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HIF-1α Is Essential for Myeloid Cell-Mediated Inflammation

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TLDR
It is found that activation of HIF-1alpha is essential for myeloid cell infiltration and activation in vivo through a mechanism independent of VEGF, and its direct regulation of survival and function in the inflammatory microenvironment is demonstrated.
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This article is published in Cell.The article was published on 2003-03-07 and is currently open access. It has received 1773 citations till now. The article focuses on the topics: Myeloid & Cell aggregation.

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The biology of VEGF and its receptors.

TL;DR: Vascular endothelial growth factor (VEGF) is a key regulator of physiological angiogenesis during embryogenesis, skeletal growth and reproductive functions and is implicated in pathologicalAngiogenesis associated with tumors, intraocular neovascular disorders and other conditions.
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The biology of cancer: metabolic reprogramming fuels cell growth and proliferation

TL;DR: This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types and regulates regulation of these fluxes by cellular mediators of signal transduction and gene expression.
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Vascular endothelial growth factor: basic science and clinical progress.

TL;DR: Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen in vitro and an angiogenic inducer in a variety of in vivo models and is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration.
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Distinct Role of Macrophages in Different Tumor Microenvironments

TL;DR: The evidence for differential regulation of TAMs in these microenvironments is discussed and an overview of current attempts to target or use TAMs for therapeutic purposes is provided.
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Tumor Cell Metabolism: Cancer's Achilles' Heel

TL;DR: The peculiarities of tumor cell metabolism are reviewed to discuss the alterations in signal transduction pathways and/or enzymatic machineries that account for metabolic reprogramming of transformed cells.
References
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The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

TL;DR: It is indicated that the interaction between HIF-1 and pVHL is iron dependent, and that it is necessary for the oxygen-dependent degradation of HIF α-subunits, which may underlie the angiogenic phenotype of VHL-associated tumours.
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Measurement of Cutaneous Inflammation: Estimation of Neutrophil Content with an Enzyme Marker

TL;DR: It is demonstrated that MPO can be used as a marker for skin neutrophil content: it is recoverable from skin in soluble form, and is directly related to neutrophIL number.
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Conditional gene targeting in macrophages and granulocytes using LysMcre mice.

TL;DR: The generation of mice that express Cre in myeloid cells due to targeted insertion of the cre cDNA into their endogenous M lysozyme locus is reported, allowing for both specific and highly efficient Cre–mediated deletion of loxP–flanked target genes in myELoid cells.
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HIF-1 alpha is required for solid tumor formation and embryonic vascularization.

TL;DR: The essential role of HIF‐1α in controlling both embryonic and tumorigenic responses to variations in microenvironmental oxygenation is demonstrated.
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The expression and distribution of the hypoxia-inducible factors HIF-1α and HIF-2α in normal human tissues, cancers, and tumor-associated macrophages

TL;DR: In the majority of solid tumors examined, including bladder, brain, breast, colon, ovarian, pancreatic, prostate, and renal carcinomas, nuclear expression of HIF-1α and -2α was observed in varying subsets of the tumor cells.
Related Papers (5)
Trending Questions (2)
How deletion of hif 1 alpha vegf and vhl in macrophages and neutrophils does not affect their number?

Deletion of HIF-1alpha, VEGF, and VHL in macrophages and neutrophils does not affect their number, but impairs their function and survival.

How HIF-1α in regulating glycolytic capacity in myeloid cells,?

HIF-1α is essential for regulating glycolytic capacity in myeloid cells, and its absence leads to a drastic reduction in the cellular ATP pool.