Abstract
FPRs: linking innate immune system and fibrosis.
Highlights
In systemic sclerosis (SSc), the tightly regulated and self-limited response to injury, normally leading to tissue regeneration, is subverted into fibrosis, with disruption of tissue architecture and loss of functional integrity; both the skin and the internal organs can be affected
After stimulation of FPRs/uPAR cross-talk by aminoterminal fragment (ATF), unmasking the uPAR88-92 region, or FPRs engagement by WKYMVm and uPAR84-95 peptides, migration and proliferation increase and a myofibroblastic phenotype is acquired, through increased α-smooth muscle actin (α-SMA) expression, matrix deposition and Radical Oxygen Species (ROS) generation
Www.impactjournals.com/oncotarget homologous domains (DI, DII, DIII) anchored to the cell surface by a glycosyl-phosphatidylinositol (GPI) tail and is able to interact with integrins, FPRs and tyrosine kinase receptors, representing a main regulator of signal transduction pathways involved in wound repair, tumor progression and angiogenesis [4]
Summary
In SSc, the tightly regulated and self-limited response to injury, normally leading to tissue regeneration, is subverted into fibrosis, with disruption of tissue architecture and loss of functional integrity; both the skin and the internal organs can be affected. After stimulation of FPRs/uPAR cross-talk by ATF, unmasking the uPAR88-92 region, or FPRs engagement by WKYMVm and uPAR84-95 peptides, migration and proliferation increase and a myofibroblastic phenotype is acquired, through increased α-SMA expression, matrix deposition and ROS generation. Membrane expression of FPRs and of a truncated uPAR form (DII-DIII-uPAR88–92), originating by uPA- or protease-mediated uPAR cleavage, is increased.
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