Hepatocyte growth factor improves viability after H2O2-induced toxicity in bile duct epithelial cells

Arends, Brigitte; Slump, Estel; Spee, Bart; Rothuizen, J.; Penning, Louis C.

doi:10.1016/j.cbpc.2007.12.001

Cited by 15 publications

(10 citation statements)

References 34 publications

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“…We observed that pretreatment with HGF protects hepatocytes against oxidative damage induced by EtOH (Fig. 2), which is in agreement with the effect observed in other cell types [7,15,16].…”

Section: Discussionsupporting

confidence: 90%

“…The same result was observed in c-Met knockout hepatocytes that present an enhanced sensitization to Fasinduced apoptosis, which was abrogated by NAC treatment [37]. On the other hand, it has been reported that HGF can induce gene expression of γ-GCS in bile duct epithelial cells [7] and an increased GSH synthesis in rat hepatocytes and H4IIE cells [33,36]. It is clear that GSH homeostasis is one of the main survival systems that are modulated by HGF in response to oxidative stress.…”

Section: Discussionsupporting

confidence: 60%

“…Liver cells possess a number of compensatory mechanisms to deal with ROS and their effects; among these are the induction of antiapoptotic and antioxidant proteins such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GSHPx), and the tripeptide glutathione (GSH), as well as others [5,7]. These mechanisms are induced in response to the actions of some growth factors and cytokines that activate survival signaling pathways, such as phosphoinositol 3-kinase (PI3K), Akt, and nuclear factor-κB (NF-κB) [8][9][10].…”

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confidence: 99%

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Hepatocyte growth factor protects hepatocytes against oxidative injury induced by ethanol metabolism

Valdes-Arzate

Luna

Bucio

et al. 2009

Free Radical Biology and Medicine

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Hepatocyte growth factor (HGF) is involved in many cellular responses, such as mitogenesis and apoptosis protection; however, its effect against oxidative injury induced by ethanol metabolism is not well understood. The aim of this work was to address the mechanism of HGF-induced protection against ethanol-generated oxidative stress damage in the human cell line VL-17A (cytochrome P450 2E1/alcohol dehydrogenase-transfected HepG2 cells). Cells were pretreated with 50 ng/ml HGF for 12 h and then treated with 100 mM ethanol for 0-48 h. Some parameters of oxidative damage were evaluated. We found that ethanol induced peroxide formation (3.3-fold) and oxidative damage as judged by lipid peroxidation (5.4-fold). Damage was prevented by HGF. To address the mechanisms of HGF-induced protection we investigated the cellular antioxidant system. We found that HGF increased the GSH/GSSG ratio, as well as SOD1, catalase, and gamma-glutamylcysteine synthetase expression. To explore the signaling pathways involved in this process, VL-17A cells were pretreated with inhibitors against PI3K, Akt, and NF-kappaB. We found that all treatments decreased the expression of the antioxidant enzymes, thus abrogating the HGF-induced protection against oxidative stress. Our results demonstrate that HGF protects cells from the oxidative damage induced by ethanol metabolism by a mechanism driven by NF-kappaB and PI3K/Akt signaling.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 60%

mentioning

confidence: 99%

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Hepatocyte growth factor protects hepatocytes against oxidative injury induced by ethanol metabolism

Valdes-Arzate

Luna

Bucio

et al. 2009

Free Radical Biology and Medicine

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“…H 2 O 2 , an inducer of apoptosis in epithelial cells [4, 18], increases the activity of a 24 pS Ca 2+ -activated, non-selective cation channel in a bronchial epithelial cell line [43], and of a 19 pS Ca 2+ -activated, ATP-sensitive non-selective cation channel in a liver-derived epithelial cell line [100]. Both of these studies are reminiscent of the effect of H 2 O 2 on TRPM4 in endothelial cells [99].…”

Section: Apoptotic Cell Deathmentioning

confidence: 99%

Transient receptor potential melastatin 4 and cell death

Simard

Woo

Gerzanich

2012

Pflugers Arch - Eur J Physiol

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Cell death proceeds by way of a variety of “cell death subroutines,” including several types of “apoptosis,” “regulated necrosis,” and others. “Accidental necrosis” due to profound adenosine triphosphate (ATP) depletion or oxidative stress is distinguished from regulated necrosis by the absence of death receptor signaling. However, both accidental and regulated necrosis have in common the process of “oncosis,” a physiological process characterized by Na+ influx and cell volume increase that, in necrotic cell death, is required to produce the characteristic features of membrane blebbing and membrane rupture. Here, we review emerging evidence that the monovalent cation channel, transient receptor potential melastatin 4 (TRPM4), is involved in the cell death process of oncosis. Potential involvement of TRPM4 in oncosis is suggested by the fact that the two principal regulators of TRPM4, intracellular ATP and Ca2+, are both altered during necrosis in the direction that causes TRPM4 channel opening. Under physiological conditions, activation of TRPM4 promotes Na+ influx and cell depolarization. Under pathological conditions, unchecked activation of TRPM4 leads to Na+ overload, cell volume increase, blebbing and cell membrane rupture, the latter constituting the irreversible end stage of necrosis. Emerging data indicate that TRPM4 plays a crucial role as end executioner in the accidental necrotic death of ATP-depleted or redox-challenged endothelial and epithelial cells, both in vitro and in vivo. Future studies will be needed to determine whether TRPM4 also plays a role in regulated necrosis and apoptosis.

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“…The reported metastasis suppressor functions of SSeCKS strongly resemble those reported for CD82. Reexpression of SSeCKS in tumor cells increases cell-cell adhesion [221], blocks Src-dependent matrigel invasion via inhibition of Rho GTPases [222], and inhibits angiogenesis [223]. The relationship to PKC signaling to SSeCKS and suppression of metastasis has not been investigated.…”

Section: Cell-ecm Adhesionmentioning

confidence: 99%

Mechanisms of KAI1/CD82-Induced Prostate Cancer Metastasis

Miranti¹

2011

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE (DD-MM-YYYY)2. REPORT TYPE 3. DATES COVERED (From -To) 4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER 5b. GRANT NUMBER 5c. PROGRAM ELEMENT NUMBER 6. AUTHOR(S) 5d. PROJECT NUMBER 5e. TASK NUMBER E-Mail:5f. WORK UNIT NUMBER Mechanisms of KAI1/CD82-Induced Prostate Cancer Metastasis Cynthia Miranti Metastatic prostate cancer kills over 28,000 American men every year. The mechanisms that drive metastasis are poorly understood. We investigated the hypothesis that loss of the metastasis suppressor gene, CD82/KAI1 in primary prostate tumors of genetically engineered mice would be sufficient to induce metastasis. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBER SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTWhile CD82 was sufficient to suppress metastasis of metastatic tumor cells lines and did so by repressing c-Met, the reverse was not true, i.e. loss of CD82 was not sufficient to induce metastasis. This was the case in at least two genetically engineered prostate cancer models. Ongoing studies in different models may yet prove otherwise.Our other hypothesis, that CD82 was suppressing c-Met and invasion through integrins, was proven invalid in these studies. Other tetraspanins that CD82 associates with, i.e. CD9 and CD151 were required to suppress cMet, but not invasion. Thus, these two events must be occurring via different mechanisms. Nonetheless, we are finding several interesting phenotypes in the CD82 null mice which will shed additional light on CD82 function overall and be useful in developing new hypotheses about how CD82 functions as a metastasis suppressor. cell biology, integrins, KAI1/CD82, tetraspanins, metastasis, c-Met, HGF, mouse models cindy.miranti@vai.org 3 INTRODUCTIONProstate cancer is the most frequently diagnosed cancer and the third leading cause of cancer deaths in men in the United States. 1 Death is due to invasion and metastasis beyond the prostate gla...

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Hepatocyte growth factor improves viability after H2O2-induced toxicity in bile duct epithelial cells

Cited by 15 publications

References 34 publications

Hepatocyte growth factor protects hepatocytes against oxidative injury induced by ethanol metabolism

Hepatocyte growth factor protects hepatocytes against oxidative injury induced by ethanol metabolism

Transient receptor potential melastatin 4 and cell death

Mechanisms of KAI1/CD82-Induced Prostate Cancer Metastasis

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