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Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis

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Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis. / Beier, Laura-Sophie; Waldow, Ayk; Khomeijani Farahani, Saeed; Mannweiler, Roman; Vidal-Y-Sy, Sabine; Brandner, Johanna M; Piontek, Jörg; Günzel, Dorothee.

in: ANN NY ACAD SCI, Jahrgang 1517, Nr. 1, 11.2022, S. 251-265.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Beier, L-S, Waldow, A, Khomeijani Farahani, S, Mannweiler, R, Vidal-Y-Sy, S, Brandner, JM, Piontek, J & Günzel, D 2022, 'Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis', ANN NY ACAD SCI, Jg. 1517, Nr. 1, S. 251-265. https://doi.org/10.1111/nyas.14879

APA

Beier, L-S., Waldow, A., Khomeijani Farahani, S., Mannweiler, R., Vidal-Y-Sy, S., Brandner, J. M., Piontek, J., & Günzel, D. (2022). Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis. ANN NY ACAD SCI, 1517(1), 251-265. https://doi.org/10.1111/nyas.14879

Vancouver

Beier L-S, Waldow A, Khomeijani Farahani S, Mannweiler R, Vidal-Y-Sy S, Brandner JM et al. Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis. ANN NY ACAD SCI. 2022 Nov;1517(1):251-265. https://doi.org/10.1111/nyas.14879

Bibtex

@article{e7f5384d061f46a39233fd454e292df6,
title = "Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis",
abstract = "Tight junction (TJ) formation is vital for epidermal barrier function. We aimed to specifically manipulate TJ barriers in the reconstructed human epidermis (RHE) by claudin-1 and -4 knockdown (KD) and by claudin-binding fusion proteins of glutathione S-transferase and modified C-terminal fragments of Clostridium perfringens enterotoxin (GST-cCPE). Impedance spectroscopy and tracer permeability imaging were employed for functional barrier assessment and investigation of claudin contribution. KD of claudin-1, but not claudin-4, impaired the paracellular barrier in vitro. Similarly, claudin-binding GST-cCPE variants weakened the paracellular but not the stratum corneum barrier. Combining both TJ targeting methods, we found that claudin-1 targeting by GST-cCPE after claudin-4 KD led to a marked decrease in paracellular barrier properties. Conversely, after claudin-1 KD, GST-cCPE did not further impair the barrier. Comparison of GST-cCPE variants with different claudin-1/claudin-4 affinities, NHS-fluorescein tracer detection, and immunostaining of RHE paraffin sections showed that GST-cCPE variants bind to extrajunctional claudin-1 and -4, which are differentially distributed along the stratum basale-stratum granulosum axis. GST-cCPE binding blocks these claudins, thereby specifically opening the paracellular barrier of RHE. The data indicate a critical role for claudin-1 in regulating paracellular permeability for ions and small molecules in the viable epidermis. Claudin targeting is presented as a proof-of-concept for precise barrier modulation.",
keywords = "Humans, Claudins/metabolism, Claudin-1/metabolism, Claudin-4/metabolism, Epidermis/metabolism, Permeability, Tight Junctions/metabolism, Claudin-5/metabolism",
author = "Laura-Sophie Beier and Ayk Waldow and {Khomeijani Farahani}, Saeed and Roman Mannweiler and Sabine Vidal-Y-Sy and Brandner, {Johanna M} and J{\"o}rg Piontek and Dorothee G{\"u}nzel",
note = "{\textcopyright} 2022 The Authors. Annals of the New York Academy of Sciences published by Wiley Periodicals LLC on behalf of New York Academy of Sciences.",
year = "2022",
month = nov,
doi = "10.1111/nyas.14879",
language = "English",
volume = "1517",
pages = "251--265",
journal = "ANN NY ACAD SCI",
issn = "0077-8923",
publisher = "Wiley-Blackwell",
number = "1",

}

RIS

TY - JOUR

T1 - Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis

AU - Beier, Laura-Sophie

AU - Waldow, Ayk

AU - Khomeijani Farahani, Saeed

AU - Mannweiler, Roman

AU - Vidal-Y-Sy, Sabine

AU - Brandner, Johanna M

AU - Piontek, Jörg

AU - Günzel, Dorothee

N1 - © 2022 The Authors. Annals of the New York Academy of Sciences published by Wiley Periodicals LLC on behalf of New York Academy of Sciences.

PY - 2022/11

Y1 - 2022/11

N2 - Tight junction (TJ) formation is vital for epidermal barrier function. We aimed to specifically manipulate TJ barriers in the reconstructed human epidermis (RHE) by claudin-1 and -4 knockdown (KD) and by claudin-binding fusion proteins of glutathione S-transferase and modified C-terminal fragments of Clostridium perfringens enterotoxin (GST-cCPE). Impedance spectroscopy and tracer permeability imaging were employed for functional barrier assessment and investigation of claudin contribution. KD of claudin-1, but not claudin-4, impaired the paracellular barrier in vitro. Similarly, claudin-binding GST-cCPE variants weakened the paracellular but not the stratum corneum barrier. Combining both TJ targeting methods, we found that claudin-1 targeting by GST-cCPE after claudin-4 KD led to a marked decrease in paracellular barrier properties. Conversely, after claudin-1 KD, GST-cCPE did not further impair the barrier. Comparison of GST-cCPE variants with different claudin-1/claudin-4 affinities, NHS-fluorescein tracer detection, and immunostaining of RHE paraffin sections showed that GST-cCPE variants bind to extrajunctional claudin-1 and -4, which are differentially distributed along the stratum basale-stratum granulosum axis. GST-cCPE binding blocks these claudins, thereby specifically opening the paracellular barrier of RHE. The data indicate a critical role for claudin-1 in regulating paracellular permeability for ions and small molecules in the viable epidermis. Claudin targeting is presented as a proof-of-concept for precise barrier modulation.

AB - Tight junction (TJ) formation is vital for epidermal barrier function. We aimed to specifically manipulate TJ barriers in the reconstructed human epidermis (RHE) by claudin-1 and -4 knockdown (KD) and by claudin-binding fusion proteins of glutathione S-transferase and modified C-terminal fragments of Clostridium perfringens enterotoxin (GST-cCPE). Impedance spectroscopy and tracer permeability imaging were employed for functional barrier assessment and investigation of claudin contribution. KD of claudin-1, but not claudin-4, impaired the paracellular barrier in vitro. Similarly, claudin-binding GST-cCPE variants weakened the paracellular but not the stratum corneum barrier. Combining both TJ targeting methods, we found that claudin-1 targeting by GST-cCPE after claudin-4 KD led to a marked decrease in paracellular barrier properties. Conversely, after claudin-1 KD, GST-cCPE did not further impair the barrier. Comparison of GST-cCPE variants with different claudin-1/claudin-4 affinities, NHS-fluorescein tracer detection, and immunostaining of RHE paraffin sections showed that GST-cCPE variants bind to extrajunctional claudin-1 and -4, which are differentially distributed along the stratum basale-stratum granulosum axis. GST-cCPE binding blocks these claudins, thereby specifically opening the paracellular barrier of RHE. The data indicate a critical role for claudin-1 in regulating paracellular permeability for ions and small molecules in the viable epidermis. Claudin targeting is presented as a proof-of-concept for precise barrier modulation.

KW - Humans

KW - Claudins/metabolism

KW - Claudin-1/metabolism

KW - Claudin-4/metabolism

KW - Epidermis/metabolism

KW - Permeability

KW - Tight Junctions/metabolism

KW - Claudin-5/metabolism

U2 - 10.1111/nyas.14879

DO - 10.1111/nyas.14879

M3 - SCORING: Journal article

C2 - 35994210

VL - 1517

SP - 251

EP - 265

JO - ANN NY ACAD SCI

JF - ANN NY ACAD SCI

SN - 0077-8923

IS - 1

ER -