Lipocalin-2 (24p3/Neutrophil Gelatinase-associated Lipocalin (NGAL)) Receptor Is Expressed in Distal Nephron and Mediates Protein Endocytosis

Langelueddecke, Christian; Roussa, Eleni; Fenton, Robert A.; Wolff, Natascha A.; Lee, Wing-Kee; Thévenod, Frank

doi:10.1074/jbc.m111.308296

Cited by 97 publications

(154 citation statements)

References 60 publications

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“…However, it is also possible that hydroxamate and acid hydrazide moieties contribute to additional iron affinity of maduraferrin (45). (iii) Finally, in contrast to the study by Correnti et al, results from our laboratory as well as others have reported interaction of 24p3 with 24p3R (46)(47)(48). Thus, noninclusion of these reports that would otherwise support our conclusions makes it difficult to interpret the observations of Correnti et al Nonetheless, in light of their study, we extensively studied the complex formation of ferric iron salts with 2,5-DHBA in pH ranges of 2.5 to 9.0 at 298.15 K in water as a solvent using kinetic and equilibrium UV spectroscopy.…”

Section: Discussioncontrasting

confidence: 54%

Endogenous Siderophore 2,5-Dihydroxybenzoic Acid Deficiency Promotes Anemia and Splenic Iron Overload in Mice

Liu

Ciocea

Devireddy

2014

Molecular and Cellular Biology

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Eukaryotes produce a siderophore-like molecule via a remarkably conserved biosynthetic pathway. 3-OH butyrate dehydrogenase (BDH2), a member of the short-chain dehydrogenase (SDR) family of reductases, catalyzes a rate-limiting step in the biogenesis of the mammalian siderophore 2,5-dihydroxybenzoic acid (2,5-DHBA). Depletion of the mammalian siderophore by inhibiting expression of bdh2 results in abnormal accumulation of intracellular iron and mitochondrial iron deficiency in cultured mammalian cells, as well as in yeast cells and zebrafish embryos We disrupted murine bdh2 by homologous recombination to analyze the effect of bdh2 deletion on erythropoiesis and iron metabolism. bdh2 null mice developed microcytic anemia and tissue iron overload, especially in the spleen. Exogenous supplementation with 2,5-DHBA alleviates splenic iron overload in bdh2 null mice. Additionally, bdh2 null mice exhibit reduced serum iron. Although BDH2 has been proposed to oxidize ketone bodies, we found that BDH2 deficiency did not alter ketone body metabolism in vivo. In sum, our findings demonstrate a key role for BDH2 in erythropoiesis.

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Section: Discussioncontrasting

confidence: 54%

Endogenous Siderophore 2,5-Dihydroxybenzoic Acid Deficiency Promotes Anemia and Splenic Iron Overload in Mice

Liu

Ciocea

Devireddy

2014

Molecular and Cellular Biology

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“…NGAL was found constitutively synthesized during a narrow window of maturation in the granulocyte precursors in the bone marrow, and is stored in specific granules of mature neutrophils in complex with gelatinase (Kjeldsen et al, 1994), but has since been described in a variety of cell-types. Other cells known to produce NGAL are renal cells (Langelueddecke et al, 2012), endothelial cells (Hamzic et al, 2013), hepatic cells (Borkham-Kamphorst et al, 2011), cardiomyocytes (Yndestad et al, 2009) and neurons (Naude et al, 2012). NGAL is involved in anti-microbial defense by sequestering iron; in vitro studies have demonstrated that NGAL has a bacteriostatic effect via the binding of siderophore molecules, thereby restricting the availability of iron to bacteria (Goetz et al, 2002).…”

Section: Neutrophil Gelatinase-associated Lipocalin (Ngal)mentioning

confidence: 98%

The role of neutrophil gelatinase associated lipocalin (NGAL) as biological constituent linking depression and cardiovascular disease

Gouweleeuw

Naudé

Rots

et al. 2015

Brain, Behavior, and Immunity

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“…Indeed, the elevated residence time of cadmium in the body after intoxication is due to its trapping in the kidneys, and renal MT hydrolysis may release a form of cadmium that cannot be mobilized further and detoxified. In a similar way, another membrane receptor, 24p3R, internalizes metal-binding proteins, including MT, thus mediating cadmium toxicity [81]. 24p3R was initially described as the tight binding receptor for lipocalin-2, a siderophore-binding protein involved in iron handling, as part of the inflammatory response [82].…”

Section: Other Ways To Cross Membranesmentioning

confidence: 99%

The Bioinorganic Chemistry of Cadmium in the Context of Its Toxicity

Maret

Moulis

2012

Cadmium: From Toxicity to Essentiality

123

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Cadmium is known for its toxicity in animals and man as it is not used in these species. Its only role in biology is as a zinc replacement at the catalytic site of a particular class of carbonic anhydrases in some marine diatoms. The toxicity of cadmium continues to be a significant public health concern as cadmium enters the food chain and it is taken up by tobacco smokers. The biochemical basis for its toxicity has been the objective of research for over 50 years. Cadmium damages the kidneys, the lungs upon inhalation, and interferes with bone metabolism. Evidence is accumulating that it affects the cardiovascular system. Cadmium is classified as a human carcinogen. It generates oxidative stress. This chapter discusses the chemistry and biochemistry of cadmium(II) ions, the only important state of cadmium in biology. This background is needed to interpret the countless effects of cadmium in laboratory experiments with cultured cells or with animals with regard to their significance for human health. Evaluation of the risks of cadmium exposure and the risk factors that affect cadmium's biological effects in tissues is an on-going process. It appears that the more we learn about the biochemistry of cadmium and the more sensitive assays we develop for determining exposure, the lower we need to set the upper limits for exposure to protect those at risk. But proper control of cadmium's presence and interactions with living species and the environment still needs to be based on improved knowledge about the mechanisms of cadmium toxicity; the gaps in our knowledge in this area are discussed herein.

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Lipocalin-2 (24p3/Neutrophil Gelatinase-associated Lipocalin (NGAL)) Receptor Is Expressed in Distal Nephron and Mediates Protein Endocytosis

Cited by 97 publications

References 60 publications

Endogenous Siderophore 2,5-Dihydroxybenzoic Acid Deficiency Promotes Anemia and Splenic Iron Overload in Mice

Endogenous Siderophore 2,5-Dihydroxybenzoic Acid Deficiency Promotes Anemia and Splenic Iron Overload in Mice

The role of neutrophil gelatinase associated lipocalin (NGAL) as biological constituent linking depression and cardiovascular disease

The Bioinorganic Chemistry of Cadmium in the Context of Its Toxicity

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