Delivery of ferric ion to mouse spermatozoa is mediated by lipocalin internalization

Elangovan, Namasivayam; Lee, Ying-Chu; Tzeng, Woan-Fang; Chu, Shao‐I

doi:10.1016/j.bbrc.2004.05.091

Cited by 34 publications

(30 citation statements)

References 32 publications

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“…There have been reports implicating lipocalin 2 as an enhancer of sperm motility (23), through the delivery and internalization of ferric ion into mouse spermatozoa (24). Consistent with these findings, we observed that female Lcn2 Ϫ/Ϫ mice were delayed in litter-bearing.…”

Section: Discussionsupporting

confidence: 91%

Lipocalin 2-deficient mice exhibit increased sensitivity toEscherichia coliinfection but not to ischemia-reperfusion injury

Berger

Togawa

Duncan

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

416

402

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Diverse functions have been reported for lipocalin 2. To investigate these functions in vivo, we generated gene-targeted lipocalin 2-deficient mice (Lcn2 ؊/؊ mice). In vitro studies have suggested that lipocalin 2 is important for cellular apoptosis induced by IL-3 withdrawal, and for the induction of kidney differentiation during embryogenesis. Analysis of Lcn2 ؊/؊ mice showed normal cell death upon IL-3 withdrawal and normal kidney development. However, we found that Lcn2 ؊/؊ mice exhibited an increased susceptibility to bacterial infections, in keeping with the proposed function of lipocalin 2 in iron sequestration. Neutrophils isolated from Lcn2 ؊/؊ mice showed significantly less bacteriostatic activity compared with WT controls. The bacteriostatic property of the WT neutrophils was abolished by the addition of exogenous iron, indicating that the main function of lipocalin 2 in the antibacterial innate immune response is to limit this essential element. Another important function ascribed to lipocalin 2 has been its protective role against kidney ischemia-reperfusion injury. We analyzed Lcn2 ؊/؊ mice using a mouse model for severe renal failure and could not detect any significant differences compared with their WT littermates.24p3 ͉ bacteriostatic ͉ kidney ischemia-reperfusion injury ͉ NGAL

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Section: Discussionsupporting

confidence: 91%

Lipocalin 2-deficient mice exhibit increased sensitivity toEscherichia coliinfection but not to ischemia-reperfusion injury

Berger

Togawa

Duncan

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

416

402

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“…LCN2 bound to the sperm membrane (Fig. 5D, middle), which was consistent with a previous report (Elangovan et al, 2004). This binding of LCN2 was suppressed by cinnamycin, a peptide toxin derived from Streptomyces that specifically binds to PE (Zhao, 2011;Makino et al, 2003), indicating that LCN2 binds to sperm membrane via PE, and possibly PPPE or SSPE (Fig.…”

Section: Lcn2 Binds To Membrane Pesupporting

confidence: 91%

“…A previous report described that LCN2 binds to the sperm surface, and is then internalized and distributed throughout the cytosol (Elangovan et al, 2004). It is well known that PE is a major phospholipid of the inner leaflet of the plasma membrane, but is present in low quantities in the outer leaflet, leading to the asymmetric localization of phospholipid.…”

Section: Discussionmentioning

confidence: 99%

“…S2) and performed further analyses in vitro. In a previous study, it was reported that LCN2 is expressed in the epididymis (Elangovan et al, 2004). Thus, to exclude epididymal LCN2 and examine LCN2 functions quantitatively by adjusting the protein concentration, we used Lcn2 knockout mouse sperm in the following studies.…”

Section: Lcn2 Promotes Sperm Capacitation In Vitromentioning

confidence: 99%

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Lipocalin 2 binds to membrane phosphatidylethanolamine to induce lipid raft movement in a PKA-dependent manner and modulates sperm maturation

et al. 2014

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Mammalian sperm undergo multiple maturation steps after leaving the testis in order to become competent for fertilization, but the molecular mechanisms underlying this process remain unclear. In terms of identifying factors crucial for these processes in vivo, we found that lipocalin 2 (Lcn2), which is known as an innate immune factor inhibiting bacterial and malarial growth, can modulate sperm maturation. Most sperm that migrated to the oviduct of wild-type females underwent lipid raft reorganization and glycosylphosphatidylinositol-anchored protein shedding, which are signatures of sperm maturation, but few did so in Lcn2 null mice. Furthermore, we found that LCN2 binds to membrane phosphatidylethanolamine to reinforce lipid raft reorganization via a PKA-dependent mechanism and promotes sperm to acquire fertility by facilitating cholesterol efflux. These observations imply that mammals possess a mode for sperm maturation in addition to the albumin-mediated pathway.

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“…Lcn2 also plays a role in normal iron metabolism (Elangovan et al, 2004). The proper functioning of Lcn2 may be especially important for myelin and oligodendrocytes, which contain particularly high levels of iron.…”

Section: Lipocalin 2-lipocalinmentioning

confidence: 99%

Effects of melatonin and age on gene expression in mouse CNS using microarray analysis

Sharman

Bondy

Sharman

et al. 2007

Neurochemistry International

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The expression levels of a number of genes associated with inflammation and immune function change with advancing age. Melatonin modulates gene expression levels of several of these genes. Therefore the declining levels of melatonin associated with age may play a role in the physiological effects of aging. We used oligonucleotide microarrays to measure age-related changes in mRNA expression in the murine CNS, and to study the effect of prolonged administration of dietary melatonin upon these changes. CB6F1 male mice were fed 40ppm melatonin for 2.1 months prior to sacrifice at age 26.5 months, and compared with both age-matched controls and young, 4.5-monthold untreated controls. Total RNA was extracted from whole brain (excluding cerebellum and brain stem) and individual samples were hybridized to Affymetrix Mouse 430-2.0 arrays. The expression of a substantial number of genes was modulated by melatonin treatment and changes in selected genes were validated by quantitative reverse transcription polymerase chain reaction (qRT-PCR). A subset of these genes did not change with age. Conversely, some genes modulated by age were also modulated by melatonin treatment. In general melatonin treatment drove the expression levels of these genes closer to the expression levels detected in the younger animals. Notably, the abundance of lipocalin 2 (Lcn2) mRNA increased with age and was decreased in old animals treated with melatonin. Lcn2 is a member of the acute phase response family of proteins and its mRNA levels in the brain increase in response to inflammation. Many of the genes with expression reduced by melatonin are involved in inflammation and the immune system. This suggests that melatonin treatment may influence the inflammatory responses of old animals, driving them to resemble more closely those occurring in young animals.

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Delivery of ferric ion to mouse spermatozoa is mediated by lipocalin internalization

Cited by 34 publications

References 32 publications

Lipocalin 2-deficient mice exhibit increased sensitivity toEscherichia coliinfection but not to ischemia-reperfusion injury

Lipocalin 2-deficient mice exhibit increased sensitivity toEscherichia coliinfection but not to ischemia-reperfusion injury

Lipocalin 2 binds to membrane phosphatidylethanolamine to induce lipid raft movement in a PKA-dependent manner and modulates sperm maturation

Effects of melatonin and age on gene expression in mouse CNS using microarray analysis

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