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Title: Recovery from temporary endoplasmic reticulum stress in plants relies on the tissue-specific and largely independent roles of bZIP28 and bZIP60, as well as an antagonizing function of BAX-Inhibitor 1 upon the pro-adaptive signaling mediated by bZIP28

Authors:
ORCiD logo [1];  [1]; ORCiD logo [1]
  1. Plant Research Laboratory, Department of Energy, Michigan State University, 612 Wilson Road East Lansing MI 48824 USA, Department of Plant Biology, Michigan State University, 612 Wilson Road East Lansing MI 48824 USA
Publication Date:
Sponsoring Org.:
USDOE Office of Science (SC), Basic Energy Sciences (BES) (SC-22)
OSTI Identifier:
1411091
Grant/Contract Number:
FG02-91ER20021
Resource Type:
Journal Article: Publisher's Accepted Manuscript
Journal Name:
The Plant Journal
Additional Journal Information:
Journal Volume: 93; Journal Issue: 1; Related Information: CHORUS Timestamp: 2017-12-16 16:59:02; Journal ID: ISSN 0960-7412
Publisher:
Wiley-Blackwell
Country of Publication:
United Kingdom
Language:
English

Citation Formats

Ruberti, Cristina, Lai, YaShiuan, and Brandizzi, Federica. Recovery from temporary endoplasmic reticulum stress in plants relies on the tissue-specific and largely independent roles of bZIP28 and bZIP60, as well as an antagonizing function of BAX-Inhibitor 1 upon the pro-adaptive signaling mediated by bZIP28. United Kingdom: N. p., 2017. Web. doi:10.1111/tpj.13768.
Ruberti, Cristina, Lai, YaShiuan, & Brandizzi, Federica. Recovery from temporary endoplasmic reticulum stress in plants relies on the tissue-specific and largely independent roles of bZIP28 and bZIP60, as well as an antagonizing function of BAX-Inhibitor 1 upon the pro-adaptive signaling mediated by bZIP28. United Kingdom. doi:10.1111/tpj.13768.
Ruberti, Cristina, Lai, YaShiuan, and Brandizzi, Federica. 2017. "Recovery from temporary endoplasmic reticulum stress in plants relies on the tissue-specific and largely independent roles of bZIP28 and bZIP60, as well as an antagonizing function of BAX-Inhibitor 1 upon the pro-adaptive signaling mediated by bZIP28". United Kingdom. doi:10.1111/tpj.13768.
@article{osti_1411091,
title = {Recovery from temporary endoplasmic reticulum stress in plants relies on the tissue-specific and largely independent roles of bZIP28 and bZIP60, as well as an antagonizing function of BAX-Inhibitor 1 upon the pro-adaptive signaling mediated by bZIP28},
author = {Ruberti, Cristina and Lai, YaShiuan and Brandizzi, Federica},
abstractNote = {},
doi = {10.1111/tpj.13768},
journal = {The Plant Journal},
number = 1,
volume = 93,
place = {United Kingdom},
year = 2017,
month =
}

Journal Article:
Free Publicly Available Full Text
This content will become publicly available on December 2, 2018
Publisher's Accepted Manuscript

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  • Long-term excessive fluoride intake is known to be toxic and can damage a variety of organs and tissues in the human body. However, the molecular mechanisms underlying fluoride-induced male reproductive toxicity are not well understood. In this study, we used a rat model to simulate the situations of human exposure and aimed to evaluate the roles of endoplasmic reticulum (ER) stress and inflammatory response in fluoride-induced testicular injury. Sprague–Dawley rats were administered with sodium fluoride (NaF) at 25, 50 and 100 mg/L via drinking water from pre-pregnancy to gestation, birth and finally to post-puberty. And then the testes of malemore » offspring were studied at 8 weeks of age. Our results demonstrated that fluoride treatment increased MDA accumulation, decreased SOD activity, and enhanced germ cell apoptosis. In addition, fluoride elevated mRNA and protein levels of glucose-regulated protein 78 (GRP78), inositol requiring ER-to-nucleus signal kinase 1 (IRE1), and C/EBP homologous protein (CHOP), indicating activation of ER stress signaling. Furthermore, fluoride also induced testicular inflammation, as manifested by gene up-regulation of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in a nuclear factor-κB (NF-κB)-dependent manner. These were associated with marked histopathological lesions including injury of spermatogonia, decrease of spermatocytes and absence of elongated spermatids, as well as severe ultrastructural abnormalities in testes. Taken together, our results provide compelling evidence that ER stress and inflammation would be novel and significant mechanisms responsible for fluoride-induced disturbance of spermatogenesis and germ cell loss in addition to oxidative stress. - Highlights: • We used a rat model to simulate the situations of human fluoride (F) exposure. • Developmental F exposure induces testicular damage related with oxidative stress. • Endoplasmic reticulum stress is involved in testis disorder and germ cell apoptosis. • Inflammatory response is implicated in impaired spermatogenesis and germ cell loss.« less
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