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It is well known that the plasminogen-activating (PA) system plays a key role in the bovine mammary gland during tissue remodelling. However, the modulation of the PA cascade after bacterial infections needs to be elucidated. This study examined the effects of Escherichia coli lipopolysaccharide (LPS) on cell viability, the modulation of cell-associated u-PA activity, and the regulation of u-PA and u-PA receptor (u-PAR) RNA expression using the BME-UV1 bovine mammary epithelial cell line. LPS did not affect cell viability, but induced an increase in u-PA activity, with the maximum response after 6 h of incubation. Moreover, u-PA and u-PAR mRNA expression were both up-regulated in BME-UV1 cells after 3 h of incubation with LPS. These data indicated that E. coli LPS led to an increase in u-PA activity and RNA expression of u-PA and u-PAR in BME-UV1 cells, thus strengthening the role of the PA system during pathological processes.
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http://dx.doi.org/10.1016/j.rvsc.2011.10.017 | DOI Listing |
J Pharmacol Exp Ther
August 2025
Animal Cancer Care and Research Program, University of Minnesota, St Paul, Minnesota; Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, Minnesota; Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota; Center for Immunology
We evaluated the antitumor effects of remodeling the MC17 mouse sarcoma microenvironment (SME) by targeting urokinase-type plasminogen activator receptor (uPAR)- and epidermal growth factor receptor (EGFR)-expressing cells. Specifically, we used eBAT (a bispecific ligand-targeted toxin directed to EGFR and uPAR), and its mouse counterpart, meBAT, to ablate uPAR- and/or EGFR-expressing cells. We chose the MC17 model because the cells are resistant to eBAT, allowing us to exclusively evaluate the role of uPAR- and EGFR-expressing cells in the SME.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
September 2025
Division of Hematology, Department of Medicine, UNC Blood Research Center, University of North Carolina at Chapel Hill.
The primary role of the fibrinolytic system is to degrade fibrin clots. However, the fibrinolytic system is often activated in patients with cancer and may affect cancer progression, metastasis, and patient survival. Clinical studies have shown that elevated plasma levels of uPA (urokinase plasminogen activator) are associated with cancer progression in patients with prostate and cervical cancers, whereas high plasma levels of soluble uPAR (uPA receptor) are associated with progression and metastasis in prostate, breast, bladder, and colorectal cancers.
View Article and Find Full Text PDFBiomed J
August 2025
Department of Dermatology, Tohoku University Graduate School of Medicine, Sendai, Japan. Electronic address:
Plasminogen activator inhibitor-1 (PAI-1), a key regulator of the fibrinolytic system, has emerged as a multifaceted contributor to the pathogenesis of systemic sclerosis (SSc). Beyond its classical role in inhibiting plasminogen activation, PAI-1 is implicated in the dysregulation of vascular remodeling, promotion of fibrosis, modulation of immune responses, and the maintenance of cellular senescence-all of which are hallmarks of SSc. Notably, elevated PAI-1 expression has been observed in both patient-derived tissues and experimental models of the disease.
View Article and Find Full Text PDFRev Assoc Med Bras (1992)
August 2025
Mersin University, Faculty of Medicine, Department of Urology - Mersin, Turkey.
Objective: Although many genes associated with prostate cancer have been identified, there are still many cases of prostate cancer whose genetics have not been identified. The urokinase-type plasminogen activator gene is thought to play a key role in cancer invasion and metastasis. The Pro141Leu polymorphism may be involved in the development of prostate cancer, although genetic evidence is lacking.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
August 2025
Department of Biology, University of Pisa, Pisa, Italy.
Purpose: Retinitis pigmentosa (RP) is characterized by primary rod degeneration followed by secondary cone death. The urokinase-type plasminogen activator (uPA) and its cognate receptor (uPAR) have been recently suggested to regulate pro-inflammatory events in RP possibly through the interaction of uPAR with its lateral partners, including formyl peptide receptors (FPRs). This study explored whether the inhibition of the crosstalk between uPAR and FPR1 may counteract photoreceptor degeneration in the rd10 mouse model of RP.
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