Retrovirus-mediated human heme oxygenase-1 (HO-1) gene transfer into rat endothelial cells: the effect of HO-1 inducers on the expression of cytokines

Abdel-Aziz, Mostafa M.; El-Asmar, M.F.; El-Miligy, Dawlat; Atta, Hazem; Shaker, Olfat G.; Ghattas, Maivel H.; Hosni, Hasnaa A.; Kamal, Nagwa

doi:10.1016/s1357-2725(02)00172-3

Cited by 23 publications

(8 citation statements)

References 34 publications

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“…This also suggests certain KSHV miRNAs may protect cells from oxidative stress, by inhibiting BACH1 from repressing HMOX1 expression. Increased HMOX1 activity also correlates with increased angiogenesis [54], [55], [56], [57]. Taken together, KSHV miRNA induction of HMOX1 can potentially protect cells from oxidative stress and increase proliferation and angiogenesis.…”

Section: Discussionmentioning

confidence: 82%

Proteomic Screening of Human Targets of Viral microRNAs Reveals Functions Associated with Immune Evasion and Angiogenesis

et al. 2013

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Kaposi's sarcoma (KS) is caused by infection with Kaposi's sarcoma-associated herpesvirus (KSHV). The virus expresses unique microRNAs (miRNAs), but the targets and functions of these miRNAs are not completely understood. In order to identify human targets of viral miRNAs, we measured protein expression changes caused by multiple KSHV miRNAs using pulsed stable labeling with amino acids in cell culture (pSILAC) in primary endothelial cells. This led to the identification of multiple human genes that are repressed at the protein level, but not at the miRNA level. Further analysis also identified that KSHV miRNAs can modulate activity or expression of upstream regulatory factors, resulting in suppressed activation of a protein involved in leukocyte recruitment (ICAM1) following lysophosphatidic acid treatment, as well as up-regulation of a pro-angiogenic protein (HIF1α), and up-regulation of a protein involved in stimulating angiogenesis (HMOX1). This study aids in our understanding of miRNA mechanisms of repression and miRNA contributions to viral pathogenesis.

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Section: Discussionmentioning

confidence: 82%

Proteomic Screening of Human Targets of Viral microRNAs Reveals Functions Associated with Immune Evasion and Angiogenesis

et al. 2013

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“…Therefore, overcoming the poor survival rate of implanted cells is clearly needed to improve stem cell therapy. In line with this, heme oxygenase-1 (HO-1), the rate-limiting enzyme in the degradation of heme, is now considered to function as a cytoprotective agent due to its multiple catalytic byproducts (Shibahara 2003); in fact, HO-1 has been shown to protect against apoptosis after oxidative stress injury in multiple cell types (Takahashi et al 1999;Abdel-Aziz et al 2003;Zeng et al 2010).…”

mentioning

confidence: 99%

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Yang

Liu

et al. 2012

Tohoku J. Exp. Med.

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Adipose tissue-derived stem cells (ADSCs) are a promising source of autologous stem cells that are used for regeneration and repair of infracted heart. However, the efficiency of their transplantation is under debate. One of the possible reasons for marginal improvement in ADSCs transplantation is the significant cell death rate of implanted cells after being grafted into injured heart. Therefore, overcoming the poor survival rate of implanted cells may improve stem cell therapy. Due to limited improvement concerning direct stem cell therapy, gene-transfer methods are used to enhance cellular cardiomyoplasty efficacy. Heme oxygenase-1 (HO-1) can provide various types of cells with protection against oxidative injury and apoptosis. However, exact effects of autologous ADSCs combined with HO-1 on cardiac performance remains unknown. In this study, rabbits were treated with ADSCs transduced with HO-1 (HO-1-ADSCs), treated with non-transduced ADSCs, or injected with phosphate buffered saline 14 days after experimental myocardial infarction was induced, when autologous ADSCs were obtained simultaneously. Four weeks after injection, echocardiography showed significant improvements for cardiac functions and left ventricular dimensions in HO-1-ADSCs-treated animals. Structural consequences of transplantation were determined by detailed histological analysis, which showed differentiation of HO-1-ADSCs to cardiomyocyte-like tissues and lumen-like structure organizations. Apart from improvement in angiogenesis and scar areas, more connexin 43-positive gap junction and greater tyrosine hydroxylase-positive cardiac sympathetic nerves sprouting were observed in the HO-1-ADSCs-treated group compared with ADSCs group. These data suggest that the transplantation of autologous ADSCs combined with HO-1 transduction is a feasible and efficacious method for improving infarcted myocardium.

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“…100 Conversely, overexpression of HO-1, using retrovirus gene transfer, markedly inhibited TGF-β mRNA and protein in a rat lung microvessel endothelial cell line. 101 Thus, TGF-β-mediated HO-1 induction may counteract the negative effects of TGF-β1 by blocking further TGF-β1 production and/or affecting cell proliferation, apoptosis and deposition of ECM.…”

Section: Molecular Regulation Of Ho-1 By Tgf-βmentioning

confidence: 99%

Heme Oxygenase-1 as a Target for TGF-β in Kidney Disease

Zarjou

Agarwal

2012

Seminars in Nephrology

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Transforming growth factor-β (TGF-β) is a multifunctional regulatory cytokine that is implicated in a variety of kidney diseases, including diabetic nephropathy and chronic transplant rejection where it promotes stimulation of the extracellular matrix deposition, cell proliferation and migration. TGF-β exerts its biological functions largely via its downstream complex signaling molecules, Smad proteins. Paradoxically, TGF-β is also essential for normal homeostasis and suppression of inflammation through mechanisms that are yet to be fully elucidated. One feasible mechanism by which TGF-β may exert its beneficial properties is through induction of heme oxygenase-1 (HO-1). Induction of this redox sensitive enzyme is known to be cytoprotective through its potent antioxidant, anti-inflammatory and anti-apoptotic properties in different conditions including several kidney diseases. In this overview, recent advances in our understanding of the role of TGF-β in kidney disease, its molecular regulation of HO-1 expression and the potential role of HO-1 induction as a therapeutic modality in TGF-β mediated kidney diseases are highlighted.

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Retrovirus-mediated human heme oxygenase-1 (HO-1) gene transfer into rat endothelial cells: the effect of HO-1 inducers on the expression of cytokines

Cited by 23 publications

References 34 publications

Proteomic Screening of Human Targets of Viral microRNAs Reveals Functions Associated with Immune Evasion and Angiogenesis

Proteomic Screening of Human Targets of Viral microRNAs Reveals Functions Associated with Immune Evasion and Angiogenesis

Transplantation of Adipose Tissue-Derived Stem Cells Overexpressing Heme Oxygenase-1 Improves Functions and Remodeling of Infarcted Myocardium in Rabbits

Heme Oxygenase-1 as a Target for TGF-β in Kidney Disease

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