Preventing oxidative stress: a new role for XBP1

Liu, Y; Adachi, Masaaki; Zhao, Shen; Hareyama, Masato; Koong, Albert C.; Luo, Dan; Rando, Thomas A.; Imai, Kohzoh; Shinomura, Yasuhisa

doi:10.1038/cdd.2009.14

Cited by 139 publications

(117 citation statements)

References 40 publications

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“…In contrast to beta cells and in accordance with previous studies [29,30], XBP1s overproduction did not induce apoptosis in the 208F rat fibroblast cell line. In fact, it protected these cells against apoptosis induced by 48 h of CPA treatment (Fig.…”

Section: Resultssupporting

confidence: 92%

Sustained production of spliced X-box binding protein 1 (XBP1) induces pancreatic beta cell dysfunction and apoptosis

et al. 2010

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Aims/hypothesis Pro-inflammatory cytokines involved in the pathogenesis of type 1 diabetes deplete endoplasmic reticulum (ER) Ca 2+ stores, leading to ER-stress and beta cell apoptosis. However, the cytokine-induced ER-stress response in beta cells is atypical and characterised by induction of the pro-apoptotic PKR-like ER kinase (PERK)-C/EBP homologous protein (CHOP) branch of the unfolded protein response, but defective X-box binding protein 1 (XBP1) splicing and activating transcription factor 6 activation. The purpose of this study was to overexpress spliced/active Xbp1 (XBP1s) to increase beta cell resistance to cytokine-induced ER-stress and apoptosis.Methods Xbp1s was overexpressed using adenoviruses and knocked down using small interference RNA in rat islet cells. In selected experiments, Xbp1 was also knocked down in FACS-purified rat beta cells and rat fibroblasts. Expression and production of XBP1s and key downstream genes and proteins was measured and beta cell function and viability were evaluated.

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Section: Resultssupporting

confidence: 92%

Sustained production of spliced X-box binding protein 1 (XBP1) induces pancreatic beta cell dysfunction and apoptosis

et al. 2010

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“…Another well-established role of XBP1 is the protection of cells against oxidative stress by regulating the expression of antioxidant genes such SOD-1 and catalase (14). The phagocytosis of parasites during infection creates an oxidative burst and induces the formation of ROS that act as a cellular defense against the parasite (20).…”

Section: Xbp1 Protects Macrophages Infected With L Amazonensis Againmentioning

confidence: 99%

“…Total RNA was extracted from RAW 264.7 cells (1 3 10 6 ) with RNeasy Plus (Qiagen, Hilden, Germany), and 1 mg total RNA was reverse transcribed into the first-strand cDNA with ImProm (Promega, Madison WI, USA) and oligo (dT) [12][13][14][15][16][17][18] primer, according to the manufacturer's instructions. Forward 59-CCGCAGCACTCAGACTATG-39 and reverse 59-GGGTCCAACTTGTCCAGAAT-39 pairs were used to amplify uXBP1 mRNA; forward 59-CTGAGTCCGCAGCAGGT-39and reverse 59-AAACATGACAGGGTCCAACTT-39 primers were used to amplify sXBP1 mRNA; forward: 59-TCCAAGAAAGGA-CGAACATTC-39 and reverse 59-TGAGGACATCTCCCACG-TCAA-39 primers were used to amplify IFN1-b; and forward 59-GTGTCCGTCGTGGATCTG-39 and reverse 59-TGCTTCAC-CACCTTCTTGA-39 primers were used to amplify GAPDH.…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

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The integrated endoplasmic reticulum stress response in Leishmania amazonensis macrophage infection: the role of X‐box binding protein 1 transcription factor

et al. 2015

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Endoplasmic reticulum (ER) stress triggers the integrated ER-stress response (IERSR) that ensures cellular survival of ER stress and represents a primordial form of innate immunity. We investigated the role of IERSR during Leishmania amazonensis infection. Treatment of RAW 264.7 infected macrophages with the ER stress-inducing agent thapsigargin (TG; 1 mM) increased L. amazonensis infectivity in an IFN1-a receptor (IFNAR)-dependent manner. In Western blot assays, we showed that L. amazonensis activates the inositol-requiring enzyme (IRE1)/ X-box binding protein (XBP)-1-splicing arms of the IERSR in host cells. In chromatin immunoprecipitation (ChIP) assays, we showed an increased occupancy of enhancer and promoter sequences for the Ifnb gene by XBP1 in infected RAW 264.7 cells. Knocking down XBP1 expression by transducing RAW 264.7 cells with the short hairpin XBP1 lentiviral vector significantly reduced the parasite proliferation associated with impaired translocation of phosphorylated IFN regulatory transcription factor (IRF)-3 to the nucleus and a decrease in IFN1-b expression. Knocking down XBP1 expression also increased NO concentration, as determined by Griess reaction and reduced the expression of antioxidant genes, such as heme oxygenase (HO)-1, that protect parasites from oxidative stress. We conclude that L. amazonensis activation of XBP1 plays a critical role in infection by protecting the parasites from oxidative stress and increasing IFN1-b expression.-

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“…In response to ER stress, IRE1, having endoribonuclease and kinase activity, cleaves X-box binding protein 1 (XBP1) mRNA unconventionally to splice out 26 nucleotides and activate XBP1, which is a member of the leucine zipper protein (bZIP) transcription factor family that can be induced by ATF6 (11). In addition, XBP1 has an important role in cell differentiation (12) and oxidative stress prevention (13), and it is necessary for survival in hypoxic conditions (14).…”

Section: Introductionmentioning

confidence: 99%

Pomegranate (Punica granatum L.) reduces endoplasmic reticulum stress induced by renal ischemia/reperfusion injury in rat

Hashemi¹,

Parivar²,

FAZLIFAR³

et al. 2013

Turk J Biol

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Ischemia/reperfusion (I/R) is one of the main causes of acute renal failure, leading to generation of reactive oxygen species (ROS) and ensuing oxidative stress, which results in unfolded/misfolded protein accumulation and its dependent response pathways, generally known as unfolded protein response (UPR), in the endoplasmic reticulum (ER). We studied the effects of renal I/R on the expression of ER-stress genes, as well as concomitant effects of oral pretreatment with pomegranate (Punica granatum L.) pith and carpellary membrane (PPCM). An in vivo model of rat kidney I/R followed by conventional and real-time RT-PCR was used to evaluate the modulation of GRP78 and XBP1 as central UPR and ER-stress markers. Ischemia followed by reperfusion (60 and 150 min, respectively) resulted in decreased antioxidant properties of plasma (lowered ferric reducing ability of plasma [FRAP] value) and GRP78 transcript levels. Oral administration of PPCM aqueous extract for 10 days with or without ischemia (PPCM and PPCM/Isc groups, respectively) was able to further decrease the GRP78 expression, while it increased the FRAP value. PPCM pretreatment also reduced the XBP1 splicing in the PPCM/Isc group compared to the Isc group. These results suggest that UPR is activated during oxidative insults induced by I/R, while PPCM can reduce I/R-induced ER stress in rat kidneys via antioxidant defense mechanisms.

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Preventing oxidative stress: a new role for XBP1

Cited by 139 publications

References 40 publications

Sustained production of spliced X-box binding protein 1 (XBP1) induces pancreatic beta cell dysfunction and apoptosis

Sustained production of spliced X-box binding protein 1 (XBP1) induces pancreatic beta cell dysfunction and apoptosis

The integrated endoplasmic reticulum stress response in Leishmania amazonensis macrophage infection: the role of X‐box binding protein 1 transcription factor

Pomegranate (Punica granatum L.) reduces endoplasmic reticulum stress induced by renal ischemia/reperfusion injury in rat

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