Effect of tumor necrosis factor-α and interleukin-1α on heme oxygenase-1 expression in human endothelial cells

Terry, Christi M.; Clikeman, Jennifer A.; Hoidal, John R.; Callahan, Karleen S.

doi:10.1152/ajpheart.1998.274.3.h883

Cited by 125 publications

(121 citation statements)

References 61 publications

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“…This native response is likely caused by I͞R-mediated activation of the inflammatory cascade and the consequent release of cytokines. Indeed, cytokines have been reported to induce HO-1 expression both at the transcriptional and posttranscriptional levels (32). Despite HO-1 protein levels that equaled or surpassed those in the hHO-1-treated rats, this ''late'' response was clearly not enough to provide significant myocardial protection in the lacZ-treated animals.…”

Section: Discussionmentioning

confidence: 98%

Hypoxia-regulated therapeutic gene as a preemptive treatment strategy against ischemia/reperfusion tissue injury

Pachori

Melo

Hart

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Ischemia and reperfusion represent major mechanisms of tissue injury and organ failure. The timing of administration and the duration of action limit current treatment approaches using pharmacological agents. In this study, we have successfully developed a preemptive strategy for tissue protection using an adenoassociated vector system containing erythropoietin hypoxia response elements for ischemia-regulated expression of the therapeutic gene human heme-oxygenase-1 (hHO-1). We demonstrate that a single administration of this vector several weeks in advance of ischemia͞reperfusion injury to multiple tissues such as heart, liver, and skeletal muscle yields rapid and timely induction of hHO-1 during ischemia that resulted in dramatic reduction in tissue damage. In addition, overexpression of therapeutic transgene prevented long-term pathological tissue remodeling and normalized tissue function. Application of this regulatable system using an endogenous physiological stimulus for expression of a therapeutic gene may be a feasible strategy for protecting tissues at risk of ischemia͞reperfusion injury.

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Section: Discussionmentioning

confidence: 98%

Hypoxia-regulated therapeutic gene as a preemptive treatment strategy against ischemia/reperfusion tissue injury

Pachori

Melo

Hart

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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“…Several authors have shown that HO-1 was induced by heat shock, heavy metals, hypoxia and endotoxin (Eyssen-Hernandez et al 1996, Carraway et al 1998, Panchenko et al 2000, Stuhlmeier 2000. Furthermore, HO-1 was induced by TNF- (Terry et al 1998), which is known to stimulate granulosa cell apoptosis (Kaipai et al 1996). In porcine granulosa cells, we have demonstrated that HO-1 was mainly expressed in granulosa cells in the atretic follicle, and was present in freshly isolated and cultured granulosa cells, but we have not studied the nature of the factors that induced HO-1.…”

Section: Discussionmentioning

confidence: 99%

Haem oxygenase augments porcine granulosa cell apoptosis in vitro

Harada¹,

Koi²,

Kubota³

et al. 2004

Journal of Endocrinology

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Haem oxygenases produce carbon monoxide, which, like nitric oxide, is a gaseous messenger molecule that is one of several important survival factors in ovarian follicles. However, little is known about the expression and possible functions of these enzymes in granulosa cells. The purpose of this study was to investigate the expression and possible role of haem oxygenases in porcine granulosa cells (PGCs). We obtained frozen sections of porcine ovaries and PGCs from ovarian follicles of various sizes by needle aspiration, and examined the expression of haem oxygenase-1 (HO-1; inducible type) and HO-2 (constitutive type) in PGCs by immunohistochemistry, RT-PCR, western blotting and flow cytometry. Both types of haem oxygenase were identified in PGCs throughout follicular development, but HO-1 was expressed primarily in granulosa cells in atretic follicles. We also investigated the effect of haem oxygenases on apoptosis of granulosa cells (flow cytometry to detect subdiploid DNA fluorescence) and on expression of Fas ligand (quantitative analysis of western blotting and flow cytometry). In tightly bound PGCs, the mean proportion of apoptotic cells treated with 1 µM haemin (a haem oxygenase substrate) was approximately 1·7-fold greater than that in untreated controls, and zinc protoporphyrin IX (ZnPP IX; a haem oxygenase inhibitor) completely inhibited the increase in apoptosis induced by haemin in 24-h culture. Conversely, in weakly associated PGCs, the proportion of apoptotic cells was not altered by haemin. The quantity of Fas ligand protein was increased in a dose-dependent manner in tightly bound PGCs treated with haemin compared with controls, and the haemin-induced increase in Fas ligand protein was inhibited by ZnPP IX. Thus we identified inducible HO-1 and constitutive HO-2 in PGCs throughout follicular development, and we conclude that products of reactions catalysed by haem oxygenases are likely to be important autocrine/paracrine factors that regulate apoptosis in PGCs.

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“…NF-E2-related factor 2 (Nrf2) is an important transcription factor that regulates expression of antioxidant defense genes through binding to antioxidant response elements in the promoter region, such as HO-1. 14 HO-1 has been reported to play a critical role in protection against oxidative tissue injury following ischemia and inflammation, 15 however, the mechanism is not clear. Therefore, we determined the role of HO-1 in TNF-␣-mediated adhesion molecules expression and airway inflammation in vitro and in vivo.…”

Section: The P47mentioning

confidence: 99%

Overexpression of HO-1 Protects against TNF-α-Mediated Airway Inflammation by Down-Regulation of TNFR1-Dependent Oxidative Stress

Lee

Luo

Lee

et al. 2009

The American Journal of Pathology

160

151

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Oxidative stresses are believed to play an important role in the induction of both cell adhesion molecules and pro-inflammatory cytokines, a key event in a variety of inflammatory processes. The enzyme heme oxygenase-1 (HO-1) functions as an antioxidant and serves to protect against tissue injury. In this study, we report that HO-1 was induced in cultured human tracheal smooth muscle cells after either treatment with a potent inducer of HO-1 activity, cobalt protoporphyrin IX, or infection with a recombinant adenovirus that carries the human HO-1 gene. Overexpression of HO-1 protected against tumor necrosis factor (TNF)-␣-mediated airway inflammation via the down-regulation of oxidative stress, adhesion molecules, and interleukin-6 in both cultured human tracheal smooth muscle cells and the airways of mice. In addition, HO-1 overexpression inhibited TNF-␣-induced intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression, adherence of THP-1 cells, generation of interleukin-6, p47 phox translocation, and nuclear factor-B activation. HO-1 overexpression also attenuated TNF-␣-induced oxidative stress, which was abrogated in the presence of both the HO-1 inhibitor, zinc protoporphyrin IX, as well as a carbon monoxide scavenger. In addition, HO-1 overexpression reduced the formation of a TNFR1/c-Src/p47 phox complex. These results suggest that HO-1 functions as a suppressor of TNF-␣ signaling, not only by inhibiting the expression of adhesion molecules and generation of interleukin-6, but also by diminishing intracellular reactive oxygen species production and nuclear factor-B activation in both cultured human tracheal smooth muscle cells and the airways of mice.

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Effect of tumor necrosis factor-α and interleukin-1α on heme oxygenase-1 expression in human endothelial cells

Cited by 125 publications

References 61 publications

Hypoxia-regulated therapeutic gene as a preemptive treatment strategy against ischemia/reperfusion tissue injury

Hypoxia-regulated therapeutic gene as a preemptive treatment strategy against ischemia/reperfusion tissue injury

Haem oxygenase augments porcine granulosa cell apoptosis in vitro

Overexpression of HO-1 Protects against TNF-α-Mediated Airway Inflammation by Down-Regulation of TNFR1-Dependent Oxidative Stress

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