scholarly journals Human Placental Hypoxia-Inducible Factor-1α Expression Correlates with Clinical Outcomes in Chronic Hypoxia in Vivo

2007 ◽  
Vol 170 (6) ◽  
pp. 2171-2179 ◽  
Author(s):  
Stacy Zamudio ◽  
Yuanhong Wu ◽  
Francesca Ietta ◽  
Alessandro Rolfo ◽  
Ashley Cross ◽  
...  
Keyword(s):  
Clinical Outcomes ◽  
Chronic Hypoxia ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α

Phosphodiesterase-5 Inhibition Abolishes Neuron Apoptosis Induced by Chronic Hypoxia Independently of Hypoxia-Inducible Factor-1α Signaling

2008 ◽  
Vol 233 (10) ◽  
pp. 1222-1230 ◽  
Author(s):  
Anna Caretti ◽  
Paola Bianciardi ◽  
Raffaella Ronchi ◽  
Monica Fantacci ◽  
Marco Guazzi ◽  
...  
Keyword(s):  
Chronic Hypoxia ◽  
Day Treatment ◽  
Hypoxia Inducible Factor ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Hypoxia Inducible Factor 1Α ◽  
Cgmp Pathway ◽  
The Impact ◽  
Phosphodiesterase 5 ◽  
Neuron Apoptosis

Exposure to hypoxia triggers a variety of adverse effects in the brain that arise from metabolic stress and induce neuron apoptosis. Overexpression of the hypoxia-inducible factor-1α (HIF-1α) is believed to be a major candidate in orchestrating the cell’s defense against stress. To test the impact of HIF-1α on apoptosis during chronic hypoxia in vivo, we examined the protective effect of modulating the nitric oxide (NO)/cGMP pathway by sildenafil, a selective inhibitor of phosphodiesterase-5 (PDE-5). Male ICR/CD-1 mice were divided into 3 groups ( n = 6/group): normoxic (21% O2), hypoxic (9.5% O2), and hypoxic with sildenafil (1.4-mg/kg intraperitoneal injections daily). At the end of the 8-day treatment period, the mice were euthanized and cerebral cortex biopsies were harvested for analyses. We found that sildenafil: (1) did not significantly alter the hypoxia-induced weight loss and hemoglobin increase, but did augment plasma nitrates+nitrites and the tissue content of cGMP and phosphorylated (P) NO synthase III; (2) reversed the hypoxia-induced neuron apoptosis (terminal deoxynucleotidyl transferase positivity and double-staining immunofluorescence, P = 0.009), presumably through increased bcl-2/Bax ( P = 0.0005); and (3) did not affect HIF-1α, but rather blunted the hypoxia-induced increase in P-ERK1/2 ( P = 0.0002) and P-p38 ( P = 0.004). We conclude that upregulating the NO/cGMP pathway by PDE-5 inhibition during hypoxia reduces neuron apoptosis, regardless of HIF-1α, through an interaction involving ERK1/2 and p38.

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.

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

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
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