FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2205000835> ?p ?o ?g. }

• W2205000835 endingPage "23527" @default.
• W2205000835 startingPage "23523" @default.
• W2205000835 abstract "Sickle cell disease (SCD) is caused by genetic defects in the β-globin chain. SCD is a frequently inherited blood disorder, and sickle cell anemia is a common type of hemoglobinopathy. During anemia, the hypoxic response via the transcription factor hypoxia-inducible factor (HIF)-2α is highly activated in the intestine and is essential in iron absorption. Intestinal disruption of HIF-2α protects against tissue iron accumulation in iron overload anemias. However, the role of intestinal HIF-2α in regulating anemia in SCD is currently not known. Here we show that in mouse models of SCD, disruption of intestinal HIF-2α significantly decreased tissue iron accumulation. This was attributed to a decrease in intestinal iron absorptive genes, which were highly induced in a mouse model of SCD. Interestingly, disruption of intestinal HIF-2α led to a robust improvement in anemia with an increase in RBC, hemoglobin, and hematocrit. This was attributed to improvement in RBC survival, hemolysis, and insufficient erythropoiesis, which is evident from a significant decrease in serum bilirubin, reticulocyte counts, and serum erythropoietin following intestinal HIF-2α disruption. These data suggest that targeting intestinal HIF-2α has a significant therapeutic potential in SCD pathophysiology. Sickle cell disease (SCD) is caused by genetic defects in the β-globin chain. SCD is a frequently inherited blood disorder, and sickle cell anemia is a common type of hemoglobinopathy. During anemia, the hypoxic response via the transcription factor hypoxia-inducible factor (HIF)-2α is highly activated in the intestine and is essential in iron absorption. Intestinal disruption of HIF-2α protects against tissue iron accumulation in iron overload anemias. However, the role of intestinal HIF-2α in regulating anemia in SCD is currently not known. Here we show that in mouse models of SCD, disruption of intestinal HIF-2α significantly decreased tissue iron accumulation. This was attributed to a decrease in intestinal iron absorptive genes, which were highly induced in a mouse model of SCD. Interestingly, disruption of intestinal HIF-2α led to a robust improvement in anemia with an increase in RBC, hemoglobin, and hematocrit. This was attributed to improvement in RBC survival, hemolysis, and insufficient erythropoiesis, which is evident from a significant decrease in serum bilirubin, reticulocyte counts, and serum erythropoietin following intestinal HIF-2α disruption. These data suggest that targeting intestinal HIF-2α has a significant therapeutic potential in SCD pathophysiology." @default.
• W2205000835 created "2016-06-24" @default.
• W2205000835 creator A5016118917 @default.
• W2205000835 creator A5040091526 @default.
• W2205000835 creator A5043313553 @default.
• W2205000835 creator A5046499318 @default.
• W2205000835 creator A5049287730 @default.
• W2205000835 creator A5051834794 @default.
• W2205000835 date "2015-09-01" @default.
• W2205000835 modified "2023-10-17" @default.
• W2205000835 title "Intestine-specific Disruption of Hypoxia-inducible Factor (HIF)-2α Improves Anemia in Sickle Cell Disease" @default.
• W2205000835 cites W1585483325 @default.
• W2205000835 cites W1965891152 @default.
• W2205000835 cites W1972406498 @default.
• W2205000835 cites W1982322827 @default.
• W2205000835 cites W2019381418 @default.
• W2205000835 cites W2022595661 @default.
• W2205000835 cites W2024654129 @default.
• W2205000835 cites W2030846356 @default.
• W2205000835 cites W2038900684 @default.
• W2205000835 cites W2053495832 @default.
• W2205000835 cites W2054380088 @default.
• W2205000835 cites W2061342616 @default.
• W2205000835 cites W2082679209 @default.
• W2205000835 cites W2094155951 @default.
• W2205000835 cites W2116854831 @default.
• W2205000835 cites W2122164678 @default.
• W2205000835 cites W2125425147 @default.
• W2205000835 cites W2125919583 @default.
• W2205000835 cites W2137367581 @default.
• W2205000835 cites W2146183954 @default.
• W2205000835 cites W2160602863 @default.
• W2205000835 cites W2163438420 @default.
• W2205000835 cites W2167845320 @default.
• W2205000835 cites W4211186710 @default.
• W2205000835 doi "https://doi.org/10.1074/jbc.c115.681643" @default.
• W2205000835 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4583015" @default.
• W2205000835 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26296885" @default.
• W2205000835 hasPublicationYear "2015" @default.
• W2205000835 type Work @default.
• W2205000835 sameAs 2205000835 @default.
• W2205000835 citedByCount "30" @default.
• W2205000835 countsByYear W22050008352016 @default.
• W2205000835 countsByYear W22050008352017 @default.
• W2205000835 countsByYear W22050008352018 @default.
• W2205000835 countsByYear W22050008352019 @default.
• W2205000835 countsByYear W22050008352020 @default.
• W2205000835 countsByYear W22050008352021 @default.
• W2205000835 countsByYear W22050008352022 @default.
• W2205000835 countsByYear W22050008352023 @default.
• W2205000835 crossrefType "journal-article" @default.
• W2205000835 hasAuthorship W2205000835A5016118917 @default.
• W2205000835 hasAuthorship W2205000835A5040091526 @default.
• W2205000835 hasAuthorship W2205000835A5043313553 @default.
• W2205000835 hasAuthorship W2205000835A5046499318 @default.
• W2205000835 hasAuthorship W2205000835A5049287730 @default.
• W2205000835 hasAuthorship W2205000835A5051834794 @default.
• W2205000835 hasBestOaLocation W22050008351 @default.
• W2205000835 hasConcept C104317684 @default.
• W2205000835 hasConcept C126322002 @default.
• W2205000835 hasConcept C134018914 @default.
• W2205000835 hasConcept C160450060 @default.
• W2205000835 hasConcept C178790620 @default.
• W2205000835 hasConcept C185592680 @default.
• W2205000835 hasConcept C203014093 @default.
• W2205000835 hasConcept C2776175824 @default.
• W2205000835 hasConcept C2778248108 @default.
• W2205000835 hasConcept C2778534260 @default.
• W2205000835 hasConcept C2778620579 @default.
• W2205000835 hasConcept C2778917026 @default.
• W2205000835 hasConcept C2779134260 @default.
• W2205000835 hasConcept C2779668550 @default.
• W2205000835 hasConcept C2779703530 @default.
• W2205000835 hasConcept C2779902561 @default.
• W2205000835 hasConcept C2780844101 @default.
• W2205000835 hasConcept C540031477 @default.
• W2205000835 hasConcept C55493867 @default.
• W2205000835 hasConcept C71924100 @default.
• W2205000835 hasConcept C7836513 @default.
• W2205000835 hasConcept C86803240 @default.
• W2205000835 hasConceptScore W2205000835C104317684 @default.
• W2205000835 hasConceptScore W2205000835C126322002 @default.
• W2205000835 hasConceptScore W2205000835C134018914 @default.
• W2205000835 hasConceptScore W2205000835C160450060 @default.
• W2205000835 hasConceptScore W2205000835C178790620 @default.
• W2205000835 hasConceptScore W2205000835C185592680 @default.
• W2205000835 hasConceptScore W2205000835C203014093 @default.
• W2205000835 hasConceptScore W2205000835C2776175824 @default.
• W2205000835 hasConceptScore W2205000835C2778248108 @default.
• W2205000835 hasConceptScore W2205000835C2778534260 @default.
• W2205000835 hasConceptScore W2205000835C2778620579 @default.
• W2205000835 hasConceptScore W2205000835C2778917026 @default.
• W2205000835 hasConceptScore W2205000835C2779134260 @default.
• W2205000835 hasConceptScore W2205000835C2779668550 @default.
• W2205000835 hasConceptScore W2205000835C2779703530 @default.
• W2205000835 hasConceptScore W2205000835C2779902561 @default.
• W2205000835 hasConceptScore W2205000835C2780844101 @default.
• W2205000835 hasConceptScore W2205000835C540031477 @default.

• next