Gprc5a-deficiency confers susceptibility to endotoxin-induced acute lung injury via NF-kB pathway

Yueling Liao, Hongyong Song, Dongliang Xu, Huike Jiao, Feng Yao, Jingyi Liu, Yadi Wu, Shuangshuang Zhong, Huijing Yin, Shuli Liu, Xiaofei Wang, Wenzheng Guo, Beibei Sun, Baohui Han, Y. Eugene Chin, Jiong Deng

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


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-1b and TNFa) and chemokine (KC) in Gprc5a-ko mouse lungs than in wild-type. The enhanced pulmonary inflammatory responses were associated with dysregulated NF-kB signaling in the bronchioalveolar epithelium of Gprc5a-ko mouse lungs. Importantly, selective inhibition of NF-kB through expression of the super-repressor IkBa 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-kB signaling in bronchioalveolar epithelium of lung.

Original languageEnglish
Pages (from-to)1403-1412
Number of pages10
JournalCell Cycle
Issue number9
StatePublished - Feb 25 2015

Bibliographical note

Publisher Copyright:
© 2015 Taylor & Francis Group, LLC.


  • Acute lung injury
  • Animal model
  • Endotoxin
  • Gprc5a
  • Inflammation
  • NF-kB

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology


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