scholarly journals Glucose, Fructose, and Urate Transporters in the Choroid Plexus Epithelium

2020 ◽  
Vol 21 (19) ◽  
pp. 7230
Author(s):  
Yoichi Chiba ◽  
Ryuta Murakami ◽  
Koichi Matsumoto ◽  
Keiji Wakamatsu ◽  
Wakako Nonaka ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
High Energy ◽  
Choroid Plexus Epithelium ◽  
Energy Demands ◽  
Total Brain ◽  
Proximal Tubular ◽  
Renal Proximal Tubular ◽  
And Function ◽  
Choroid Plexus Epithelial

The choroid plexus plays a central role in the regulation of the microenvironment of the central nervous system by secreting the majority of the cerebrospinal fluid and controlling its composition, despite that it only represents approximately 1% of the total brain weight. In addition to a variety of transporter and channel proteins for solutes and water, the choroid plexus epithelial cells are equipped with glucose, fructose, and urate transporters that are used as energy sources or antioxidative neuroprotective substrates. This review focuses on the recent advances in the understanding of the transporters of the SLC2A and SLC5A families (GLUT1, SGLT2, GLUT5, GLUT8, and GLUT9), as well as on the urate-transporting URAT1 and BCRP/ABCG2, which are expressed in choroid plexus epithelial cells. The glucose, fructose, and urate transporters repertoire in the choroid plexus epithelium share similar features with the renal proximal tubular epithelium, although some of these transporters exhibit inversely polarized submembrane localization. Since choroid plexus epithelial cells have high energy demands for proper functioning, a decline in the expression and function of these transporters can contribute to the process of age-associated brain impairment and pathophysiology of neurodegenerative diseases.

Na+-dependent HCO3− uptake into the rat choroid plexus epithelium is partially DIDS sensitive

2005 ◽  
Vol 289 (6) ◽  
pp. C1448-C1456 ◽  
Author(s):  
Elena V. Bouzinova ◽  
Jeppe Praetorius ◽  
Leila V. Virkki ◽  
Søren Nielsen ◽  
Walter F. Boron ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Choroid Plexus ◽  
Brush Border Membrane ◽  
Bicarbonate Transport ◽  
Excitation Wavelength ◽  
Membrane Domain ◽  
Choroid Plexus Epithelium ◽  
Transport Inhibitor ◽  
Acid Loading ◽  
Choroid Plexus Epithelial

Several studies suggest the involvement of Na+ and HCO3− transport in the formation of cerebrospinal fluid. Two Na+-dependent HCO3− transporters were recently localized to the epithelial cells of the rat choroid plexus (NBCn1 and NCBE), and the mRNA for a third protein was also detected (NBCe2) (Praetorius J, Nejsum LN, and Nielsen S. Am J Physiol Cell Physiol 286: C601–C610, 2004). Our goal was to immunolocalize the NBCe2 to the choroid plexus by immunohistochemistry and immunogold electronmicroscopy and to functionally characterize the bicarbonate transport in the isolated rat choroid plexus by measurements of intracellular pH (pHi) using a dual-excitation wavelength pH-sensitive dye (BCECF). Both antisera derived from COOH-terminal and NH2-terminal NBCe2 peptides localized NBCe2 to the brush-border membrane domain of choroid plexus epithelial cells. Steady-state pHi in choroidal cells increased from 7.03 ± 0.02 to 7.38 ± 0.02 ( n = 41) after addition of CO2/HCO3− into the bath solution. This increase was Na+ dependent and inhibited by the Cl− and HCO3− transport inhibitor DIDS (200 μM). This suggests the presence of Na+-dependent, partially DIDS-sensitive HCO3− uptake. The pHi recovery after acid loading revealed an initial Na+ and HCO3−-dependent net base flux of 0.828 ± 0.116 mM/s ( n = 8). The initial flux in the presence of CO2/HCO3− was unaffected by DIDS. Our data support the existence of both DIDS-sensitive and -insensitive Na+- and HCO3−-dependent base loader uptake into the rat choroid plexus epithelial cells. This is consistent with the localization of the three base transporters NBCn1, Na+-driven Cl− bicarbonate exchanger, and NBCe2 in this tissue.

scholarly journals The murine choroid plexus epithelium expresses the 2Cl−/H+ exchanger ClC-7 and Na+/H+ exchanger NHE6 in the luminal membrane domain

2018 ◽  
Vol 314 (4) ◽  
pp. C439-C448 ◽  
Author(s):  
Helle H. Damkier ◽  
Henriette L. Christensen ◽  
Inga B. Christensen ◽  
Qi Wu ◽  
Robert A. Fenton ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Epithelial Cells ◽  
Choroid Plexus ◽  
Intracellular Ph ◽  
Ph Regulation ◽  
Membrane Domain ◽  
Choroid Plexus Epithelium ◽  
Acid Base ◽  
Luminal Membrane ◽  
Choroid Plexus Epithelial

The choroid plexus epithelium within the brain ventricles secretes the majority of the cerebrospinal fluid (CSF). The luminal Na+-K+-ATPase acts in concert with a host of other transport proteins to mediate efficient fluid secretion across the epithelium. The CSF contains little protein buffer, but the pH value seems nonetheless maintained within narrow limits, even when faced with acid-base challenges. The involvement of choroid plexus acid-base transporters in CSF pH regulation is highlighted by the expression of several acid-base transporters in the epithelium. The aim of the present study was to identify novel acid-base transporters expressed in the luminal membrane of the choroid plexus epithelium to pave the way for systematic investigations of each candidate transporter in the regulation of CSF pH. Mass spectrometry analysis of proteins from epithelial cells isolated by fluorescence-activated cell sorting identified the Cl−/H+ exchangers ClC-3, -4, -5, and -7 in addition to known choroid plexus acid-base transporters. RT-PCR on FACS isolated epithelial cells confirmed the expression of the corresponding mRNAs, as well as Na+/H+ exchanger NHE6 mRNA. Both NHE6 and ClC-7 were immunolocalized to the luminal plasma membrane domain of the choroid plexus epithelial cells. Dynamic imaging of intracellular pH and membrane potential changes in isolated choroid plexus epithelial cells demonstrated Cl− gradient-driven changes in intracellular pH and membrane potential that are consistent with Cl−/H+ exchange. In conclusion, we have detected for the first time NHE6 and ClC-7 in the choroid plexus, which are potentially involved in pH regulation of the CSF.

Is there a role of cyclosporine A on total homocysteine export from human renal proximal tubular epithelial cells?

2001 ◽  
Vol 59 (s78) ◽  
pp. 258-261 ◽  
Author(s):  
Mihaela C. Ignatescu ◽  
Manuela Fodiger ◽  
Josef Kletzmayr ◽  
Christian Bieglmayer ◽  
Walter H. Horl ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cyclosporine A ◽  
Tubular Epithelial Cells ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Total Homocysteine ◽  
Renal Proximal Tubular

scholarly journals LincRNA-p21 Inhibits Cisplatin-Induced Apoptosis of Human Renal Proximal Tubular Epithelial Cells by Sponging miR-449a

2021 ◽  
pp. 1-7
Author(s):  
Zhen Li ◽  
Gang Hou
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Kidney Injury ◽  
Protective Role ◽  
Tubular Epithelial Cells ◽  
Breast Cancer Patients ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular ◽  
Induced Apoptosis

<b><i>Introduction:</i></b> LincRNA-p21 is predicted to interact with miR-449a, which plays a protective role in cisplatin-induced acute kidney injury (CIA). <b><i>Objective:</i></b> This study aimed to analyze the involvement of lincRNA-p21 in breast cancer patients with CIA. <b><i>Methods:</i></b> Levels of lincRNA-p21 in plasma from CIA, triple negative breast cancer, and control groups were measured by performing RT-qPCR. The potential interaction between lincRNA-p21 and miR-449a was first predicted by RT-qPCR. The relationship between lincRNA-p21 and miR-449a was analyzed by overexpression experiment. <b><i>Results:</i></b> We found that lincRNA-p21 is downregulated in CIA. Dual luciferase activity assay showed that lincRNA-p21 and miR-449a can interact with each other, while overexpression of lincRNA-p21 and miR-449a failed to affect the expression of each other. In human renal proximal tubular epithelial cells (HRPTEpCs), cisplatin led to the upregulated miR-449a but downregulated lincRNA-p21. Interestingly, lincRNA-p21 overexpression led to reduced enhancing effects of miR-449a on the cisplatin-induced apoptosis of HRPTEpCs. <b><i>Conclusion:</i></b> Therefore, lincRNA-p21 is downregulated in CIA and may sponge miR-449a to inhibit cisplatin-induced apoptosis of HRPTEpCs.

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