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Syndecan-1 Attenuates Lung Injury during Influenza Infection by Potentiating c-Met Signaling to Suppress Epithelial Apoptosis.

Rena BrauerLingyin GeSaundra Y SchlesingerTimothy P BirklandYing HuangTanyalak ParimonVivian S Lee-KimBonnie L McKinneyJohn K McGuireWilliam C ParksPeter Chen
Published in: American journal of respiratory and critical care medicine (2017)
Our work shows that cell-associated syndecan-1 has an important role in regulating lung injury. Our findings demonstrate a novel mechanism in which cell membrane-associated syndecan-1 regulates the innate immune response to influenza infection by facilitating cytoprotective signals through c-Met signaling to limit bronchial epithelial apoptosis, thereby attenuating lung injury and inflammation.
Keyphrases
  • oxidative stress
  • innate immune
  • endoplasmic reticulum stress
  • cell cycle arrest
  • cell death
  • tyrosine kinase
  • single cell
  • pi k akt
  • bone marrow
  • cell proliferation