The Role of Formyl Peptide Receptor 1 Gene Polymorphisms in Human Colorectal Cancer

Parturition involves the transformation of the quiescent myometrium into a highly excitable and contractile state, a process that is driven by changes in myometrial gene expression. This study aimed to identify myometrial transcriptomic signatures and potential novel hub genes in parturition, which have great significance for understanding the underlying mechanisms of successful parturition and treating labor-associated pathologies such as preterm birth. In our study, comparative transcriptome analysis was carried out on human myometrial tissues collected from women undergoing caesarean section at term in the presence (TL = 8) and absence of labor (TNL = 8). A total of 582 differentially expressed genes (DEGs) between TL and TNL tissues were identified. Gene ontology (GO), Kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA) revealed that the DEGs were enriched in signal transduction, regulation of signaling receptor activity, inflammatory response, cytokine-cytokine receptor interaction, IL-17 signaling pathway, TNF signaling pathway, among others. Thus, transcriptome analysis of the myometrium during term labor revealed that labor onset was associated with an inflammatory response. Moreover, protein-protein interactions network analysis identified FPR1, CXCL8, CXCL1, BDKRB2, BDKRB1, and CXCL2 as the hub genes associated with onset of labor. Formyl peptide receptor 1 (FPR1) was highly expressed in laboring myometrial tissues, with the activation of FPR1 in vitro experiments resulting in increased myometrial contraction. Our findings demonstrate the novel role of FPR1 as a modulator of myometrial contraction.

Download Full-text

Faculty Opinions recommendation of Anti-inflammatory role of the murine formyl-peptide receptor 2: ligand-specific effects on leukocyte responses and experimental inflammation.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.4480966.4335065 ◽

2010 ◽

Author(s):

Andrew S Neish

Keyword(s):

Formyl Peptide Receptor ◽

Peptide Receptor ◽

Specific Effects ◽

Formyl Peptide ◽

Experimental Inflammation ◽

Anti Inflammatory

Download Full-text

Role of GDP in formyl-peptide-receptor-induced activation of guanine-nucleotide-binding proteins in membranes of HL 60 cells

European Journal of Biochemistry ◽

10.1111/j.1432-1033.1992.tb16891.x ◽

1992 ◽

Vol 205 (3) ◽

pp. 1201-1206 ◽

Cited By ~ 15

Author(s):

Thomas WIELAND ◽

Janine KREISS ◽

Peter GIERSCHIK ◽

Karl H. JAKOBS

Keyword(s):

Binding Proteins ◽

Nucleotide Binding ◽

Formyl Peptide Receptor ◽

Guanine Nucleotide ◽

Peptide Receptor ◽

Formyl Peptide ◽

Guanine Nucleotide Binding ◽

Nucleotide Binding Proteins ◽

Guanine Nucleotide Binding Proteins

Download Full-text

Detrimental Role of miRNA-144-3p in Intracerebral Hemorrhage Induced Secondary Brain Injury is Mediated by Formyl Peptide Receptor 2 Downregulation BothIn VivoandIn Vitro

Cell Transplantation ◽

10.1177/0963689718817219 ◽

2018 ◽

Vol 28 (6) ◽

pp. 723-738 ◽

Cited By ~ 2

Author(s):

Weijian Fan ◽

Xiang Li ◽

Dongping Zhang ◽

Haiying Li ◽

Haitao Shen ◽

...

Keyword(s):

Brain Injury ◽

Intracerebral Hemorrhage ◽

Formyl Peptide Receptor ◽

Akt Pathway ◽

Secondary Brain Injury ◽

Peptide Receptor ◽

Formyl Peptide

Although microRNA-144-3p (miRNA-144-3p) has been shown to suppress tumor proliferation and invasion, its function in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI) remains unclear. Thus, this study was designed to investigate the role of miRNA-144-3p in ICH. To accomplish this, we used adult male Sprague-Dawley rats to establish an in vivo ICH model by injecting autologous blood, while cultured primary rat cortical neurons were exposed to oxyhemoglobin (OxyHb) to mimic ICH in vitro. To examine the role of miRNA-144-3p in ICH-induced SBI, we used an miRNA-144-3p mimic and inhibitor both in vivo and in vitro. Following ICH induction, we found miRNA-144-3p expression to increase. Additionally, we predicted the formyl peptide receptor 2 (FPR2) to be a potential miRNA-144-3p target, which we validated experimentally, with FPR2 expression downregulated when miRNA-144-3p was upregulated. Furthermore, elevated miRNA-144-3p levels aggravated brain edema and neurobehavioral disorders and induced neuronal apoptosis via the downregulation of FPR2 both in vivo and in vitro. We suspected that these beneficial effects provided by FPR2 were associated with the PI3K/AKT pathway. We validated this finding by overexpressing FPR2 while inhibiting PI3K/AKT in vitro and in vivo. In conclusion, miRNA-144-3p aggravated ICH-induced SBI by targeting and downregulating FPR2, thereby contributing to neurological dysfunction and neural apoptosis via PI3K/AKT pathway activation. These findings suggest that inhibiting miRNA-144-3p may offer an effective approach to attenuating brain damage incurred after ICH and a potential therapy to improve ICH-induced SBI.

Download Full-text