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. 2022 Jan 8;11(1):137. doi: 10.3390/antiox11010137

Figure 5.

Figure 5

PKD1 increases acinar cell survival and drives ADM through canonical NF-κB signaling. (A): Primary mouse acinar cells were isolated, lentivirally-infected with control vector or GFP-tagged PKD1, and then subjected to a CyQUANT Cell Proliferation Assay kit over the indicated time period. (B): Mouse pancreatic acinar cells were isolated, adenovirally-infected with control virus or superdominant IκBα (IκBα.SD) and lentivirally-infected with control or GFP-PKD1.CA (GFP-PKD1.SSEE) and then seeded in 3D collagen culture. ADM and ducts formed were quantified as described in the Methods section. (C): Schematic summarizing current data and previously published work, demonstrating how ROS-PKD1 signaling is a key factor downstream of different inducers of acinar-to-ductal (ADM) metaplasia. Macrophage-conditioned medium (M-CM) with its two major drivers TNFα and CCL5 (published in [10]; (a)), TGFα (here), or expression of oncogenic KRAS (published in [15]; (b)) all induce mitochondrial reactive oxygen species (mROS), which have been shown to activate PKD1 (published in [17]; [c] and (here)). PKD1 is a key driver of ADM (published in [14]; (d) and (here)).