Genetic Recombinant Expression and Characterization of Human Augmenter of Liver Regeneration

Gao, Chunfang; Fei, Zhou; Wang, Hao; Huang, Yingfeng; Ji, Qiang; Chen, Jie

doi:10.1007/s10620-008-0372-1

Cited by 12 publications

(6 citation statements)

References 19 publications

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“…In our experiments, as other investigators, 4, 10, 12, 14, 15, 29 we used a small 15-kDa recombinant form of ALR that, mainly reported as an extracellular cytokine, 12, 26 represents the smallest yet functional protein capable of participating in the intracellular redox-dependent signalling pathways. 12 Indeed, the small 15-kDa ALR form, similarly to other ALR homologous proteins identified in all organisms from viruses to mammals, 6 maintains a well conserved amino-acid domain, CxxC, at the C-terminus part of the molecule, responsible for its sulfhydryl oxidase enzymatic activity.…”

Section: Discussionmentioning

confidence: 99%

“…In line with other investigators, in the present experiments, we used a rALR form of 15 kDa, containing the well-conserved, biologically active, C-terminal domain of the molecule. 29, 30, 39 All the chemical reagents were purchased, if not specifically reported, from Sigma-Aldrich (Milan, Italy). The polyclonal antibody against ALR (MultiBind GmbH, Cologne, Germany; a gift from Dr. Thomas Lisowsky) has already been employed for specific identification of ALR.…”

Section: Methodsmentioning

confidence: 99%

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Decreased expression of the Augmenter of Liver Regeneration results in increased apoptosis and oxidative damage in human-derived glioma cells

et al. 2012

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The mammalian growth factor erv1-like (GFER) gene encodes a sulfhydryl oxidase enzyme, named Augmenter of Liver Regeneration (ALR). Recently it has been demonstrated that ALR supports cell proliferation acting as an anti-apoptotic factor. This effect is determined by ALR ability to support the anti-apoptotic gene expression and to preserve cellular normoxic conditions. We recently demonstrated that the addition of recombinant ALR (rALR) in the culture medium of H2O2-treated neuroblastoma cells reduces the lethal effects induced by the hydrogen peroxide. Similar data have been reported in the regenerating liver tissue from partially hepatectomized rats treated with rALR. The purpose of the present study was to evaluate the effect of the GFER inhibition, via the degradation of the complementary mRNA by the specific siRNA, on the behaviour of the apoptosis (apoptotic gene and caspase expression and apoptotic cell number) and of the oxidative stress-induced parameters (reactive oxygen species (ROS), clusterin expression and mitochondrial integrity) in T98G glioma cells. The results revealed a reduction of (i) ALR, (ii) clusterin and (iii) bcl-2 and an increase of (iv) caspase-9, activated caspase-3, ROS, apoptotic cell number and mitochondrial degeneration. These data confirm the anti-apoptotic role of ALR and its anti-oxidative properties, and shed some light on the molecular pathways through which ALR modulates its biological effects.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Decreased expression of the Augmenter of Liver Regeneration results in increased apoptosis and oxidative damage in human-derived glioma cells

et al. 2012

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“…18 Augmenter of liver regeneration (ALR) was purified from the liver of newborn rats and cloned by Hagiya et al 19 Several studies have found that ALR can stimulate hepatocyte proliferation and protect the liver from acute liver failure. [20][21][22] Recent studies have shown that depletion of ALR in hepatocytes by anti-sense oligonucleotide transfection induced hepatocyte apoptosis, while recombinant human ALR (rhALR) significantly decreased hepatocyte apoptosis in vitro. 23,24 The expression of exogenous ALR increased the survival of hepatoma cells, accompanied by a decrease in apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Augmenter of Liver Regeneration Attenuates Tubular Cell Apoptosis in Acute Kidney Injury in Rats: The Possible Mechanisms

Liao

Chen

et al. 2012

Renal Failure

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Augmenter of liver regeneration (ALR), the expression of which increased in rat kidneys after renal ischemia/reperfusion (I/R) injury, enhances renal tubular cell regeneration in vivo and in vitro. We aimed to investigate the effects of ALR on apoptosis of renal tubular cells after renal I/R injury in vivo and consider the possible mechanisms. Rats that were subjected to bilateral renal ischemia for 60 min followed by reperfusion were administered with either vehicle or recombinant human ALR (rhALR). Renal dysfunction and histologic injury were assessed by the measurement of serum biochemical markers and histological grading. Apoptosis was assessed by terminal deoxynucleotidyl transferasemediated dUTP-biotin nick-end labeling (TUNEL). Caspase-3 activity was measured using a colorimetric protease assay. Expression of Bcl-2, Bax Fas, phosphorylated-Akt (p-Akt), and phosphorylated-p53 (p-p53) was determined by western blotting. Compared with vehicle-treated rats, renal dysfunction and histologic injury were significantly attenuated by administration of rhALR. The number of TUNEL-positive tubular cells and caspase-3 activity were decreased, Bcl-2 and p-Akt expression was up-regulated, and Bax and p-p53 expression was down-regulated by administration of rhALR. However, administration of rhALR had no effect on Fas protein expression. These results indicate that the protective effect of rhALR on renal I/R injury is associated with its anti-apoptotic action in renal tubular cells. RhALR inhibits apoptosis by increasing the ratio of Bcl-2 to Bax and by decreasing the activity of caspase-3. The activation of Akt and inactivation of p53 are involved in the rhALR anti-apoptosis process.

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“…Erv1/ALR has been described to enhance the regenerative capacities of liver tissue [95–97]. For this role of Erv1/ALR two different mechanisms were proposed.…”

Section: Physiological Impact Of Mia40 and Erv1/alrmentioning

confidence: 99%

The Mitochondrial Disulfide Relay System: Roles in Oxidative Protein Folding and Beyond

Fischer

Riemer

2013

International Journal of Cell Biology

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Disulfide bond formation drives protein import of most proteins of the mitochondrial intermembrane space (IMS). The main components of this disulfide relay machinery are the oxidoreductase Mia40 and the sulfhydryl oxidase Erv1/ALR. Their precise functions have been elucidated in molecular detail for the yeast and human enzymes in vitro and in intact cells. However, we still lack knowledge on how Mia40 and Erv1/ALR impact cellular and organism physiology and whether they have functions beyond their role in disulfide bond formation. Here we summarize the principles of oxidation-dependent protein import mediated by the mitochondrial disulfide relay. We proceed by discussing recently described functions of Mia40 in the hypoxia response and of ALR in influencing mitochondrial morphology and its importance for tissue development and embryogenesis. We also include a discussion of the still mysterious function of Erv1/ALR in liver regeneration.

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Genetic Recombinant Expression and Characterization of Human Augmenter of Liver Regeneration

Abstract: The rhALR is successfully expressed highly effectively with anticipated MW, N-terminal, and antigenicity. It could play an important role in relieving acute hepatic injury and hepatic failure by promoting hepatic cell proliferation and improving liver function in CCl(4)-intoxicated mice.

Cited by 12 publications

References 19 publications

Decreased expression of the Augmenter of Liver Regeneration results in increased apoptosis and oxidative damage in human-derived glioma cells

Decreased expression of the Augmenter of Liver Regeneration results in increased apoptosis and oxidative damage in human-derived glioma cells

Augmenter of Liver Regeneration Attenuates Tubular Cell Apoptosis in Acute Kidney Injury in Rats: The Possible Mechanisms

The Mitochondrial Disulfide Relay System: Roles in Oxidative Protein Folding and Beyond

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