The Experts below are selected from a list of 11214 Experts worldwide ranked by ideXlab platform
Susan M Dymecki - One of the best experts on this subject based on the ideXlab platform.
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sonic hedgehog is required for vascular outgrowth in the hindbrain Choroid Plexus
Developmental Biology, 2010Co-Authors: Corinne M Nielsen, Susan M DymeckiAbstract:Critical to the exchange and metabolic functions served by tissues like brain Choroid plexi and lung is the coherent development of an epithelial sheet of large surface area in tight apposition to an extensive vascular bed. Here, we present functional experiments in the mouse demonstrating that Sonic hedgehog (Shh) produced by hindbrain Choroid Plexus epithelium induces the extensive vascular outgrowths and vascular surface area fundamental to Choroid Plexus functions, but does not induce the more specialized endothelial cell features of fenestrations and bore size. Our findings indicate that these Shh-dependent vascular elaborations occur even in the presence of Vegf and other established angiogenic factors, suggesting either that the levels of these factors are inadequate in the absence of Shh or that a different set of factors may be more essential to Choroid Plexus outgrowth. Transducing Shh signal is a perivascular cell – the pericyte – rather than the more integral vascular endothelial cell itself. Moreover, our findings suggest that hindbrain Choroid Plexus endothelial cells, as compared to other vascular endothelial cells, are more dependent upon pericytes for instruction. Thus, in addition to Shh acting on the progenitor pool for Choroid Plexus epithelial cells, as previously shown, it also acts on Choroid Plexus pericytes, and together serves the important role of coordinating the development of two disparate yet functionally dependent structures – the Choroid Plexus vasculature and its ensheathing epithelium.
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sonic hedgehog is required for vascular outgrowth in the hindbrain Choroid Plexus
Developmental Biology, 2010Co-Authors: Corinne M Nielsen, Susan M DymeckiAbstract:Critical to the exchange and metabolic functions served by tissues like brain Choroid plexi and lung is the coherent development of an epithelial sheet of large surface area in tight apposition to an extensive vascular bed. Here, we present functional experiments in the mouse demonstrating that Sonic hedgehog (Shh) produced by hindbrain Choroid Plexus epithelium induces the extensive vascular outgrowths and vascular surface area fundamental to Choroid Plexus functions, but does not induce the more specialized endothelial cell features of fenestrations and bore size. Our findings indicate that these Shh-dependent vascular elaborations occur even in the presence of Vegf and other established angiogenic factors, suggesting either that the levels of these factors are inadequate in the absence of Shh or that a different set of factors may be more essential to Choroid Plexus outgrowth. Transducing the Shh signal is a perivascular cell-the pericyte-rather than the more integral vascular endothelial cell itself. Moreover, our findings suggest that hindbrain Choroid Plexus endothelial cells, as compared to other vascular endothelial cells, are more dependent upon pericytes for instruction. Thus, in addition to Shh acting on the progenitor pool for Choroid Plexus epithelial cells, as previously shown, it also acts on Choroid Plexus pericytes, and together serves the important role of coordinating the development of two disparate yet functionally dependent structures-the Choroid Plexus vasculature and its ensheathing epithelium.
Corinne M Nielsen - One of the best experts on this subject based on the ideXlab platform.
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sonic hedgehog is required for vascular outgrowth in the hindbrain Choroid Plexus
Developmental Biology, 2010Co-Authors: Corinne M Nielsen, Susan M DymeckiAbstract:Critical to the exchange and metabolic functions served by tissues like brain Choroid plexi and lung is the coherent development of an epithelial sheet of large surface area in tight apposition to an extensive vascular bed. Here, we present functional experiments in the mouse demonstrating that Sonic hedgehog (Shh) produced by hindbrain Choroid Plexus epithelium induces the extensive vascular outgrowths and vascular surface area fundamental to Choroid Plexus functions, but does not induce the more specialized endothelial cell features of fenestrations and bore size. Our findings indicate that these Shh-dependent vascular elaborations occur even in the presence of Vegf and other established angiogenic factors, suggesting either that the levels of these factors are inadequate in the absence of Shh or that a different set of factors may be more essential to Choroid Plexus outgrowth. Transducing Shh signal is a perivascular cell – the pericyte – rather than the more integral vascular endothelial cell itself. Moreover, our findings suggest that hindbrain Choroid Plexus endothelial cells, as compared to other vascular endothelial cells, are more dependent upon pericytes for instruction. Thus, in addition to Shh acting on the progenitor pool for Choroid Plexus epithelial cells, as previously shown, it also acts on Choroid Plexus pericytes, and together serves the important role of coordinating the development of two disparate yet functionally dependent structures – the Choroid Plexus vasculature and its ensheathing epithelium.
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sonic hedgehog is required for vascular outgrowth in the hindbrain Choroid Plexus
Developmental Biology, 2010Co-Authors: Corinne M Nielsen, Susan M DymeckiAbstract:Critical to the exchange and metabolic functions served by tissues like brain Choroid plexi and lung is the coherent development of an epithelial sheet of large surface area in tight apposition to an extensive vascular bed. Here, we present functional experiments in the mouse demonstrating that Sonic hedgehog (Shh) produced by hindbrain Choroid Plexus epithelium induces the extensive vascular outgrowths and vascular surface area fundamental to Choroid Plexus functions, but does not induce the more specialized endothelial cell features of fenestrations and bore size. Our findings indicate that these Shh-dependent vascular elaborations occur even in the presence of Vegf and other established angiogenic factors, suggesting either that the levels of these factors are inadequate in the absence of Shh or that a different set of factors may be more essential to Choroid Plexus outgrowth. Transducing the Shh signal is a perivascular cell-the pericyte-rather than the more integral vascular endothelial cell itself. Moreover, our findings suggest that hindbrain Choroid Plexus endothelial cells, as compared to other vascular endothelial cells, are more dependent upon pericytes for instruction. Thus, in addition to Shh acting on the progenitor pool for Choroid Plexus epithelial cells, as previously shown, it also acts on Choroid Plexus pericytes, and together serves the important role of coordinating the development of two disparate yet functionally dependent structures-the Choroid Plexus vasculature and its ensheathing epithelium.
Lisa M Korst - One of the best experts on this subject based on the ideXlab platform.
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the isolated Choroid Plexus cyst
Obstetrics & Gynecology, 1998Co-Authors: Carol L Morcos, Naomi Greene, Kimberly D Gregory, Lawrence D. Platt, Dru E. Carlson, Lisa M KorstAbstract:Abstract Objective: To describe the karyotypes of a population of fetuses with Choroid Plexus cysts and compare affected fetuses with and without additional ultrasonographic findings. Methods: The study population included all patients undergoing second-trimester ultrasound examination in a prenatal diagnostic program between January 1993 and October 1995. The records of all cases in which a Choroid Plexus cyst was found were reviewed, and information was abstracted regarding the fetal karyotype and the presence of other sonographic abnormalities. Results: Two hundred ten cases of Choroid Plexus cysts were identified among 7617 patients (2.8%) who underwent second-trimester ultrasound examination. The majority of the cases (181, or 86%) involved isolated Choroid Plexus cysts and the remaining 29 (14%) were associated with additional ultrasonographic findings. Autosomal aneuploidy was found in one patient with an isolated Choroid Plexus cyst (trisomy 21) and in another with additional findings (trisomy 18); the mothers of both of these patients were at least 35 years old. For those fetuses with known outcome, the risk of aneuploidy with isolated Choroid Plexus cyst (one in 180) was not statistically significantly different from that associated with Choroid Plexus cyst accompanied by other sonographic findings (one in 26). More than 1000 fetuses with Choroid Plexus cysts would have to be studied to determine whether such a difference was real. Conclusion: Because of the rarity of aneuploidy, the reported risk for a fetus with an isolated Choroid Plexus cyst must be interpreted cautiously and should include the baseline risk.
Virginia B. Kalish - One of the best experts on this subject based on the ideXlab platform.
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Fetal Choroid Plexus cysts in association with cri du chat (5p-) syndrome
American Journal of Obstetrics and Gynecology, 1993Co-Authors: Albert P. Sarno, William Polzin, Virginia B. KalishAbstract:The significance of fetal Choroid Plexus cysts is controversial. We report a case of antenatally detected cri du chat syndrome (5p-) in one fetus of a twin pregnancy in association with bilateral fetal Choroid Plexus cysts and unassociated with other structural malformations. Choroid Plexus cysts may be nonspecific markers for chromosomal anomalies.
Eva Carro - One of the best experts on this subject based on the ideXlab platform.
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neurogenic effects of β amyloid in the Choroid Plexus epithelial cells in alzheimer s disease
Cellular and Molecular Life Sciences, 2013Co-Authors: Marta Bolos, Carlos Spuch, Lara Ordonezgutierrez, Francisco Wandosell, Isidro Ferrer, Eva CarroAbstract:β-amyloid (Aβ) can promote neurogenesis, both in vitro and in vivo, by inducing neural progenitor cells to differentiate into neurons. The Choroid Plexus in Alzheimer’s disease (AD) is burdened with amyloid deposits and hosts neuronal progenitor cells. However, neurogenesis in this brain tissue is not firmly established. To investigate this issue further, we examined the effect of Aβ on the neuronal differentiation of Choroid Plexus epithelial cells in several experimental models of AD. Here we show that Aβ regulates neurogenesis in vitro in cultured Choroid Plexus epithelial cells as well as in vivo in the Choroid Plexus of APP/Ps1 mice. Treatment with oligomeric Aβ increased proliferation and differentiation of neuronal progenitor cells in cultured Choroid Plexus epithelial cells, but decreased survival of newly born neurons. These Aβ-induced neurogenic effects were also observed in Choroid Plexus of APP/PS1 mice, and detected also in autopsy tissue from AD patients. Analysis of signaling pathways revealed that pre-treating the Choroid Plexus epithelial cells with specific inhibitors of TyrK or MAPK diminished Aβ-induced neuronal proliferation. Taken together, our results support a role of Aβ in proliferation and differentiation in the Choroid Plexus epithelial cells in Alzheimer’s disease.
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clearance of amyloid β peptide across the Choroid Plexus in alzheimer s disease
Current Aging Science, 2010Co-Authors: Ximena Alvirabotero, Eva CarroAbstract:Aging and several neurodegenerative diseases bring about changes in the anatomy and physiology of the Choroid Plexus. The identification of specific membrane receptors that bind and internalize extracellular ligands has revolutionized the traditional roles of this tissue. Amyloid beta peptide (Aβ), the major constituent of the amyloid core of senile plaques in patients with Alzheimer's disease (AD) is known to contribute to disease neuropathology and progression. Recent emphasis on comorbidity of AD and a deficient clearance of Aβ across the blood-brain barrier and blood-cerebrospinal fluid barrier have highlighted the importance of brain Aβ clearance in AD. The megalin receptor has also been implicated in the pathogenesis of AD. Faulty Aβ clearance from the brain across the Choroid Plexus epithelium by megalin appears to mediate focal Aβ accumulation in AD. Patients with AD have reduced levels of megalin at the Choroid Plexus, which in turn seem to increase brain levels of Aβ through a decreased efflux of brain Aβ. Therapies that increase megalin expression at the Choroid Plexus could potentially control accumulation of brain Aβ. This review covers in depth the anatomy and function of the Choroid Plexus, focusing on the brain barrier at the Choroid Plexus, as it actively participates in Aβ clearance. In addition, we describe the role of the Choroid Plexus in brain functions, aging and AD, as well as the role of megalin in the process of Aβ clearance. Finally, we present current data on the use of Choroid Plexus cells to repair the damaged brain.