Midkine is regulated by hypoxia and causes pulmonary vascular remodeling
Paul R. Reynolds,Michael L. Mucenski,Timothy D. Le Cras,William C. Nichols,Jeffrey A. Whitsett +4 more
TLDR
Data provide a model wherein the respiratory epithelium responds to hypoxia via HIF-1α-dependent regulation of MK, enhancing myocardin expression to influence pulmonary vascular gene expression.About:
This article is published in Journal of Biological Chemistry.The article was published on 2004-08-27 and is currently open access. It has received 161 citations till now. The article focuses on the topics: Myocardin & Lung morphogenesis.read more
Citations
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Neurovascular mechanisms and blood–brain barrier disorder in Alzheimer’s disease
TL;DR: In this article, the role of the neurovascular unit and molecular mechanisms in vascular cells behind Alzheimer's disease and CAA pathogenesis was discussed. But, the authors did not consider the effect of microglia and perivascular macrophages in Aβ clearance from the brain.
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Oxygen-dependent regulation of mitochondrial respiration by hypoxia-inducible factor 1
TL;DR: COX subunit switching occurs in yeast, but by a completely different regulatory mechanism, suggesting that selection for O2-dependent homoeostatic regulation of mitochondrial respiration is ancient and likely to be shared by all eukaryotic organisms.
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Hypoxia-Inducible Factor 1 and Cardiovascular Disease
TL;DR: Analysis of animal models suggests that by activation of these homeostatic mechanisms, HIF-1 plays a critical protective role in the pathophysiology of ischemic heart disease and pressure-overload heart failure.
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The Transcription Factor Gene Nfib Is Essential for both Lung Maturation and Brain Development
George Steele-Perkins,Celine Plachez,Kenneth G. Butz,Guanhu Yang,Cindy J. Bachurski,Stephen L. Kinsman,E. David Litwack,Linda J. Richards,Richard M. Gronostajski +8 more
TL;DR: It is shown that Nfib-deficient mice possess unique defects in lung maturation and exhibit callosal agenesis and forebrain defects that are similar to, but more severe than, those seen in Nfia- deficient animals.
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Neurovascular Dysfunction and Faulty Amyloid β-Peptide Clearance in Alzheimer Disease
TL;DR: The data reviewed here support an essential role of the neurovascular and BBB mechanisms in AD pathogenesis, and focus on blood-brain barrier dysfunction, decreased cerebral blood flow, and impaired vascular clearance of Aβ from brain.
References
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A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation.
Gregg L. Semenza,Guang L. Wang +1 more
TL;DR: A functionally tripartite, 50-nt hypoxia-inducible enhancer which binds several nuclear factors, one of which is induced by Hypoxia via de novo protein synthesis.
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Regulation of hypoxia-inducible factor 1α is mediated by an O2-dependent degradation domain via the ubiquitin-proteasome pathway
TL;DR: The identification of an oxygen-dependent degradation (ODD) domain within HIF-1alpha that controls its degradation by the ubiquitin-proteasome pathway is reported and may provide a means of controlling gene expression by changes in oxygen tension.
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General involvement of hypoxia-inducible factor 1 in transcriptional response to hypoxia.
Guang L. Wang,Gregg L. Semenza +1 more
TL;DR: It is demonstrated that Hif-1 DNA binding activity is also induced by hypoxia in a variety of mammalian cell lines in which the EPO gene is not transcribed, providing evidence that HIF-1 and its recognition sequence are common components of a general mammalian cellular response to Hypoxia.
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HIF-1, O2, and the 3 PHDs: How Animal Cells Signal Hypoxia to the Nucleus
TL;DR: A molecular basis for O(2)-regulated expression of the HIF-1 alpha subunit has now been determined, providing a mechanism for changes in gene expression in response to changes in cellular oxygenation.