ArticleCell cycle (Georgetown, Tex.)2015
Gprc5a-deficiency confers susceptibility to endotoxin-induced acute lung injury via NF-κB pathway.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Down-regulation of GPRC5A Confers Protection Against Periodontitis.Inflammation · 2026Article
- Increased metallopeptidase activity, compromised endothelial integrity and impaired pathogen recognition revealed by transcriptomics inCurrent research in parasitology & vector-borne diseases · 2026Article
- Mitochondrial components secretion in extracellular vesicles promotes alveolar epithelial mitochondrial quality control.Nature communications · 2025Article
- NF-κB-mediated EAAT3 upregulation in antioxidant defense and ferroptosis sensitivity in lung cancer.Cell death & disease · 2025Article
- Molecular signatures of alveolar type II cell differentiation in acute respiratory distress syndrome.Frontiers in medicine · 2025Article
- NF-κB represses retinoic acid receptor-mediated GPRC5A transactivation in lung epithelial cells to promote neoplasia.JCI insight · 2023Article
- BMSC-derived exosomes ameliorate sulfur mustard-induced acute lung injury by regulating the GPRC5A-YAP axis.Acta pharmacologica Sinica · 2021Article
- IMUP and GPRC5A: two newly identified risk score indicators in pancreatic ductal adenocarcinoma.Cancer cell international · 2021Article
- Derangement of cell cycle markers in peripheral blood mononuclear cells of asthmatic patients as a reliable biomarker for asthma control.Scientific reports · 2021Article
- Article
- Crystalline silica particles cause rapid NLRP3-dependent mitochondrial depolarization and DNA damage in airway epithelial cells.Particle and fibre toxicology · 2020Article
- PTGES/PGEOncogene · 2020Article
- Effect of Thymoquinone on Acute Kidney Injury Induced by Sepsis in BALB/c Mice.BioMed research international · 2020Article
- GPRC5A: An Emerging Biomarker in Human Cancer.BioMed research international · 2018Review
- Osthole Protects against Acute Lung Injury by Suppressing NF-Mediators of inflammation · 2018Article
- Osthole protects sepsis-induced acute kidney injury via down-regulating NF-κB signal pathway.Oncotarget · 2017Article
- Autocrine epiregulin activates EGFR pathway for lung metastasis via EMT in salivary adenoid cystic carcinoma.Oncotarget · 2016Article
- Epithelial neoplasia coincides with exacerbated injury and fibrotic response in the lungs of Gprc5a-knockout mice following silica exposure.Oncotarget · 2015Article
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Authors and funding
16 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Susceptibility to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) varies greatly among patients in sepsis/septic shock. The genetic and biochemical reasons for the difference are not fully understood. G protein coupled receptor family C group 5 member A (GPRC5A), a retinoic acid target gene, is predominately expressed in the bronchioalveolar epithelium of lung. We hypothesized that Gprc5a is important in controlling the susceptibility to ALI or ARDS. In this study, we examined the susceptibility of wild-type and Gprc5a-knockout (ko) mice to induced ALI. Administration of endotoxin LPS induced an increased pulmonary edema and injury in Gprc5a-ko mice, compared to wild-type counterparts. Consistently, LPS administration induced higher levels of inflammatory cytokines (IL-1β and TNFα) and chemokine (KC) in Gprc5a-ko mouse lungs than in wild-type. The enhanced pulmonary inflammatory responses were associated with dysregulated NF-κB signaling in the bronchioalveolar epithelium of Gprc5a-ko mouse lungs. Importantly, selective inhibition of NF-κB through expression of the super-repressor IκBα in the bronchioalveolar epithelium of Gprc5a-ko mouse lungs alleviated the LPS-induced pulmonary injury, and inflammatory response. Thus, Gprc5a is critical for lung homeostasis, and Gprc5a deficiency confers the susceptibility to endotoxin-induced pulmonary edema and injury, mainly through NF-κB signaling in bronchioalveolar epithelium of lung.
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