Abstract
During vascular aging or in pathological conditions in humans, elastin is degraded and its by-products, the elastin-derived peptides (EDPs), enter the blood circulation. EDPs may be detected in the serum of healthy subjects or people who suffered a stroke. Moreover, recent evidence suggests a potential role of inflammatory mechanisms in neurological conditions, which are usually not categorized as inflammatory. Therefore, the present in vitro study was conducted to investigate the impact of the VGVAPG peptide on the activation of inflammatory process in mouse primary astrocytes, which were maintained in phenol red-free DMEM/F12 supplemented with 10% fetal bovine serum. The cells were exposed to VGVAPG or VVGPGA peptides for 24 and 48 h; this was followed by the determination of the activity of caspase-1 and levels of SOD, CAT, PPARγ, NF-κB, IL-1β, and IL-1βR1. Furthermore, rosiglitazone-a PPARγ agonist-was applied. Our study pioneered the finding that the VGVAPG peptide increases caspase-1 activity in astrocytes in vitro. The VGVAPG peptide simultaneously decreases the release of IL-1β into the cell-culture medium from astrocytes. The ELISA method revealed that the VGVAPG peptide increases the protein expression of SOD1 whereas it decreases the expression of IL-1βR1, CAT, and NF-κB. Therefore, the available data suggest that the VGVAPG peptide (concentration 10 nM) synergistically acts with agonists of PPARγ in mouse astrocytes. However, given the lack of sufficient data to explain the molecular mechanism of action of the VGVAPG peptide in the nervous system, more studies in this area are necessary.