scholarly journals The Role of Formyl Peptide Receptor 1 in Uterine Contraction During Parturition

2021 ◽  
Vol 12 ◽  
Author(s):  
Chaolu Chen ◽  
Shuaiying Zhu ◽  
Long Bai ◽  
Meihua Sui ◽  
Danqing Chen
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Transcriptome Analysis ◽  
Gene Set Enrichment Analysis ◽  
Formyl Peptide Receptor ◽  
Receptor Interaction ◽  
Hub Genes ◽  
Peptide Receptor ◽  
Formyl Peptide

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.

scholarly journals The Role of Circular RNA CDR1as/ciRS-7 in Regulating Tumor Microenvironment: A Pan-Cancer Analysis

Biomolecules ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 429 ◽  
Author(s):  
Zou ◽  
Zheng ◽  
Deng ◽  
Yang ◽  
Xie ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Signaling Pathway ◽  
Malignant Tumors ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Circular Rna ◽  
Gene Set Enrichment Analysis ◽  
Functional Enrichment ◽  
Receptor Interaction

Circular RNA CDR1as/ciRS-7 functions as an oncogenic regulator in various cancers. However, there has been a lack of systematic and comprehensive analysis to further elucidate its underlying role in cancer. In the current study, we firstly performed a bioinformatics analysis of CDR1as among 868 cancer samples by using RNA-seq datasets of the MiOncoCirc database. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), gene set enrichment analysis (GSEA), CIBERSORT, Estimating the Proportion of Immune and Cancer cells (EPIC), and the MAlignant Tumors using Expression data (ESTIMATE) algorithm were applied to investigate the underlying functions and pathways. Functional enrichment analysis suggested that CDR1as has roles associated with angiogenesis, extracellular matrix (ECM) organization, integrin binding, and collagen binding. Moreover, pathway analysis indicated that it may regulate the TGF-β signaling pathway and ECM-receptor interaction. Therefore, we used CIBERSORT, EPIC, and the ESTIMATE algorithm to investigate the association between CDR1as expression and the tumor microenvironment. Our data strongly suggest that CDR1as may play a specific role in immune and stromal cell infiltration in tumor tissue, especially those of CD8+ T cells, activated NK cells, M2 macrophages, cancer-associated fibroblasts (CAFs) and endothelial cells. Generally, systematic and comprehensive analyses of CDR1as were conducted to shed light on its underlying pro-cancerous mechanism. CDR1as regulates the TGF-β signaling pathway and ECM-receptor interaction to serve as a mediator in alteration of the tumor microenvironment.

Abstract 3283: The role of formyl peptide receptor 1 (FPR1) in neuroblastoma tumorigenesis

2015 ◽  
Author(s):  
Igor Snapkov ◽  
Carl Otto Öqvist ◽  
Yngve Anton Figenschau ◽  
Per Kogner ◽  
John Inge Johnsen ◽  
...  
Keyword(s):  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Formyl Peptide

scholarly journals Human neutrophil formyl peptide receptor phosphorylation and the mucosal inflammatory response

2014 ◽  
Vol 97 (1) ◽  
pp. 87-101 ◽  
Author(s):  
Giovanna Leoni ◽  
Jeannie Gripentrog ◽  
Connie Lord ◽  
Marcia Riesselman ◽  
Ronen Sumagin ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Human Neutrophil ◽  
Formyl Peptide Receptor ◽  
Receptor Phosphorylation ◽  
Peptide Receptor ◽  
Formyl Peptide

The role of Formyl Peptide Receptor 1 in the development of non-alcoholic steatohepatitis

2019 ◽  
Author(s):  
M Nati ◽  
A Chatzigeorgiou ◽  
LS Chen ◽  
A Neuwirth ◽  
P Subramanian ◽  
...  
Keyword(s):  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Alcoholic Steatohepatitis ◽  
Formyl Peptide

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

2020 ◽  
Vol 11 (12) ◽  
pp. 3580-3587
Author(s):  
Shu-Qin Li ◽  
Yang Yu ◽  
Yan Zhang ◽  
Yan-Ping Sun ◽  
Xin-xing Li ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gene Polymorphisms ◽  
Formyl Peptide Receptor ◽  
Human Colorectal Cancer ◽  
Peptide Receptor ◽  
Formyl Peptide

scholarly journals Anti-Inflammatory Role of the Murine Formyl-Peptide Receptor 2: Ligand-Specific Effects on Leukocyte Responses and Experimental Inflammation

2010 ◽  
Vol 184 (5) ◽  
pp. 2611-2619 ◽  
Author(s):  
Neil Dufton ◽  
Robert Hannon ◽  
Vincenzo Brancaleone ◽  
Jesmond Dalli ◽  
Hetal B. Patel ◽  
...  
Keyword(s):  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Specific Effects ◽  
Formyl Peptide ◽  
Experimental Inflammation ◽  
Anti Inflammatory

scholarly journals The role of formyl peptide receptor 1 (FPR1) in neuroblastoma tumorigenesis

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Igor Snapkov ◽  
Carl Otto Öqvist ◽  
Yngve Figenschau ◽  
Per Kogner ◽  
John Inge Johnsen ◽  
...  
Keyword(s):  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Formyl Peptide

scholarly journals Suppression of FPR2 expression inhibits inflammation in preeclampsia by improving the biological functions of trophoblast via NF-κB pathway

2022 ◽  
Author(s):  
Shuxian Li ◽  
Anna Li ◽  
Liping Zhai ◽  
Yaqiong Sun ◽  
Ling Yu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Western Blotting ◽  
Immunohistochemical Staining ◽  
Tube Formation ◽  
Formyl Peptide Receptor ◽  
Cellular Model ◽  
Biological Functions ◽  
Peptide Receptor ◽  
Formyl Peptide ◽  
Potential Strategy

Abstract Purpose The dysfunction of trophoblast during inflammation plays an important role in PE. Formyl peptide receptor 2 (FPR2) plays crucial roles in the development of inflammation-associated disease. This present study aimed to explore the effect of FPR2 on a trophoblast cellular model of preeclampsia. Methods The expression of FPR2 in placenta was detected by immunohistochemical staining and western blotting. Transfection of siRNA was used to knockdown FPR2 in HTR-8/SVneo cells. Inflammatory cytokines were detected by ELISA. CCK8, Transwell, wound healing, FACS and tube formation assays were performed to observe the abilities of cell proliferation, migration, invasion, apoptosis and angiogenesis. Western blotting was implemented to clarify that NF-κB signaling pathway was downstream of FPR2. Results The expression levels of FPR2 were higher in placental tissues of patients with PE. Knockdown of FPR2 expression by siFPR2 or inhibition of its activity by WRW4 decreased the release of proinflammatory cytokines in HTR8/SVneo cells treated with LPS. Knockdown of FPR2 expression or inhibition of its activity further reversed the LPS-induced attenuation of the proliferation, migration, invasion and angiogenesis and increase in apoptosis in HTR8/SVneo cells. Moreover, the NF-κB signaling pathway was activated in both placental tissues of patients with PE and LPS-treated HTR8/SVneo cells. However, the activation was attenuated when FPR2 was knocked down or inhibited. Conclusion Suppression of FPR2 expression alleviated the effects of inflammation induced by LPS on trophoblasts via the NF-κB signaling pathway, which provided a novel and potential strategy for the treatment of PE.

Sign in / Sign up

Export Citation Format

Share Document