Rat cerebral endothelial cells express trk C and are regulated by neurotrophin-3

Takeo, Chikari; Nakamura, Susumu; Tanaka, Tomoaki; Uchida, Daigaku; Noguchi, Yoshihiko; Nagao, Toshitaka; Saitō, Yasushi; Tatsuno, Ichiro

doi:10.1016/s0006-291x(03)00770-8

Cited by 24 publications

(18 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is also widely expressed by neurons in the PNS and the ENS (4,32,35). TrkC is expressed in endothelial cells, dendritic cells, glial Schwann cells, and astrocytes (16,20,21,37,38), in addition to neurons. The expression of TrkC is in contrast to that of TrkA, which earlier studies showed to be a T. cruzi cellular invader (12).…”

Section: Discussionmentioning

confidence: 99%

Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells

2011

View full text Add to dashboard Cite

Trypanosoma cruzi, the agent of Chagas' disease, infects a variety of mammalian cells in a process that includes multiple cycles of intracellular division and differentiation starting with host receptor recognition by a parasite ligand(s). Earlier work in our laboratory showed that the neurotrophin-3 (NT-3) receptor TrkC is activated by T. cruzi surface trans-sialidase, also known as parasite-derived neurotrophic factor (PDNF). However, it has remained unclear whether TrkC is used by T. cruzi to enter host cells. Here, we show that a neuronal cell line (PC12-NNR5) relatively resistant to T. cruzi became highly susceptible to infection when overexpressing human TrkC but not human TrkB.

show abstract

Section: Discussionmentioning

confidence: 99%

Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells

2011

View full text Add to dashboard Cite

show abstract

“…In the present study, we used CECs isolated from rat brain with the Percoll-gradient method as reported (8). More than 95% of these cultured cells were immunohistochemically stained by the antibody against vWf, and showed the ability to take up oxidized LDL, both specific markers for endothelial cells (9,11).…”

Section: Resultsmentioning

confidence: 99%

“…Rat CECs were isolated and cultured as described previously (8). Briefly, the isolated brains from 3-to 5-weekold male Wistar rats were dissected out and minced into small pieces that were then incubated with dispase and collagenase.…”

Section: Cell Culturesmentioning

confidence: 99%

“…The cells were collected, washed several times with PBS, and cultured in DMEM with 20% FBS, endothelial cell growth factor (ECGF) (150 µg/ml), penicillin-streptomycin mixture (50 U/ml) and porcine heparin (10 U/ml). AECs were isolated from the thoracic aorta of 3-to 5-week-old Wistar rats as described previously (8), and cultured in Medium 199 supplemented with 10% FBS, the penicillin-streptomycin mixture (50 U/ml), endothelial growth supplement (50 µg/ml), and porcine heparin (10 U/ml). Both endothelial cells were incubated at 37°C in a humidified atmosphere containing 5% CO2.…”

Section: Cell Culturesmentioning

confidence: 99%

See 1 more Smart Citation

Analysis of Genes Dominantly Expressed in Rat Cerebral Endothelial Cells Using Suppression Subtractive Hybridization

Shibata

Misawa

Takeo

et al. 2005

JAT

Self Cite

View full text Add to dashboard Cite

In mammals, a fully developed, highly branched vascular system specialized for each particular organ or tissue is essential for obtaining metabolic nutrients supply. The formation of a blood-brain barrier that protects against environmental insults is a distinguishing feature of the brain's vascular system. Since this is accomplished by cerebral endothelial cells (CECs), we analyzed the genes specifically and/or dominantly expressed in rat CECs using Suppression Subtractive Hybridization (SSH). We found 39 genes specifically and/or dominantly expressed in CECs. 24 genes of known function (thrombospondin-2, vimentin, etc.), 13 genes of known sequence but unknown function including 7 of ESTs (SNERG1, rat GPCR, etc.), and 2 novel genes. The physiological significance of these genes in CECs has been under investigation. SSH is useful for identifying genes regulated in an organ-specific manner in cells such as CECs to obtain clarification of their physiological roles. J Atheroscler Thromb, 2005; 12: 330-337.

show abstract

“…A remarkable feature in this study was the occurrence of some capillaries in the injury/graft site. Furthermore, the cells in the injury/graft comprising the endothelial cells, neurons, astrocytes and oligodendrocytes expressed NT‐3's high‐affinity receptor TrkC 43, 44. This suggests that the migration of endogenous cells may be directly induced by the interaction of ligand and receptor 45.…”

Section: Discussionmentioning

confidence: 99%

Neurotrophin‐3 released from implant of tissue‐engineered fibroin scaffolds inhibits inflammation, enhances nerve fiber regeneration, and improves motor function in canine spinal cord injury

Che

Zeng

et al. 2018

J Biomedical Materials Res

View full text Add to dashboard Cite

Spinal cord injury (SCI) normally results in cell death, scarring, cavitation, inhibitory molecules release, etc., which are regarded as a huge obstacle to reconnect the injured neuronal circuits because of the lack of effective stimulus. In this study, a functional gelatin sponge scaffold was used to inhibit local inflammation, enhance nerve fiber regeneration, and improve neural conduction in the canine. This scaffold had good porosity and modified with neurotrophin‐3 (NT‐3)/fibroin complex, which showed sustained release in vitro. After the scaffold was transplanted into canine spinal cord hemisection model, hindlimb movement, and neural conduction were improved evidently. Migrating host cells, newly formed neurons with associated synaptic structures together with functional blood vessels with intact endothelium in the regenerating tissue were identified. Taken together, the results demonstrated that using bioactive scaffold could establish effective microenvironment stimuli for endogenous regeneration, providing a potential and practical strategy for treatment of spinal cord injury. © 2018 The Authors Journal of Biomedical Materials Research Part A Published by Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 2158‐2170, 2018.

show abstract

Rat cerebral endothelial cells express trk C and are regulated by neurotrophin-3

Cited by 24 publications

References 32 publications

Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells

Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells

Analysis of Genes Dominantly Expressed in Rat Cerebral Endothelial Cells Using Suppression Subtractive Hybridization

Neurotrophin‐3 released from implant of tissue‐engineered fibroin scaffolds inhibits inflammation, enhances nerve fiber regeneration, and improves motor function in canine spinal cord injury

Contact Info

Product

Resources

About