Autophagy augmented by troglitazone is independent of EGFR transactivation and correlated with AMP-activated protein kinase signaling.

Troglitazone is a synthetic ligand of peroxisome proliferators activated receptor-gamma (PPARgamma) and induces apoptosis in a variety of malignant cells. However, the underlying mechanism of its regulatory role in macroautophagy (hereafter autophagy) remains largely unknown. Using fluorescence and electron microscopy, we observed that autophagosomes could be induced and identified upon troglitazone challenge in both primary and epidermal growth factor receptor (EGFR)-expressed porcine aortic endothelial (PAE) cells.

Autophagy is involved in influenza A virus replication.

Autophagy is involved in the replication of viruses, especially those that perform RNA assembly on the surface of cytoplasmic membrane in host cells. However, little is known about the regulatory role of autophagy in influenza A virus replication. Using fluorescence and electron microscopy, we observed that autophagosomes can be induced and identified upon influenza A virus infection.

[Stimulating autophagosome formation and inducing mixed cell death in HeLa cells by troglitazone].

Objective: To study the effect of troglitazone on autophagy and programmed cell death of HeLa cells.

Methods: Fluorescence microscopy, electron microscopy, western-blotting and flow cytometry were used.

Results: Troglitazone increased the autophagosome formation of HeLa cell as observed by fluorescence and electron microscopy.