The evolutionary relationship and functional correlation between human formyl peptide receptors (FPRs) and their mouse counterparts remain incompletely understood. We examined three members of the mouse formyl peptide receptor subfamily (mFprs) and found that they differ in agonist preference and cellular distributions. When stably expressed in transfected rat basophilic leukemia (RBL-2H3) cells, mFpr1 was readily activated by N-formylated peptides derived from Listeria monocytogenes (fMIVTLF), Staphylococcus aureus (fMIFL), and mitochondria (fMMYALF). In contrast, the Escherichia coliderived fMLF was 1000-fold less potent. The aforementioned peptides were much less efficacious at mFpr2, which responded better to the synthetic hexapeptide WKYMVm, the synthetic agonists Quin-C1 (a substituted quinazolinone), and compound 43 (a nitrosylated pyrazolone derivative). Saturation binding assays showed that mFpr1 and mFpr2 were expressed at similar levels on the cell surface, although their affinity for N-formyl-Met-Leu-Phe-Ile-Ile-Lys-fluorescein isothiocyanate varied by more than 1000-fold [dissociation constant (K d ) values of 2.8 nM for mFpr1 and 4.8 mM for mFpr2]). Contrary to these receptors, mFpr-rs1 responded poorly to all the previously mentioned peptides that were tested. Fluorescent microscopy revealed an intracellular distribution pattern of mFpr-rs1. On the basis of these results, we conclude that mFpr1 is an ortholog of human FPR1 with certain pharmacologic properties of human FPR2/ALX, whereas mFpr2 has much lower affinity for formyl peptides. The intracellular distribution of mFpr-rs1 suggests an evolutionary correlation with human FPR3.
a b s t r a c t RIG-G is a retinoic acid-or interferon-induced gene with potential anti-proliferation function. However, the mechanism underlying ATRA-induced RIG-G induction is not completely understood. Here, we demonstrate that ATRA up-regulates the expression of PU.1, which in turn directly binds to the promoter and increases the expression of RIG-G gene. Luciferase reporter assay and electrophoretic mobility shift assay reveal that PU.1 preferentially binds to one of the two putative binding sites on the RIG-G promoter. Moreover, silencing of PU.1 by shRNA markedly inhibited ATRA-but not IFNainduced expression of RIG-G. These data provide new insight into the mechanism of ATRA-induced RIG-G expression.
Contrary to most signal decomposition methods that usually decompose an original signal into a series of components simultaneously, a novel approach based on repeated extraction of Maximum Energy Component (MEC) is proposed. The approach starts from determination of the MEC referring to the estimated Power Spectral Density (PSD) function, and then represents the MEC by employing an exponential function to fit the original signal. By defining a stopping criterion based on two adjacent estimated PSDs, each MEC can be accurately extracted with an improved performance throughout the entire signal decomposition. To verify the proposed method, a single degree-of-freedom system subject to harmonic loads has been examined. Numerical results show that the analytical response can not only be decomposed into four MECs corresponding to the excitation and the system, respectively, but also provide an accurate estimation of natural frequency and damping ratio of the system. Meanwhile, by observing results from the Ensemble Empirical Mode Decomposition (EEMD), Variational Mode Decomposition (VMD) and Prony based on state-space model (Prony-SS), an improved decomposition accuracy has been achieved from the proposed approach. Furthermore, experimental data from the Norwegian Deepwater Programme and two sets of field-test data from one fixed offshore platform and an offshore wind turbine have been used to demonstrate the correctness of the developed signal decomposition method. It is noted that divergence in results by Prony-SS can be observed when a very large model order is used, while the proposed method provides the better decomposition and reconstruction of signals.
Cerebral stroke is one of the highest-ranking causes of death and the leading cause of disability globally, particularly with an increasing incidence and prevalence in developing countries. Steadily more evidence has indicated that micro ribonucleic acids (miRNAs) have important regulatory functions in gene transcription and translation in the course of cerebral stroke. It is beyond arduous to understand the pathophysiology of cerebral stroke, due in part to the perplexity of influencing the network of the inflammatory response, brain edema, autophagy and neuronal apoptosis. The recent research shows miRNA plays a key role in regulating aquaporin 4 (AQP4), and many essential pathological processes after cerebral stroke. This article reviews the recent knowledge on how miRNA influences the inflammatory response, brain edema, infarction size, and neuronal injury after cerebral stroke. In addition, some miRNAs may serve as potential biomarkers in stroke diagnosis and therapy since the expression of some miRNAs in the blood is stable after cerebral stroke.
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