Bax-inhibiting peptide attenuates bleomycin-induced lung injury in mice | Zendy

Kunihiro Suzuki | Zendy; Toyoshi Yanagihara | Zendy; Tetsuya Yokoyama | Zendy; Takashige Maeyama | Zendy; Saiko Ogata-Suetsugu | Zendy; Masako ArimuraOmori | Zendy; Hironori Mikumo | Zendy; Naoki Hamada | Zendy; Eiji Harada | Zendy; Kazuyoshi Kuwano | Zendy; Taishi Harada | Zendy; Yoichi Nakanishi | Zendy

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Bax-inhibiting peptide attenuates bleomycin-induced lung injury in mice

Author(s) -

Kunihiro Suzuki,

Toyoshi Yanagihara,

Tetsuya Yokoyama,

Takashige Maeyama,

Saiko Ogata-Suetsugu,

Masako ArimuraOmori,

Hironori Mikumo,

Naoki Hamada,

Eiji Harada,

Kazuyoshi Kuwano,

Taishi Harada,

Yoichi Nakanishi

Publication year - 2017

Publication title -

biology open

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.936

H-Index - 41

ISSN - 2046-6390

DOI - 10.1242/bio.026005

Subject(s) - bleomycin , apoptosis , pulmonary fibrosis , bronchoalveolar lavage , a549 cell , bcl 2 associated x protein , lung , biology , idiopathic pulmonary fibrosis , cancer research , fibroblast , alveolar epithelium , immunology , cell culture , programmed cell death , medicine , chemotherapy , caspase 3 , biochemistry , genetics

Bax is a pro-apoptotic member of the Bcl-2 family of proteins, and plays a central role in mitochondria-dependent apoptosis. Several lines of evidence have implied that Bax is involved in both epithelial apoptosis and fibroblast proliferation in idiopathic pulmonary fibrosis; however, the mechanisms remain unknown. Bax-inhibiting peptide V5 (BIP-V5) exhibits membrane permeability and inhibits the activation of Bax.The purpose of this study was to investigate whether the control of Bax activity by BIP-V5 reduces the degree of bleomycin-induced lung injury. C57BL/6J mice were administered bleomycin and BIP-V5 intratracheally on day 0. Bronchoalveolar lavage fluid and lung tissue were obtained on day 7. Human pulmonary alveolar epithelial cells (A549 cells) and mouse pulmonary alveolar epithelial cells (LA-4 cells) were stimulated with bleomycin to induce apoptosis.Administration of BIP-V5 improved the survival rate and degree of bleomycin-induced lung injury by suppressing Bax activation in mice. BIP-V5 treatment decreased bleomycin-induced apoptosis of alveolar epithelial cell lines (A549 cells and LA-4 cells) by suppressing Bax activation. These results indicate that administration of BIP-V5 may constitute a novel therapeutic strategy against lung injury.

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