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Scatena, Roberto,Messana, Irene,Martorana, Giuseppe Ettore,Gozzo, Maria Luisa,Lippa, Silvio,Maccaglia, Alessandro,Bottoni, Patrizia,Vincenzoni, Federica,Nocca, Giuseppina,Castagnola, Massimo,Giardina, Korean Society for Biochemistry and Molecular Biol 2004 Journal of biochemistry and molecular biology Vol.37 No.4
Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and toxicity. In this study, a modified experimental set up was adopted to accomplish a model of moderate hyperoxia (50% $O_2$, 96 h culture) to induce oxidative stress in the human leukemia cell line, U-937. Spectrophotometric measurements of mitochondrial respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, and cell proliferation and differentiation assays were performed. The data showed that moderate hyperoxia in this myeloid cell line causes: i) intriguing alterations in the mitochondrial activities at the levels of succinate dehydrogenase and succinate-cytochrome c reductase; ii) induction of metabolic compensatory adaptations, with significant shift to glycolysis; iii) induction of different antioxidant enzyme activities; iv) significant cell growth inhibition and v) no significant apoptosis. This work will permit better characterization the mitochondrial damage induced by hyperoxia. In particular, the data showed a large increase in the succinate cytochrome c reductase activity, which could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.
( Roberto Scatena ),( Irene Messana ),( Giuseppe Ettore Martorana ),( Maria Luisa Gozzo ),( Silvio Lippa ),( Alessandro Maccaglia ),( Patrizia Bottoni ),( Federica Vincenzoni ),( Giuseppina Nocca ),( 생화학분자생물학회 2004 BMB Reports Vol.37 No.4
Experimental hyperoxia represents a suitable in vitro model to study some pathogenic mechanisms related to oxidative stress. Moreover, it allows the investigation of the molecular pathophysiology underlying oxygen therapy and toxicity. In this study, a modified experimental set up was adopted to accomplish a model of moderate hyperoxia (50% 0₂, 96 h culture) to induce oxidative stress in the human leukemia cell line, U-937. Spectrophotometric measurements of mitochondria) respiratory enzyme activities, NMR spectroscopy of culture media, determination of antioxidant enzyme activities, and cell proliferation and differentiation assays were performed. The data showed that moderate hyperoxia in this myeloid cell line causes: i) intriguing alterations in the mitochondria) activities at the levels of succinate dehydrogenase and succinate-cytochrome c reductase; ⅱ) induction of metabolic compensatory adaptations, with significant shift to glycolysis; ⅲ) induction of different antioxidant enzyme activities; ⅳ) significant cell growth inhibition and ⅴ) no significant apoptosis. This work will permit better characterization the mitochondrial damage induced by hyperoxia. In particular, the data showed a large increase in the succinate cytochrome c reductase activity, which could be a fundamental pathogenic mechanism at the basis of oxygen toxicity.
Tae, Giyoong,Scatena, Marta,Stayton, Patrick S.,Hoffman, Allan S. Informa UK (TaylorFrancis) 2006 Journal of biomaterials science, Polymer edition Vol.17 No.1
<P>An affinity-based controlled release system for growth factors having heparin-binding domains was prepared using a cross-linked heparin gel. The heparin gel was made by reacting hydrazide-functionalized heparin (Hep-ADH) with the N-hydroxysuccinimidyl ester of poly(ethylene glycol)-bis-butanoic acid (SBA-PEG-SBA). The degree of cross-linking could be controlled by defining the stoichiometry of hydrazide modification and the PEG cross-linker addition. The release of vascular endothelial growth factor (VEGF) was characterized as a heparin-binding growth factor. VEGF was directly injected into the heparin gel and the loaded VEGF displayed a slow, controlled release over 3 weeks with little initial burst phase. The biological activity of the released VEGF was measured with a proliferation assay utilizing human umbilical vein endothelial cells. The released VEGF maintained its biological activity at all time points investigated. The heparin gel with loaded VEGF was implanted sub-cutaneously in the dorsal region of mice. A significantly increased density of the endothelial cell marker platelet endothelial adhesion molecule (PECAM-1) was observed in histological specimens of the tissues surrounding the implanted gel.</P>
Heparin-regulated delivery of osteoprotegerin promotes vascularization of implanted hydrogels
McGonigle, Joseph S.,Tae, Giyoong,Stayton, Patrick S.,Hoffman, Allan S.,Scatena, Marta Informa UK (TaylorFrancis) 2008 Journal of biomaterials science, Polymer edition Vol.19 No.8
<P>Localized, controlled delivery of pro-angiogenic agents is an important component of therapies for chronic wound treatment and regenerative medicine. Osteoprotegerin (OPG), a tumor necrosis factor receptor (TNFR) superfamily member has recently been shown to be pro-angiogenic in vitro, and we hypothesized that controlled delivery of OPG could induce angiogenesis in vivo. OPG contains a highly basic heparin-binding domain, suggesting that affinity interactions could be used to control the rate of its ion-exchange-driven release from drug-delivery devices. Here, we describe the use of a hydrogel consisting of thiol-modified heparin which can be readily and controllably cross-linked using a bi-functional PEG-diacrylate. These hydrogels were found to retain between 750 and 900 ng of immunoreactive OPG for up to 500 h in in vitro release studies. OPG containing hydrogels were evaluated in a subcutaneous mouse implant model, and exhibited little degradation and retained OPG as indicated by immunohistochemistry at 2 weeks post-implantation. Immunohistochemical analysis of implanted gels indicated that OPG induced nearly a 2-fold increase in vascular density in the surrounding foreign body capsule. These results suggest that the controlled delivery of OPG can stimulate angiogenesis in vivo and may be of use for wound healing therapies as well as other inflammatory and bone disorders in which OPG plays a role.</P>