Self-regulatory role of 4-hydroxynonenal in signaling for stress-induced programmed cell death

Awasthi, Yogesh C.; Sharma, Rajendra; Sharma, Abha; Yadav, Sushma; Singhal, Sharad S.; Chaudhary, Pankaj; Awasthi, Sanjay

doi:10.1016/j.freeradbiomed.2008.04.007

Cited by 97 publications

(108 citation statements)

References 115 publications

(188 reference statements)

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“…The latter, in turn, might foster cell damage via the release of ferrous ions, ROS and cathepsins, cytosolic amplification of LPO, aldehyde-mediated protein/DNA modification and mitochondrial outer membrane permeabilization, leading to Fas-and p53-mediated apoptosis or necrosis, depending on the severity of oxidative stress (19). HNE itself was able to trigger p53 and Fas-dependent apoptosis (11). The conclusions drawn in the study cited (19) had some limitations, in that: a) HNE-His-P immunoreactivity (71).…”

Section: Hne-protein Adducts In Chronic Inflammatory Diseasesmentioning

confidence: 99%

Role of 4-Hydroxynonenal-Protein Adducts in Human Diseases

Barrera

Pizzimenti

Ciamporcero

et al. 2015

Antioxidants & Redox Signaling

107

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However, in some cases, the generation of HNE-protein adducts can represent a contrast to the progression of disease or can promote adaptive cell responses, demonstrating that HNE is not only a toxic product of lipid peroxidation, but also a regulatory molecule, involved in several biochemical pathways.Future directions. In the coming years, the refinement of proteomical techniques, allowing the individuation of novel cellular targets of HNE, will lead to a better understanding the role of HNE in human diseases.

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Section: Hne-protein Adducts In Chronic Inflammatory Diseasesmentioning

confidence: 99%

Role of 4-Hydroxynonenal-Protein Adducts in Human Diseases

Barrera

Pizzimenti

Ciamporcero

et al. 2015

Antioxidants & Redox Signaling

107

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“…From the viewpoint of production of free radicals, ROS/RNS can attack and damage a variety of critical biological molecules, including lipids, essential cellular proteins and DNA [9][10][11] . Products of lipid peroxidation can be easily detected in biological fluids and tissues and can reliably and rapidly reflect the sensitive and specific signals of lipid peroxidation that occur in vivo [35,36] . The compound 4-HNE is an end product of lipoperoxidation with antiproliferative and proapoptotic properties [35,36] .…”

Section: Discussionmentioning

confidence: 99%

“…Products of lipid peroxidation can be easily detected in biological fluids and tissues and can reliably and rapidly reflect the sensitive and specific signals of lipid peroxidation that occur in vivo [35,36] . The compound 4-HNE is an end product of lipoperoxidation with antiproliferative and proapoptotic properties [35,36] . Our results with MDA and 4-HNE confirmed that OS occurred even in the early postoperative period.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress and extracellular matrices after hepatectomy and liver transplantation in rats

Hori¹,

Üemoto²,

Chen³

et al. 2014

WJH

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AIM:To investigate oxidative stress (OS)-mediated damage and the behavior of extracellular matrices in various rat models because shear stress with portal hypertension and cold ischemia/warm reperfusion injury trigger the liver regeneration cascade after surgery. These injuries also cause fatal liver damage. METHODS:Rats were divided into four groups according to the surgery performed: control; hepatectomy with 40% liver remnant (60% hepatectomy); orthotopic liver transplantation (OLT) with whole liver graft (100% OLT); and split OLT (SOLT) with 40% graft (40% SOLT). Survival was evaluated. Blood and liver samples were collected at 6 h after surgery. Biochemical and histopathological examinations were performed. OSinduced damage, 4-hydroxynonenal, ataxia-telangiectasia mutated kinase, histone H2AX, phosphatidylinositol 3-kinase (PI3K) and Akt were evaluated by western blotting. Behavior of extracellular matrices, matrix metalloproteinase (MMP)-9, MMP-2, tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 were also evaluated by western blotting and zymography. RESULTS:Although 100% OLT survived, 60% hepatectomy and 40% SOLT showed poor survival. Histopathological, immunohistological, biochemical and protein assays revealed that 60% hepatectomy, 100% OLT and 40% SOLT showed liver damage. PI3K and Akt were decreased in 60% hepatectomy and 40% SOLT. For protein expression, 40% SOLT showed differences in MMP-9, MMP-2 and TIMP-2. TIMP-1 showed differences in 60% hepatectomy and 40% SOLT. For protein activity, MMP-9 demonstrated significant differences in 60% hepatectomy, 100% OLT and 40% SOLT. CONCLUSION: Under conditions with an insufficient liver remnant, prevention of OS-induced damage viathe Akt/PI3K pathway may be key to improve the postoperative course. MMP-9 may be also a therapeutic target after surgery. Hori T et al . Hepatic damage after liver surgeryCore tip: Although shear stress with portal hypertension and cold ischemia/warm reperfusion injury trigger the liver regeneration cascade after surgery, these injuries also cause fatal liver damage. Postoperative liver damage is still a critical matter in the field of liver surgery. Oxidative stress and extracellular matrices are important for liver regeneration after surgery and these may be important keys to overcome current problems in the field of liver surgery. Here, we investigated oxidative stress-mediated damage and the behavior of extracellular matrices in various rat models with liver surgery.Hori T, Uemoto S, Chen F, Gardner LB, Baine AMT, Hata T, Kogure T, Nguyen JH. ��idative stress and e�tracellular ma��idative stress and e�tracellular matrices after hepatectomy and liver transplantation in rats. World

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“…Such compounds have been amply documented to alkylate particular protein thiols under oxidative or nitrosative stress and therefore may be implicated as stress signaling molecules that are sensed via S-alkylation. The best known example of a regulatory protein modified this way is kelch-like ECH-associated protein-1 (Keap1), which plays a pivotal role in responding to oxidative challenge with an adaptive response via activation of the transcription factor Nrf2 (6, 94-98, 254, 479, 481) (see section III), but analogous stress sensing has also been implicated in the NF-jB pathway (408) and in apoptosis (12).…”

Section: Signals Of Free Radical Damagementioning

confidence: 99%

Basic Principles and Emerging Concepts in the Redox Control of Transcription Factors

Brigelius‐Flohé

Flohé

2011

Antioxidants & Redox Signaling

522

442

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Convincing concepts of redox control of gene transcription have been worked out for prokaryotes and lower eukaryotes, whereas the knowledge on complex mammalian systems still resembles a patchwork of poorly connected findings. The article, therefore, reviews principles of redox regulation with special emphasis on chemical feasibility, kinetic requirements, specificity, and physiological context, taking well investigated mammalian transcription factor systems, nuclear transcription factor of bone marrow-derived lymphocytes (NFjB), and kelch-like ECH-associated protein-1 (Keap1)/Nrf2, as paradigms. Major conclusions are that (i) direct signaling by free radicals is restricted to O 2 -and NO and can be excluded for fast reacting radicals such as OH, OR, or Cl ; (ii) oxidant signals are H 2 O 2 , enzymatically generated lipid hydroperoxides, and peroxynitrite; (iii) free radical damage is sensed via generation of Michael acceptors; (iv) protein thiol oxidation/alkylation is the prominent mechanism to modulate function; (v) redox sensors must be thiol peroxidases by themselves or proteins with similarly reactive cysteine or selenocysteine (Sec) residues to kinetically compete with glutathione peroxidase (GPx)-and peroxiredoxin (Prx)-type peroxidases or glutathione-S-transferases, respectively, a postulate that still has to be verified for putative mammalian sensors. S-transferases and Prxs are considered for system complementation. The impact of NF-jB and Nrf2 on hormesis, management of inflammatory diseases, and cancer prevention is critically discussed. Antioxid. Redox Signal. 15, 2335-2381.

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Self-regulatory role of 4-hydroxynonenal in signaling for stress-induced programmed cell death

Cited by 97 publications

References 115 publications

Role of 4-Hydroxynonenal-Protein Adducts in Human Diseases

Role of 4-Hydroxynonenal-Protein Adducts in Human Diseases

Oxidative stress and extracellular matrices after hepatectomy and liver transplantation in rats

Basic Principles and Emerging Concepts in the Redox Control of Transcription Factors

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