Effects of Hyperbaric Oxygen on Proliferative and Apoptotic Activities and Reactive Oxygen Species Generation in Mouse Fibroblast 3T3/J2 Cell Line

Conconi, Maria Teresa; Baiguera, Silvia; Guidolin, Diego; Furlan, Claudia; Menti, Anna Michela; Vigolo, Simonetta; Belloni, Anna S.; Parnigotto, Pier Paolo; Nussdorfer, Gastone G.

doi:10.1136/jim-51-04-24

Cited by 49 publications

(36 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, an enhanced generation of both intracellular and extracellular ROS was observed after a 24-hour exposure. This finding seems to be consistent with another study that found an increase of ROS production in 3T3/J2 fibroblasts exposed to HBOT [8], where it was suggested that intracellular ROS generation could be directly related to cell apoptosis.…”

Section: Discussionsupporting

confidence: 93%

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes

et al. 2012

View full text Add to dashboard Cite

Adipose tissue often becomes poorly oxygenated in obese subjects. This feature may provide cellular mechanisms involving chronic inflammation processes such as the release of proinflammatory cytokines and macrophage infiltration. In this context, the purpose of the present study was to determine whether a hyperoxia exposure on mature adipocytes may influence the expression of some adipokines and involve favorable changes in specific metabolic variables. 3T3-L1 adipocytes (14 days differentiated) were treated with 95% oxygen for 24 h. Cell viability, intra and extracellular reactive oxygen especies (ROS) content, glucose uptake and lactate and glycerol concentrations were measured in the culture media. Also, mRNA levels of HIF-1, leptin, IL-6, MCP-1, PPAR-, adiponectin, and ANGPTL-4 were analyzed.Hyperoxia treatment increased intra and extracellular ROS content, reduced glucose uptake and lactate release and increased glucose release. It also led to an upregulation of the expression of IL-6, MCP-1 and PPAR-, while ANGPTL4 was downregulated in the hyperoxia group with respect to control. The present data shows that hyperoxia treatment seems to provoke an inflammatory response due to the release of ROS and the upregulation of pro-inflammatory adipokines, such as IL-6 and MCP-1. On the other hand, hyperoxia may have an indirect effect on the improvement of insulin sensitivity, due to the upregulation of PPAR- gene expression as well as a possible modulation of both glucose and lipid metabolic markers. To our knownledge, this is the first study analyzing the effect of hyperoxia in 3T3-L1 adipocytes.

show abstract

Section: Discussionsupporting

confidence: 93%

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes

et al. 2012

View full text Add to dashboard Cite

show abstract

“…HBO also attenuates microvascular dysfunction and reperfusion microvascular ischemia, as demonstrated in both experimental models and patients with acute myocardial infarction [5]. Since molecular oxygen is one of the critical nutrients and plays a central role in the reparative process of wound [6], the beneficial effects of HBO in treating ischemia-related wounds may be mediated by stimulating collagen synthesis [7], cell proliferation [8][9][10][11], and promoting angiogenesis [12][13][14]. However, the mechanism(s) accounting for HBO-induced vessel formation is still not well documented.…”

Section: Introductionmentioning

confidence: 99%

Hyperbaric oxygen induces VEGF expression through ERK, JNK and c-Jun/AP-1 activation in human umbilical vein endothelial cells

Lee

Chen

Tsai³

et al. 2005

J Biomed Sci

View full text Add to dashboard Cite

SummaryHyperbaric oxygen (HBO) is increasingly used in a number of areas of medical practice, such as selected problem infections and wounds. The beneficial effects of HBO in treating ischemia-related wounds may be mediated by stimulating angiogenesis. We sought to investigate VEGF, the main angiogenic regulator, regulated by HBO in human umbilical vein endothelial cells (HUVECs). In this study, we found that VEGF was up regulated both at mRNA and protein levels in HUVECs treated with HBO dose-and timedependently. Since there are several AP-1 sites in the VEGF promoter, and the c-Jun/AP-1 is activated through stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) and extracellular signal regulated kinase (ERK), we further examined the c-Jun, JNK and ERK that might be involved in the VEGF induced by HBO. The VEGF mRNA induced by HBO was blocked by both PD98059 and SP600125, the ERK and JNK inhibitors respectively. HBO induced phospho-ERK and phospho-JNK expressions within 15 min. We further demonstrated that c-Jun phosphorylation was induced within 60 min of HBO treatment. HBO also induced the nuclear AP-1 binding ability within 30-60 min, but the AP-1 induction was blocked by treatment with either the ERK or JNK inhibitor. To verify that the VEGF expression induced by HBO is through the AP-1 trans-activation and VEGF promoter, both the VEGF promoter and AP-1 driving luciferase activity were found increased by the cells treated with HBO. The c-Jun mRNA, which is also driven by AP-1, was also induced by HBO, and the induction of c-Jun was blocked by ERK and JNK inhibitors. We suggest that VEGF induced by HBO is through c-Jun/AP-1 activation, and through simultaneous activation of ERK and JNK pathways.

show abstract

“…Although the mechanism of tumor cell suppression by uncombined HBO treatment remains unclear in detail, it has been reported that cell damage due to reactive oxygen species (ROS) or free radicals plays a role in mediating this effect of HBO (29). More specifically, tumor cells are destroyed if ROS level rises beyond the limit of a tumor's resistance to oxidative stress following treatment with HBO.…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric oxygen as a chemotherapy adjuvant in the treatment of osteosarcoma

Kawasoe

Yokouchi²,

Ueno³

et al. 2009

Oncol Rep

View full text Add to dashboard Cite

Abstract. Although hyperbaric oxygen has been shown to enhance the efficacy of radiotherapy and chemotherapy for the treatment of several malignant tumors, the impact of hyperbaric oxygen on osteosarcoma has not yet been demonstrated. In this study, we investigated the efficacy of hyperbaric oxygen alone and in combination with an anticancer drug as an adjuvant to chemotherapy. In vitro, highly metastatic murine osteosarcoma cell lines were exposed to hyperbaric oxygen and cell viability was examined. Hyperbaric oxygen alone significantly suppressed cell proliferation, and hyperbaric oxygen plus carboplatin exhibited significant synergism in suppression of cell proliferation. In vivo, C3H mice were subcutaneously inoculated with osteosarcoma cells and divided into four groups: control, hyperbaric oxygen, carboplatin, and carboplatin plus hyperbaric oxygen. After 5 weeks, increase in both tumor volume and number of lung metastases was significantly suppressed in the hyperbaric oxygen group. Concomitant hyperbaric oxygen clearly enhanced the chemotherapeutic effects of carboplatin on both tumor growth and lung metastasis in osteosarcoma-bearing mice. Moreover, mortality in the carboplatin plus hyperbaric oxygen group was significantly lower than in the other three groups. These findings suggest that hyperbaric oxygen plus carboplatin combination therapy could be an appropriate therapeutic regimen for the treatment of patients with osteosarcoma.

show abstract

Effects of Hyperbaric Oxygen on Proliferative and Apoptotic Activities and Reactive Oxygen Species Generation in Mouse Fibroblast 3T3/J2 Cell Line

Cited by 49 publications

References 0 publications

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes

Hyperbaric oxygen induces VEGF expression through ERK, JNK and c-Jun/AP-1 activation in human umbilical vein endothelial cells

Hyperbaric oxygen as a chemotherapy adjuvant in the treatment of osteosarcoma

Contact Info

Product

Resources

About