ArticleJournal of molecular neuroscience : MN2013
Saturable leptin transport across the BBB persists in EAE mice.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Leptin as a Potential Modifier of Neuroinflammation: Contrasting Roles in Alzheimer's Disease and Multiple Sclerosis.International journal of molecular sciences · 2025Review
- Genetic causal role of body mass index in multiple neurological diseases.Scientific reports · 2024Article
- Obesity and Multiple Sclerosis-A Multifaceted Association.Journal of clinical medicine · 2021Review
- Multiple Sclerosis and Obesity: Possible Roles of Adipokines.Mediators of inflammation · 2016Review
- Sleep restriction impairs blood-brain barrier function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Leukocyte infiltration into spinal cord of EAE mice is attenuated by removal of endothelial leptin signaling.Brain, behavior, and immunity · 2014Article
- Loss of astrocytic leptin signaling worsens experimental autoimmune encephalomyelitis.Brain, behavior, and immunity · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We have shown that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, have upregulated leptin receptor expression in reactive astrocytes of the hippocampus, a region involved in sickness behavior. Leptin can exacerbate EAE when its serum concentration is high. Although leptin receptors in astrocytes modulate leptin transport across cultured endothelial cell monolayers, it is not known how leptin transport in EAE mice is regulated. Here, we determined brain and cervical spinal cord uptake of leptin in early and recovery stages of EAE, after either intravenous delivery or in situ brain perfusion of (125)I-leptin and the vascular marker (131)I-albumin. While increased vascular space and general blood-brain barrier (BBB) permeability after EAE were expected, the specific saturable transport system for leptin crossing the BBB also persisted. Moreover, there was upregulation of leptin transport in hippocampus and cervical spinal cord in the early stage of EAE, shown by higher leptin uptake in these regions and by competitive inhibition with coadministered excess unlabeled leptin. We conclude that EAE induced a time- and region-specific increase of leptin transport. The results provide a link between circulating leptin and enhanced leptin signaling that may play a crucial role in disease progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.