Mechanical stretch enhances IL-8 production in pulmonary microvascular endothelial cells

Mai Iwaki, Satoru Ito, Masataka Morioka, Susumu Iwata, Yasushi Numaguchi, Masakazu Ishii, Masashi Kondo, Hiroaki Kume, Keiji Naruse, Masahiro Sokabe, Yoshinori Hasegawa

Research output: Contribution to journalArticlepeer-review

68 Citations (Scopus)


In patients with acute respiratory distress syndrome, mechanical over-distension of the lung by a large tidal volume causes further damage and inflammation, called ventilator-induced lung injury (VILI), however, it is unclear how mechanical stretch affects the cellular functions or morphology in human pulmonary microvascular endothelial cells (HPMVECs). IL-8 has been proposed to play an important role in the progression of VILI by activating neutrophils. We demonstrated that HPMVECs exposed to cyclic uni-axial stretch produce IL-8 protein with p38 activation in strain- and time-dependent manners. The IL-8 synthesis was not regulated by other signal transduction pathways such as ERK1/2, JNK, or stretch-activated Ca2+ channels. Moreover, cyclic stretch enhanced IL-6 and monocyte chemoattractant protein-1 production and reoriented cell perpendicularly to the stretch axis accompanied by actin polymerization. Taken together, IL-8 production by HPMVECs due to excessive mechanical stretch may activate neutrophilic inflammation, which leads to VILI.

Original languageEnglish
Pages (from-to)531-536
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number3
Publication statusPublished - Nov 2009


  • ARDS
  • Barotraumas
  • Mechanotransduction
  • Stretch
  • Ventilator-induced lung injury
  • p38

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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