ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
Lipocalin-2 mediates the rejection of neural transplants.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- RNA Interference and Its Key Targets for Spinal Cord Injury Therapy: What Is Known So Far?International journal of molecular sciences · 2025Review
- The interaction of lipocalin-2 and astrocytes in neuroinflammation: mechanisms and therapeutic application.Frontiers in immunology · 2024Review
- DUSP6 Deficiency Attenuates Neurodegeneration after Global Cerebral Ischemia.International journal of molecular sciences · 2023Article
- Up-regulation of LCN2 in the anterior cingulate cortex contributes to neural injury-induced chronic pain.Frontiers in cellular neuroscience · 2023Article
- An exome-wide study of renal operational tolerance.Frontiers in medicine · 2022Article
- Lipocalin-2 and Cerebral Stroke.Frontiers in molecular neuroscience · 2022Review
- Chronic cerebral lipocalin 2 exposure elicits hippocampal neuronal dysfunction and cognitive impairment.Brain, behavior, and immunity · 2021Article
- Lipocalin-2 mediates the rejection of neural transplants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipocalin-2 (LCN2) has been implicated in promoting apoptosis and neuroinflammation in neurological disorders; however, its role in neural transplantation remains unknown. In this study, we cultured and differentiated Lund human mesencephalic (LUHMES) cells into human dopaminergic-like neurons and found that LCN2 mRNA was progressively induced in mouse brain after the intrastriatal transplantation of human dopaminergic-like neurons. The induction of LCN2 protein was detected in a subset of astrocytes and neutrophils infiltrating the core of the engrafted sites, but not in neurons and microglia. LCN2-immunoreactive astrocytes within the engrafted sites expressed lower levels of A1 and A2 astrocytic markers. Recruitment of microglia, neutrophils, and monocytes after transplantation was attenuated in LCN2 deficiency mice. The expression of M2 microglial markers was significantly elevated and survival of engrafted neurons was markedly improved after transplantation in LCN2 deficiency mice. Brain type organic cation transporter (BOCT), the cell surface receptor for LCN2, was induced in dopaminergic-like neurons after differentiation, and treatment with recombinant LCN2 protein directly induced apoptosis in dopaminergic-like neurons in a dose-dependent manner. Our results, therefore, suggested that LCN2 is a neurotoxic factor for the engrafted neurons and a modulator of neuroinflammation. LCN2 inhibition may be useful in reducing rejection after neural transplantation.
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