effectively decreased the activation of AKT and NF-κB signals and the exocytosis of gal-3 induced by Ang II, but it had a little effect on the endocytosis of gal-3. Ang II increased the phosphorylation of AKT and NF-κB through integrin αv. AKT is the upstream signal of the NF-κB signaling pathway. LY294002 or Bay11-7082 could decrease Ang II-induced exocytosis of gal-3 in VSMCs.

CONCLUSIONS: Ang II, depending on integrin αv/AKT/NF-κB signaling pathway, induced the exocytosis of gal-3.

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