scholarly journals 473 Investigation of cell death patterns of SJS/TEN model cells harboring formyl peptide receptor 1

2021 ◽  
Vol 141 (5) ◽  
pp. S82
Author(s):  
T. Nishiguchi ◽  
R. Abe
Keyword(s):  
Cell Death ◽  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Formyl Peptide

scholarly journals FPR-1 (Formyl Peptide Receptor-1) Activation Promotes Spontaneous, Premature Hypertension in Dahl Salt-Sensitive Rats

Hypertension ◽  
2021 ◽  
Author(s):  
Jonnelle M. Edwards ◽  
Shaunak Roy ◽  
Sarah L. Galla ◽  
Jeremy C. Tomcho ◽  
Nicole R. Bearss ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cell Death ◽  
Protein Translation ◽  
Synergistic Action ◽  
Formyl Peptide Receptor ◽  
Leaky Gut ◽  
Salt Diet ◽  
Peptide Receptor ◽  
Low Salt ◽  
Formyl Peptide

Cell death has long been a characteristic phenotype of organ damage in hypertension, and recently, leaky gut has been revealed as a novel hypertensive phenotype. However, despite the increase in bacterial and damaged mitochondrial products in the circulation of hypertensive patients and animals, the mechanistic contribution of these two phenomena to hypertension pathophysiology is unknown. Mitochondria and bacteria both start protein translation with an N-formyl methionine residue and thus are the only sources of NFPs (N-formyl peptides), which activate the FPR-1 (formyl peptide receptor-1). We hypothesized that the synergistic action of bacterial and mitochondrial NFPs would cause the spontaneous elevation of blood pressure and vascular remodeling in male Dahl salt-sensitive rats via FPR-1. We observed that mitochondria-derived peptides originating from cell death in the kidneys are responsible for FPR-1–induced vascular hypercontractility and remodeling and premature elevation of BP in Dahl salt-sensitive rats fed a low-salt diet. However, a high-salt diet leads to gut barrier disruption and, subsequently, a synergistic action of mitochondria, and bacteria-derived leaky gut NFPs lead to a severe and established hypertension. Administration of an FPR-1 antagonist lowered blood pressure in Dahl salt-sensitive rats on a low-salt diet but amoxicillin administration did not. These results reveal for the first time that cell death can be a cause of hypertensive pathophysiology, whereas leaky gut is a consequence.

scholarly journals Processing of the formyl peptide receptor by HL-60 cells.

1984 ◽  
Vol 259 (21) ◽  
pp. 13309-13315
Author(s):  
R Anderson ◽  
J Niedel
Keyword(s):  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Formyl Peptide

scholarly journals From immune to olfactory expression: neofunctionalization of formyl peptide receptors

2021 ◽  
Vol 383 (1) ◽  
pp. 387-393
Author(s):  
Madlaina Boillat ◽  
Alan Carleton ◽  
Ivan Rodriguez
Keyword(s):  
Expression Patterns ◽  
Vomeronasal Organ ◽  
Formyl Peptide Receptor ◽  
Regulatory Sequence ◽  
Powerful Source ◽  
Peptide Receptor ◽  
Gene Shuffling ◽  
Evolutionary Innovation ◽  
Vomeronasal Receptor ◽  
Formyl Peptide

Abstract Variations in gene expression patterns represent a powerful source of evolutionary innovation. In a rodent living about 70 million years ago, a genomic accident led an immune formyl peptide receptor (FPR) gene to hijack a vomeronasal receptor regulatory sequence. This gene shuffling event forced an immune pathogen sensor to transition into an olfactory chemoreceptor, which thus moved from sensing the internal world to probing the outside world. We here discuss the evolution of the FPR gene family, the events that led to their neofunctionalization in the vomeronasal organ and the functions of immune and vomeronasal FPRs.

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