Transport of Human Lactoferrin into Mouse Brain: Administration Routes and Distribution

Kopaeva, Marina Yu.; Cherepov, Anton; Zarayskaya, Irina Yu.; Nesterenko, Mikhail

doi:10.1007/s10517-019-04572-3

Cited by 14 publications

(11 citation statements)

References 22 publications

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“…As mentioned above, Lf was found in the lesion areas of a variety of neurodegenerative diseases, indicating that it is closely related to the pathogenesis of neurodegenerative diseases. Due to the presence of LfR on brain capillary endothelial cells and neurons, exogenous Lf can easily cross the blood-brain barrier (BBB) and reach neural tissues; thus, Lf was successfully used as a potential brain-targeting delivery system [ 55 , 56 , 57 , 58 , 59 ]. Increasing numbers of studies indirectly suggest that the Lf-mediated neuroprotection against neurodegenerative disorders is attributed to its biological characteristics.…”

Section: Lf In Neurodegenerative Diseasesmentioning

confidence: 99%

“…Although the precise origin of Lf in AD remains unknown, a previous study suggested that the Lf protein is mainly synthesized in the brain by reactive microglia and/or infiltrating monocytes/macrophages [ 77 ], suggesting an endogenous neuroprotective mechanism. Of course, the possibility that some Lf protein is transported from peripheral circulation into the brain cannot be excluded [ 55 , 58 , 59 , 76 , 79 ]. The role of Lf in the brains of patients with AD remains to be further elucidated, but inhibiting the inflammatory response is at least one of its important functions.…”

Section: Lf In Neurodegenerative Diseasesmentioning

confidence: 99%

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A Review on Lactoferrin and Central Nervous System Diseases

Guo

2021

Cells

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Central nervous system (CNS) diseases are currently one of the major health issues around the world. Most CNS disorders are characterized by high oxidative stress levels and intense inflammatory responses in affected tissues. Lactoferrin (Lf), a multifunctional iron-binding glycoprotein, plays a significant role in anti-inflammatory, antibacterial, antiviral, reactive oxygen species (ROS) modulator, antitumor immunity, and anti-apoptotic processes. Previous studies have shown that Lf is abnormally expressed in a variety of neurological diseases, especially neurodegenerative diseases. Recently, the promotion of neurodevelopment and neuroprotection by Lf has attracted widespread attention, and Lf could be exploited both as an active therapeutic agent and drug nanocarrier. However, our understanding of the roles of Lf proteins in the initiation or progression of CNS diseases is limited, especially the roles of Lf in regulating neurogenesis. This review highlights recent advances in the understanding of the major pharmacological effects of Lf in CNS diseases, including neurodegenerative diseases, cerebrovascular disease, developmental delays in children, and brain tumors.

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Section: Lf In Neurodegenerative Diseasesmentioning

confidence: 99%

Section: Lf In Neurodegenerative Diseasesmentioning

confidence: 99%

A Review on Lactoferrin and Central Nervous System Diseases

Guo

2021

Cells

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“…За 24 часа до стимуляции, смены среды или фиксации в культуральную среду групп «KCl+Лф», «АК+Лф» и «ПК+Лф», соответственно, добавляли чЛф (1мг/мл). В работе был использован человеческий Лф, выделенный из женского молозива методом препаративной ионообменной хроматографии [8].…”

Section: материалы и методы исследованияunclassified

“…Ранее было показано, что электрическая стимуляция вызывает значительное увеличение экспрессии c-Fos в нейрональной культуре [6], а аппликация KCl -появление белка c-Fos в культурах срезов гиппокампа [7]. В наших предыдущих исследованиях методами иммуногистохимии были выявлены высокоспецифичные места связывания лактоферрина человека (чЛф) в ядрах нейронов в мозге мыши [8]. В то же время возможная связь между Лф и индукцией c-Fos на уровне отдельных клеток еще не изучена.…”

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Human lactoferrin enhances the expression of transcription factor c-Fos in neuronal cultures under stimulated conditions

Копаева¹,

Азиева²,

Cherepov³

et al. 2021

Nauchno-Prakticheskii Zhurnal «Patogenez»

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Целью настоящей работы стало исследование влияния лактоферрина (Лф) человека на экспрессию транскрипционного фактора c-Fos в первичных нейрональных культурах после физиологической стимуляции, определение клеточной локализации Лф человека и возможной колокализации экзогенного белка с индуцированной экспрессией c-Fos. Методы. Первичные диссоциированные клеточные культуры получали из гиппокампа головного мозга новорожденных мышей (Р0-Р1) линии С57Вl/6. Индукцию экспрессии белка c-Fos в клетках осуществляли путем трехкратного добавления 50 мМ KСl в культуральную среду на 8-й день культивирования in vitro. Анализ содержания c-Fos проводили иммунофлюоресцентным методом через 2 часа после стимуляции. Результаты. Лф детектировался как в цитоплазме, так и в ядрах отдельных клеток культуры после стимуляции KСl. В ядрах некоторых клеток была выявлена колокализация включения Лф и экспрессии c-Fos. Было обнаружено, что предварительное введение Лф в культуральную среду увеличивало количество клеток, экспрессирующих c-Fos после добавления 50 мМ KСl. The aims of this research were 1) to study the effect of human lactoferrin (Lf) on the expression of the c-Fos transcription factor in primary neuronal cultures after physiological stimulation; 2) to determine the cellular localization of human Lf and possible colocalization of an exogenous protein with induced c-Fos expression. Methods. Primary dissociated cell cultures were obtained from the hippocampus of newborn C57Bl/6 mice (P0-P1). The expression of c-Fos was induced by addition of 50 mM KCl to the culture medium at 8 day in vitro. c-Fos content was analyzed by immunofluorescence 2 hrs after stimulation. Results. Lf was detected in cytoplasm and in nuclei after stimulation KCl. Lf inclusion and c-Fos expression were colocalized in the nuclei of some cells. Thus, results showed that pretreatment with Lf led to increase in the number of cells expressing c-Fos after exposure to 50 mM KCl.

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“…LF has the capacity to penetrate into the brain parenchyma via receptor-mediated transcytosis [ 16 – 18 ]. Thus, exogenous administration of LF has been associated with improved spatial cognition through reductions in oxidative stress and inflammation in the hippocampus of aged mice [ 19 ], with reduced motor deficits in an induced mouse model of Parkinson disease (PD) [ 20 , 21 ] and with decreased amyloid-beta (Aβ) aggregation and enhanced cognition in transgenic mouse models of Alzheimer’s disease (AD) [ 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

Salivary lactoferrin is associated with cortical amyloid-beta load, cortical integrity, and memory in aging

et al. 2021

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Background Aging is associated with declining protective immunity and persistent low-grade inflammatory responses, which significantly contribute to Alzheimer’s disease (AD) pathogenesis. Detecting aging-related cerebral vulnerability associated with deterioration of the immune system requires from non-invasive biomarkers able to detect failures in the brain-immunity connection. Reduced levels of salivary lactoferrin (sLF), an iron-binding protein with immunomodulatory activity, have been related to AD diagnosis. However, it remains unknown whether decreased sLF is associated with increased cortical amyloid-beta (Aβ) load and/or with loss of cortical integrity in normal aging. Methods Seventy-four cognitively normal older adults (51 females) participated in the study. We applied multiple linear regression analyses to assess (i) whether sLF is associated with cortical Aβ load measured by 18F-Florbetaben (FBB)-positron emission tomography (PET), (ii) whether sLF-related variations in cortical thickness and cortical glucose metabolism depend on global Aβ burden, and (iii) whether such sLF-related cortical abnormalities moderate the relationship between sLF and cognition. Results sLF was negatively associated with Aβ load in parieto-temporal regions. Moreover, sLF was related to thickening of the middle temporal cortex, increased FDG uptake in the posterior cingulate cortex, and poorer memory. These associations were stronger in individuals showing the highest Aβ burden. Conclusions sLF levels are sensitive to variations in cortical Aβ load, structural and metabolic cortical abnormalities, and subclinical memory impairment in asymptomatic older adults. These findings provide support for the use of sLF as a non-invasive biomarker of cerebral vulnerability in the general aging population.

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Transport of Human Lactoferrin into Mouse Brain: Administration Routes and Distribution

Cited by 14 publications

References 22 publications

A Review on Lactoferrin and Central Nervous System Diseases

A Review on Lactoferrin and Central Nervous System Diseases

Human lactoferrin enhances the expression of transcription factor c-Fos in neuronal cultures under stimulated conditions

Salivary lactoferrin is associated with cortical amyloid-beta load, cortical integrity, and memory in aging

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