Expression and localisation of brain-type organic cation transporter (BOCT/24p3R/LCN2R) in the normal rat hippocampus and after kainate-induced excitotoxicity

Chia, Wan-Jie; Tan, Francis Chee Kuan; Ong, Wei‐Yi; Dawe, Gavin S.

doi:10.1016/j.neuint.2015.04.009

Cited by 23 publications

(15 citation statements)

References 53 publications

(64 reference statements)

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“…Under physiological conditions in a murine model, the expression of LCN2 mRNA and LCN2 protein in the brain appears to be very low to absent . However, only a few studies have reported LCN2 protein expression in the hippocampus, cortex and amygdala of normal mice and the hippocampus of normal adult rats …”

Section: Lcn2 With Respect To Physiological Condition and Cognitionmentioning

confidence: 97%

“…6,8,11,[24][25][26] However, only a few studies have reported LCN2 protein expression in the hippocampus, 27,28 cortex and amygdala 28 of normal mice and the hippocampus of normal adult rats. 10 Several studies have shown no significant difference between the cognitive function of wild-type mice and LCN2 null mice (Table 1). 11,24,25,30 These findings suggest that LCN2 may not have a role in the cognitive process under normal physiological conditions.…”

Section: ↔ Cognitionmentioning

confidence: 99%

“…The expression of 24p3R has been reported in the choroid plexus, neurones and astrocytes . However, it has been found primarily in the hippocampus . Another receptor called megalin, or LRP‐2, is a low‐density lipoprotein with multi‐ligand binding sites located in the ependymal cells in the ventricular wall of the brain, endothelial cells and choroid plexus .…”

Section: Introductionmentioning

confidence: 99%

“…22 Although previous studies have shown that LCN2 is undetectable in the brain under physiological conditions, 6,8,11,[24][25][26] other studies showed that LCN2 is expressed only in specific brain regions. 10,27,28 In addition, the up-regulation of brain LCN2 expression has been found to occur in response to injury and inflammation 7 and it has been suggested that LCN2 could modulate cognitive function in Alzheimer's disease (AD). 29 Despite this, from the available evidence to date, any association between LCN2 and cognitive function remains unclear.…”

mentioning

confidence: 99%

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Lipocalin‐2: Its perspectives in brain pathology and possible roles in cognition

Pinyopornpanish

Chattipakorn

2019

J Neuroendocrinology

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Lipocalin‐2 (LCN2) has been known to play an important role in pathological conditions, specifically in response to inflammation, infection and injury to cells. Recently, several research teams have been interested in investigating its association with cognition during the progression of pathology. Previous studies have demonstrated that LCN2 is not correlated with cognitive function under normal physiological conditions, although LCN2 has been negatively associated with cognition and some neuropathologies. Increasing LCN2 production is associated with reduced cognitive performance in a rodent model. However, further studies are needed to explore the potential underlying mechanisms of LCN2 on cognitive dysfunction, as well as its clinical relevance. This review aims to summarise the evidence available from in vitro, in vivo and clinical studies concerning the possible role of LCN2 on cognitive function following the onset of pathological conditions. Any contradictory evidence is also assessed and presented.

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Section: Lcn2 With Respect To Physiological Condition and Cognitionmentioning

confidence: 97%

Section: ↔ Cognitionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Lipocalin‐2: Its perspectives in brain pathology and possible roles in cognition

Pinyopornpanish

Chattipakorn

2019

J Neuroendocrinology

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“…Such reduced sensitivity correlates with the downregulation of LCN‐2R/24p3R mRNA levels in p50KO ahNPC. Although it has been demonstrated that LCN‐2R is constitutively expressed at high levels in brain, including the hippocampus (Chia et al, ), to our knowledge, this is the first demonstration that this receptor is expressed in aNPC. Interestingly, NF‐κB signaling activation has been shown to occur downstream of LCN‐2/24p3R activation (Dizin et al, ).…”

Section: Discussionmentioning

confidence: 67%

Cell autonomous and noncell‐autonomous role of NF‐κB p50 in astrocyte‐mediated fate specification of adult neural progenitor cells

Cvijetic

Bortolotto

Manfredi

et al. 2016

Glia

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In previous work, we demonstrated that NF-κB p50 acts as crucial regulator of adult hippocampal neural progenitor cells (ahNPC). Indeed, NF-κB p50 knockout (KO) mice are characterized by remarkably reduced hippocampal neurogenesis. As a follow up to that work, herein we show that when cultured in vitro, ahNPC from wild type (WT) and p50KO mice are not significantly different in their neurogenic potential. This observation prompted us to investigate cell-autonomous and noncell-autonomous consequences of p50 absence on neuronal fate specification of ahNPC. In particular, we focused our attention on astrocytes, known to provide soluble proneurogenic signals, and investigated the influence of WT and p50KO astrocyte conditioned media (ACM) on WT and p50KO ahNPC differentiation. Interestingly, while WT ACM promoted both neuronal and astroglial differentiations, p50KO ACM only supported astroglial differentiation of WT ahNPC. By using a LC-MS/MS approach, we identified some proteins, which are significantly upregulated in p50KO compared with WT astrocytes. Among them, lipocalin-2 (LCN-2) was recognized as a novel astroglial-derived signal regulating neuronal fate specification of ahNPC. Interestingly, LCN-2 proneurogenic effect was greatly reduced in p50KO NPC, where LCN-2 receptor gene expression appeared downregulated. In addition to that, we demonstrated p50KO NPC unresponsiveness to both neuronal and astroglial fate specification signals from WT and p50KO ACM, and we identified a reduced expression of α2δ1, a thrombospondin-1 receptor, as another phenotypic change occurring in ahNPC in the absence of p50. Altogether, our data suggest that dysregulated NPC-astrocyte communication may contribute to a reduced hippocampal neurogenesis in p50KO mice in vivo. GLIA 2016 GLIA 2017;65:169-181.

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Integrated Bioinformatics Analysis for the Identification of Key Molecules and Pathways in the Hippocampus of Rats After Traumatic Brain Injury

et al. 2020

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Expression and localisation of brain-type organic cation transporter (BOCT/24p3R/LCN2R) in the normal rat hippocampus and after kainate-induced excitotoxicity

Cited by 23 publications

References 53 publications

Lipocalin‐2: Its perspectives in brain pathology and possible roles in cognition

Lipocalin‐2: Its perspectives in brain pathology and possible roles in cognition

Cell autonomous and noncell‐autonomous role of NF‐κB p50 in astrocyte‐mediated fate specification of adult neural progenitor cells

Integrated Bioinformatics Analysis for the Identification of Key Molecules and Pathways in the Hippocampus of Rats After Traumatic Brain Injury

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