Chronic in vivo hypoxia in various organs: Hypoxia-inducible factor-1α and apoptosis

2006 ◽  
Vol 342 (3) ◽  
pp. 875-880 ◽  
Author(s):  
Paola Bianciardi ◽  
Monica Fantacci ◽  
Anna Caretti ◽  
Raffaella Ronchi ◽  
Giuseppina Milano ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α

Hypoxic Stress Upregulates the Expression of Slc38a1 in Brown Adipocytes via Hypoxia-Inducible Factor-1α

Pharmacology ◽  
2017 ◽  
Vol 101 (1-2) ◽  
pp. 64-71 ◽  
Author(s):  
Tetsuhiro Horie ◽  
Kazuya Fukasawa ◽  
Takashi Iezaki ◽  
Gyujin Park ◽  
Yuki Onishi ◽  
...  
Keyword(s):  
Amino Acid ◽  
Hypoxia Inducible Factor ◽  
Amino Acid Transporters ◽  
Hypoxic Stress ◽  
Gene Encoding ◽  
Brown Adipocytes ◽  
Hypoxia Inducible Factor 1Α ◽  
Brown Adipose

The availability of amino acid in the brown adipose tissue (BAT) has been shown to be altered under various conditions; however, little is known about the possible expression and pivotal role of amino acid transporters in BAT under physiological and pathological conditions. The present study comprehensively investigated whether amino acid transporters are regulated by obesogenic conditions in BAT in vivo. Moreover, we investigated the mechanism underlying the regulation of the expression of amino acid transporters by various stressors in brown adipocytes in vitro. The expression of solute carrier family 38 member 1 (Slc38a1; gene encoding sodium-coupled neutral amino acid transporter 1) was preferentially upregulated in the BAT of both genetic and acquired obesity mice in vivo. Moreover, the expression of Slc38a1 was induced by hypoxic stress through hypoxia-inducible factor-1α, which is a master transcription factor of the adaptive response to hypoxic stress, in brown adipocytes in vitro. These results indicate that Slc38a1 is an obesity-associated gene in BAT and a hypoxia-responsive gene in brown adipocytes.

scholarly journals In Vivo Topoisomerase I Inhibition Attenuates the Expression of Hypoxia-Inducible Factor 1α Target Genes and Decreases Tumor Angiogenesis

2011 ◽  
Vol 18 (1) ◽  
pp. 83-94 ◽  
Author(s):  
Eric Guérin ◽  
Wolfgang Raffelsberger ◽  
Erwan Pencreach ◽  
Armin Maier ◽  
Agnès Neuville ◽  
...  
Keyword(s):  
Tumor Angiogenesis ◽  
Topoisomerase I ◽  
Target Genes ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α

Silencing of Hypoxia Inducible Factor-1α by RNA Interference Attenuates Human Glioma Cell Growth In vivo

2007 ◽  
Vol 13 (8) ◽  
pp. 2441-2448 ◽  
Author(s):  
David L. Gillespie ◽  
Kum Whang ◽  
Brian T. Ragel ◽  
Jeannette R. Flynn ◽  
David A. Kelly ◽  
...  
Keyword(s):  
Rna Interference ◽  
Cell Growth ◽  
Glioma Cell ◽  
Hypoxia Inducible Factor ◽  
Human Glioma ◽  
Human Glioma Cell ◽  
Hypoxia Inducible Factor 1Α

scholarly journals Activation of hypoxia-inducible factor-1α (Hif-1α) delays inflammation resolution by reducing neutrophil apoptosis and reverse migration in a zebrafish inflammation model

Blood ◽  
2011 ◽  
Vol 118 (3) ◽  
pp. 712-722 ◽  
Author(s):  
Philip M. Elks ◽  
Fredericus J. van Eeden ◽  
Giles Dixon ◽  
Xingang Wang ◽  
Constantino Carlos Reyes-Aldasoro ◽  
...  
Keyword(s):  
Cell Function ◽  
Genetic Manipulation ◽  
Tissue Injury ◽  
Critical Role ◽  
Hypoxia Inducible Factor ◽  
Site Directed Mutagenesis ◽  
Neutrophil Apoptosis ◽  
Hypoxia Inducible Factor 1Α ◽  
Inflammation Resolution

Abstract The oxygen-sensing transcription factor hypoxia-inducible factor-1α (HIF-1α) plays a critical role in the regulation of myeloid cell function. The mechanisms of regulation are not well understood, nor are the phenotypic consequences of HIF modulation in the context of neutrophilic inflammation. Species conservation across higher metazoans enables the use of the genetically tractable and transparent zebrafish (Danio rerio) embryo to study in vivo resolution of the inflammatory response. Using both a pharmacologic approach known to lead to stabilization of HIF-1α, and selective genetic manipulation of zebrafish HIF-1α homologs, we sought to determine the roles of HIF-1α in inflammation resolution. Both approaches reveal that activated Hif-1α delays resolution of inflammation after tail transection in zebrafish larvae. This delay can be replicated by neutrophil-specific Hif activation and is a consequence of both reduced neutrophil apoptosis and increased retention of neutrophils at the site of tissue injury. Hif-activated neutrophils continue to patrol the injury site during the resolution phase, when neutrophils would normally migrate away. Site-directed mutagenesis of Hif in vivo reveals that hydroxylation of Hif-1α by prolyl hydroxylases critically regulates the Hif pathway in zebrafish neutrophils. Our data demonstrate that Hif-1α regulates neutrophil function in complex ways during inflammation resolution in vivo.

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