Functional role of intracellular labile zinc in pulmonary endothelium
Abstract After iron, zinc is the most abundant essential trace metal. Intracellular zinc ([Zn]i) is maintained across a wide range of cells and species in a tight quota (100 to 500 μM) by a dynamic process of transport, intracellular vesicular storage, and binding to a large number of proteins (estimated at 3–10% of human proteome). As such, zinc is an integral component of numerous metalloenzymes, structural proteins, and transcription factors. It is generally assumed that a vanishingly small component of [Zn]i, referred to as free or labile zinc, and operationally defined as the pool sensitive to chelation (by agents such as N, N, N’, N’-tetrakis [2-pyridylmethyl] ethylenediamine [TPEN]) and capable of detection by a variety of chemical and genetic sensors, participates in signal transduction pathways. Zinc deficiencies, per se, can arise from acquired (malnutrition, alcoholism) or genetic (mutations in molecules affecting zinc homeostasis, the informative and first example being acrodermatitis enteropathica) factors or as a component of various diseases (e.g., sickle cell disease, cystic fibrosis, sepsis). Hypozincemia has profound effects on developing humans, and all facets of physiological function (neuronal, endocrine, immunological) are affected, although considerably less is known regarding cardiovascular pathophysiology. In this review, we provide an update on current knowledge of molecular and cellular aspects of zinc homeostasis and then focus on implications of zinc signaling in pulmonary endothelium as it relates to programmed cell death, altered contractility, and septic and aseptic injury to this segment of the lung..
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2012 |
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| Erschienen: |
2012 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:2 |
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| Sprache: |
en |
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| Beteiligte Personen: |
Thambiayya, Kalidasan [VerfasserIn] |
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| Links: |
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| doi: |
10.4103/2045-8932.105032 |
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| funding: |
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| PPN (Katalog-ID): |
JST135547989 |
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| 245 | 1 | 0 | |a Functional role of intracellular labile zinc in pulmonary endothelium |
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| 520 | |a Abstract After iron, zinc is the most abundant essential trace metal. Intracellular zinc ([Zn]i) is maintained across a wide range of cells and species in a tight quota (100 to 500 μM) by a dynamic process of transport, intracellular vesicular storage, and binding to a large number of proteins (estimated at 3–10% of human proteome). As such, zinc is an integral component of numerous metalloenzymes, structural proteins, and transcription factors. It is generally assumed that a vanishingly small component of [Zn]i, referred to as free or labile zinc, and operationally defined as the pool sensitive to chelation (by agents such as N, N, N’, N’-tetrakis [2-pyridylmethyl] ethylenediamine [TPEN]) and capable of detection by a variety of chemical and genetic sensors, participates in signal transduction pathways. Zinc deficiencies, per se, can arise from acquired (malnutrition, alcoholism) or genetic (mutations in molecules affecting zinc homeostasis, the informative and first example being acrodermatitis enteropathica) factors or as a component of various diseases (e.g., sickle cell disease, cystic fibrosis, sepsis). Hypozincemia has profound effects on developing humans, and all facets of physiological function (neuronal, endocrine, immunological) are affected, although considerably less is known regarding cardiovascular pathophysiology. In this review, we provide an update on current knowledge of molecular and cellular aspects of zinc homeostasis and then focus on implications of zinc signaling in pulmonary endothelium as it relates to programmed cell death, altered contractility, and septic and aseptic injury to this segment of the lung. | ||
| 540 | |a © 2012 by the Pulmonary Vascular Research Institute. All rights reserved. | ||
| 650 | 4 | |a zinc homeostasis | |
| 650 | 4 | |a pulmonary endothelium | |
| 650 | 4 | |a apoptosis | |
| 650 | 4 | |a SLC39A14 or ZIP14 | |
| 650 | 4 | |a metallothionien (MT) | |
| 650 | 4 | |a acute lung injury (ALI) | |
| 650 | 4 | |a Physical sciences |x Chemistry |x Chemical elements |x Transition metals |x Zinc | |
| 650 | 4 | |a Biological sciences |x Biology |x Cytology |x Cell biology |x Cell physiology |x Cell death |x Apoptosis | |
| 650 | 4 | |a Biological sciences |x Biology |x Physiology |x System physiology |x Cardiovascular physiology |x Circulatory system |x Cardiovascular system |x Blood vessels |x Endothelium | |
| 650 | 4 | |a Biological sciences |x Biology |x Cytology |x Cell biology |x Cells |x Epithelial cells |x Endothelial cells | |
| 650 | 4 | |a Health sciences |x Medical conditions |x Diseases |x Skin diseases |x Dermatitis |x Acrodermatitis | |
| 650 | 4 | |a Biological sciences |x Biology |x Physiology |x Physiological regulation |x Homeostasis | |
| 650 | 4 | |a Biological sciences |x Biology |x Anatomy |x Respiratory system |x Lungs | |
| 650 | 4 | |a Biological sciences |x Biology |x Cytology |x Cell biology |x Cells |x Epithelial cells | |
| 650 | 4 | |a Behavioral sciences |x Sociology |x Human societies |x Social institutions |x Families |x Family members | |
| 650 | 4 | |a Biological sciences |x Biology |x Zoology |x Animals |x Mammals |x Rodents |x Mice |x Review Article | |
| 655 | 4 | |a research-article | |
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| 700 | 1 | |a St. Croix, Claudette M. |e verfasserin |4 aut | |
| 700 | 1 | |a Pitt, Bruce R. |e verfasserin |4 aut | |
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