Stress to endoplasmic reticulum of mouse osteoblasts induces apoptosis and transcriptional activation for bone remodeling | Zendy

Hamamura Kazunori | Zendy; Yokota Hiroki | Zendy

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Stress to endoplasmic reticulum of mouse osteoblasts induces apoptosis and transcriptional activation for bone remodeling

Author(s) -

Hamamura Kazunori,

Yokota Hiroki

Publication year - 2007

Publication title -

febs letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.593

H-Index - 257

eISSN - 1873-3468

pISSN - 0014-5793

DOI - 10.1016/j.febslet.2007.03.063

Subject(s) - atf4 , endoplasmic reticulum , unfolded protein response , thapsigargin , tunicamycin , microbiology and biotechnology , runx2 , apoptosis , downregulation and upregulation , chemistry , bone remodeling , regulator , osteoblast , medicine , endocrinology , biology , biochemistry , gene , in vitro

ATF4 is an essential regulator in osteogenesis as well as in stress responses to the endoplasmic reticulum (ER). We addressed a question: Does ER stress to osteoblasts upregulate ATF4 expression? If so, do they exhibit ATF4‐mediated bone remodeling or apoptosis? ER stress, induced by Thapsigargin and tunicamycin, elevated a phosphorylated form of eIF2α and ATF4, but the cellular fate depended on treatment duration. The treatment for 1 h, for instance, activated Runx2, and type I collagen, while the treatment for 24 h induced apoptosis. Our observations suggest that there is a threshold for ER stress and osteoblasts present a bi‐phasic pattern of their fate.

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