Difference between revisions of "Sanjuán-Pla 2005 FEBS Lett"
(Created page with "{{Publication |title=Sanjuán-Pla A, Cervera AM, Apostolova N, Garcia-Bou R, Víctor VM, Murphy MP, McCreath KJ (2005) A targeted antioxidant reveals the importance of mitocho...") |
|||
Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title= | |title=Sanjuan-Pla A, Cervera AM, Apostolova N, Garcia-Bou R, Victor VM, Murphy MP, McCreath KJ (2005) A targeted antioxidant reveals the importance of mitochondrial reactive oxygen species in the hypoxic signaling of HIF-1alpha. FEBS Lett 579:2669-74. | ||
|info=[https://pubmed.ncbi.nlm.nih.gov/15862307/ PMID:15862307 Open Access] | |info=[https://pubmed.ncbi.nlm.nih.gov/15862307/ PMID:15862307 Open Access] | ||
|authors=Sanjuán-Pla A, Cervera AM, Apostolova N, Garcia-Bou R, Víctor VM, Murphy MP, McCreath KJ | |authors=Sanjuán-Pla A, Cervera AM, Apostolova N, Garcia-Bou R, Víctor VM, Murphy MP, McCreath KJ | ||
Line 7: | Line 7: | ||
|abstract=Exposure to limiting oxygen in cells and tissues induce the stabilization and transcriptional activation of the hypoxia-inducible factor 1 alpha (HIF-1alpha) protein, a key regulator of the hypoxic response. Reactive oxygen species (ROS) generation has been implicated in the stabilization of HIF-1alpha during this response, but this is still a matter of some debate. In this study we utilize a mitochondria-targeted antioxidant, mitoubiquinone (MitoQ), and examine its effects on the hypoxic stabilization of HIF-1alpha. Our results show that under conditions of reduced oxygen (3% O(2)), MitoQ ablated the hypoxic induction of ROS generation and destabilized HIF-1alpha protein. This in turn led to an abrogation of HIF-1 transcriptional activity. Normoxic stabilization of HIF-1alpha, on the other hand, was unchanged in the presence of MitoQ suggesting that ROS were not involved. This study strongly suggests that mitochondrial ROS contribute to the hypoxic stabilization of HIF-1alpha. | |abstract=Exposure to limiting oxygen in cells and tissues induce the stabilization and transcriptional activation of the hypoxia-inducible factor 1 alpha (HIF-1alpha) protein, a key regulator of the hypoxic response. Reactive oxygen species (ROS) generation has been implicated in the stabilization of HIF-1alpha during this response, but this is still a matter of some debate. In this study we utilize a mitochondria-targeted antioxidant, mitoubiquinone (MitoQ), and examine its effects on the hypoxic stabilization of HIF-1alpha. Our results show that under conditions of reduced oxygen (3% O(2)), MitoQ ablated the hypoxic induction of ROS generation and destabilized HIF-1alpha protein. This in turn led to an abrogation of HIF-1 transcriptional activity. Normoxic stabilization of HIF-1alpha, on the other hand, was unchanged in the presence of MitoQ suggesting that ROS were not involved. This study strongly suggests that mitochondrial ROS contribute to the hypoxic stabilization of HIF-1alpha. | ||
}} | }} | ||
== Cited by == | |||
{{Template:Cited by Komlodi 2021 MitoFit AmR}} | |||
{{Labeling | {{Labeling | ||
|additional=MitoFit 2021 AmR | |additional=MitoFit 2021 AmR | ||
}} | }} |
Revision as of 16:14, 23 March 2021
Sanjuan-Pla A, Cervera AM, Apostolova N, Garcia-Bou R, Victor VM, Murphy MP, McCreath KJ (2005) A targeted antioxidant reveals the importance of mitochondrial reactive oxygen species in the hypoxic signaling of HIF-1alpha. FEBS Lett 579:2669-74. |
Sanjuán-Pla A, Cervera AM, Apostolova N, Garcia-Bou R, Víctor VM, Murphy MP, McCreath KJ (2005) FEBS Lett
Abstract: Exposure to limiting oxygen in cells and tissues induce the stabilization and transcriptional activation of the hypoxia-inducible factor 1 alpha (HIF-1alpha) protein, a key regulator of the hypoxic response. Reactive oxygen species (ROS) generation has been implicated in the stabilization of HIF-1alpha during this response, but this is still a matter of some debate. In this study we utilize a mitochondria-targeted antioxidant, mitoubiquinone (MitoQ), and examine its effects on the hypoxic stabilization of HIF-1alpha. Our results show that under conditions of reduced oxygen (3% O(2)), MitoQ ablated the hypoxic induction of ROS generation and destabilized HIF-1alpha protein. This in turn led to an abrogation of HIF-1 transcriptional activity. Normoxic stabilization of HIF-1alpha, on the other hand, was unchanged in the presence of MitoQ suggesting that ROS were not involved. This study strongly suggests that mitochondrial ROS contribute to the hypoxic stabilization of HIF-1alpha.
Cited by
- Komlódi T, Schmitt S, Zdrazilova L, Donnelly C, Zischka H, Gnaiger E. Oxygen dependence of hydrogen peroxide production in isolated mitochondria and permeabilized cells. MitoFit Preprints (in prep).
Labels:
MitoFit 2021 AmR