| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2129977 | Experimental Cell Research | 2016 | 9 Pages |
•The expression and subcellular distribution of Foxp3, is modulated by PMA and preS1/2.•PMA and preS1/2 increase Foxp3 expression on HepG2.•PMA and preS1/2 induce foxp3 enrichment at mitochondrial, microsomal and nuclear compartments.•Results suggest a non-canonical function of Foxp3 or a mitochondrial transcriptional activity.
Foxp3 is considered to be the master regulator for the development and function of regulatory T cells (Treg). Recently Foxp3, has been detected in extra lymphoid tissue, and in hepatocytes and has been associated with hepatocellular carcinoma (HCC), although its role has not been defined. Since it is expected that there is a relationship between protein localization, activity and cellular function, the aim of this study was to explore the subcellular localization of Foxp3 in resting and stimulated human hepatocytes. Foxp3 expression was measured by flow cytometry, subcellular fractioning, and immunofluorescence, and this data was used to track the shuttling of Foxp3 in different subcellular compartments in hepatocytes (HepG2 cell line), stimulated by using the PKC activators (PMA), core and preS1/2 antigen from hepatitis B virus (HBV). Our data shows that besides the nuclear location, mitochondrial translocation was detected after stimulation with PMA and at to a lesser extent, with preS1/2. In addition, Foxp3 is localizes at outer mitochondrial membrane. These results suggest a non-canonical role of Foxp3 in the mitochondrial compartment in human hepatocytes, and opens a new field about their role in liver damages during HBV infection.
