Dopamine enhances duodenal epithelial permeability via the dopamine D5 receptor in rodent.
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| Title: | Dopamine enhances duodenal epithelial permeability via the dopamine D |
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| Authors: | Feng, X.‐Y., Zhang, D.‐N., Wang, Y.‐A., Fan, R.‐F., Hong, F., Zhang, Y., Li, Y., Zhu, J.‐X. |
| Source: | Acta Physiologica. May2017, Vol. 220 Issue 1, p113-123. 11p. |
| Subjects: | Dopamine receptors, Duodenal diseases, Epithelial cells, Junctional complexes (Epithelium), Enzyme-linked immunosorbent assay, Therapeutics |
| Abstract: | Aim The intestinal barrier is made up of epithelial cells and intercellular junctional complexes to regulate epithelial ion transport and permeability. Dopamine ( DA) is able to promote duodenal epithelial ion transport through D1-like receptors, which includes subtypes of D1 (D1R) and D5 (D5R), but whether D1-like receptors influence the duodenal permeability is unclear. Methods FITC-dextran permeability, short-circuit current ( ISC), Western blot, immunohistochemistry and ELISA were used in human D5R transgenic mice and hyperendogenous enteric DA ( HEnD) rats in this study. Results Dopamine induced a downward deflection in ISC and an increase in FITC-dextran permeability of control rat duodenum, which were inhibited by the D1-like receptor antagonist, SCH-23390. However, DA decreased duodenal transepithelial resistance ( TER), an effect also reversed by SCH-23390. A strong immunofluorescence signal for D5R, but not D1R, was observed in the duodenum of control rat. In human D5R knock-in transgenic mice, duodenal mucosa displayed an increased basal ISC with high FITC-dextran permeability and decreased TER with a lowered expression of tight junction proteins, suggesting attenuated duodenal barrier function in these transgenic mice. D5R knock-down transgenic mice manifested a decreased basal ISC with lowered FITC-dextran permeability. Moreover, an increased FITC-dextran permeability combined with decreased TER and tight junction protein expression in duodenal mucosa were also observed in HEnD rats. Conclusion This study demonstrates, for the first time, that DA enhances duodenal permeability of control rat via D5R, which provides new experimental and theoretical evidence for the influence of DA on duodenal epithelial barrier function. [ABSTRACT FROM AUTHOR] |
| Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 122576307 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Dopamine enhances duodenal epithelial permeability via the dopamine D<subscript>5</subscript> receptor in rodent. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Feng%2C+X%2E‐Y%2E%22">Feng, X.‐Y.</searchLink><br /><searchLink fieldCode="AR" term="%22Zhang%2C+D%2E‐N%2E%22">Zhang, D.‐N.</searchLink><br /><searchLink fieldCode="AR" term="%22Wang%2C+Y%2E‐A%2E%22">Wang, Y.‐A.</searchLink><br /><searchLink fieldCode="AR" term="%22Fan%2C+R%2E‐F%2E%22">Fan, R.‐F.</searchLink><br /><searchLink fieldCode="AR" term="%22Hong%2C+F%2E%22">Hong, F.</searchLink><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Y%2E%22">Zhang, Y.</searchLink><br /><searchLink fieldCode="AR" term="%22Li%2C+Y%2E%22">Li, Y.</searchLink><br /><searchLink fieldCode="AR" term="%22Zhu%2C+J%2E‐X%2E%22">Zhu, J.‐X.</searchLink> – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Acta+Physiologica%22">Acta Physiologica</searchLink>. May2017, Vol. 220 Issue 1, p113-123. 11p. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Dopamine+receptors%22">Dopamine receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Duodenal+diseases%22">Duodenal diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Epithelial+cells%22">Epithelial cells</searchLink><br /><searchLink fieldCode="DE" term="%22Junctional+complexes+%28Epithelium%29%22">Junctional complexes (Epithelium)</searchLink><br /><searchLink fieldCode="DE" term="%22Enzyme-linked+immunosorbent+assay%22">Enzyme-linked immunosorbent assay</searchLink><br /><searchLink fieldCode="DE" term="%22Therapeutics%22">Therapeutics</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Aim The intestinal barrier is made up of epithelial cells and intercellular junctional complexes to regulate epithelial ion transport and permeability. Dopamine ( DA) is able to promote duodenal epithelial ion transport through D1-like receptors, which includes subtypes of D1 (D1R) and D5 (D5R), but whether D1-like receptors influence the duodenal permeability is unclear. Methods FITC-dextran permeability, short-circuit current ( ISC), Western blot, immunohistochemistry and ELISA were used in human D5R transgenic mice and hyperendogenous enteric DA ( HEnD) rats in this study. Results Dopamine induced a downward deflection in ISC and an increase in FITC-dextran permeability of control rat duodenum, which were inhibited by the D1-like receptor antagonist, SCH-23390. However, DA decreased duodenal transepithelial resistance ( TER), an effect also reversed by SCH-23390. A strong immunofluorescence signal for D5R, but not D1R, was observed in the duodenum of control rat. In human D5R knock-in transgenic mice, duodenal mucosa displayed an increased basal ISC with high FITC-dextran permeability and decreased TER with a lowered expression of tight junction proteins, suggesting attenuated duodenal barrier function in these transgenic mice. D5R knock-down transgenic mice manifested a decreased basal ISC with lowered FITC-dextran permeability. Moreover, an increased FITC-dextran permeability combined with decreased TER and tight junction protein expression in duodenal mucosa were also observed in HEnD rats. Conclusion This study demonstrates, for the first time, that DA enhances duodenal permeability of control rat via D5R, which provides new experimental and theoretical evidence for the influence of DA on duodenal epithelial barrier function. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1111/apha.12806 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 11 StartPage: 113 Subjects: – SubjectFull: Dopamine receptors Type: general – SubjectFull: Duodenal diseases Type: general – SubjectFull: Epithelial cells Type: general – SubjectFull: Junctional complexes (Epithelium) Type: general – SubjectFull: Enzyme-linked immunosorbent assay Type: general – SubjectFull: Therapeutics Type: general Titles: – TitleFull: Dopamine enhances duodenal epithelial permeability via the dopamine D5 receptor in rodent. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Feng, X.‐Y. – PersonEntity: Name: NameFull: Zhang, D.‐N. – PersonEntity: Name: NameFull: Wang, Y.‐A. – PersonEntity: Name: NameFull: Fan, R.‐F. – PersonEntity: Name: NameFull: Hong, F. – PersonEntity: Name: NameFull: Zhang, Y. – PersonEntity: Name: NameFull: Li, Y. – PersonEntity: Name: NameFull: Zhu, J.‐X. IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 05 Text: May2017 Type: published Y: 2017 Identifiers: – Type: issn-print Value: 17481708 Numbering: – Type: volume Value: 220 – Type: issue Value: 1 Titles: – TitleFull: Acta Physiologica Type: main |
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