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Bone Marrow-Derived Stem Cells Migrate into Intraepidermal Skin Defects of a Desmoglein-3 Knockout Mouse Model but Preserve their Mesodermal Differentiation

Standard

Bone Marrow-Derived Stem Cells Migrate into Intraepidermal Skin Defects of a Desmoglein-3 Knockout Mouse Model but Preserve their Mesodermal Differentiation. / Hünefeld, Christian; Mezger, Markus; Müller-Hermelink, Eva; Schaller, Martin; Müller, Ingo; Amagai, Masayuki; Handgretinger, Rupert; Röcken, Martin.

In: J INVEST DERMATOL, Vol. 138, No. 5, 05.2018, p. 1157-1165.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Hünefeld, C, Mezger, M, Müller-Hermelink, E, Schaller, M, Müller, I, Amagai, M, Handgretinger, R & Röcken, M 2018, 'Bone Marrow-Derived Stem Cells Migrate into Intraepidermal Skin Defects of a Desmoglein-3 Knockout Mouse Model but Preserve their Mesodermal Differentiation', J INVEST DERMATOL, vol. 138, no. 5, pp. 1157-1165. https://doi.org/10.1016/j.jid.2017.10.035

APA

Hünefeld, C., Mezger, M., Müller-Hermelink, E., Schaller, M., Müller, I., Amagai, M., Handgretinger, R., & Röcken, M. (2018). Bone Marrow-Derived Stem Cells Migrate into Intraepidermal Skin Defects of a Desmoglein-3 Knockout Mouse Model but Preserve their Mesodermal Differentiation. J INVEST DERMATOL, 138(5), 1157-1165. https://doi.org/10.1016/j.jid.2017.10.035

Vancouver

Hünefeld C, Mezger M, Müller-Hermelink E, Schaller M, Müller I, Amagai M et al. Bone Marrow-Derived Stem Cells Migrate into Intraepidermal Skin Defects of a Desmoglein-3 Knockout Mouse Model but Preserve their Mesodermal Differentiation. J INVEST DERMATOL. 2018 May;138(5):1157-1165. https://doi.org/10.1016/j.jid.2017.10.035

Bibtex

@article{e82efe70a0bf48b5959c6967b9fbce6e,
title = "Bone Marrow-Derived Stem Cells Migrate into Intraepidermal Skin Defects of a Desmoglein-3 Knockout Mouse Model but Preserve their Mesodermal Differentiation",
abstract = "Inherited forms of epidermolysis bullosa are blistering diseases of the skin and mucosa resulting from various gene mutations. Transplantation of bone marrow-derived stem cells might be a promising systemic treatment for severe dystrophic or junctional epidermolysis bullosa, but many key questions remain unresolved. Two open questions of clinical interest are whether systemically transplanted bone marrow-derived stem cells of mesodermal origin might be able to transdifferentiate into keratinocytes with an ectodermal phenotype and whether these cells are also capable of repairing a specific intraepidermal gene defect. To address these questions, we transplanted bone marrow-derived stem cells into mice with a blistering disease exclusively localized to the epidermis resulting from a functional knockout of desmoglein-3 (Dsg3). We found that Dsg3+ donor-derived cells migrate into the recipient epidermis. However, these cells failed to restore the missing Dsg3 mRNA and DSG3 protein expression in the transplanted Dsg3-/- mice. The donor-derived cells found in the epidermis preserved their CD45+ hematopoietic origin, and no transdifferentiation into integrin α6+ keratinocytes or integrin α6+/CD34+ epidermal stem cells occurred. Our results indicate that bone marrow-derived stem cells preserve their mesodermal fate after systemic transplantation and are not capable of treating patients with epidermolysis bullosa with an intraepidermal skin defect.",
keywords = "Journal Article",
author = "Christian H{\"u}nefeld and Markus Mezger and Eva M{\"u}ller-Hermelink and Martin Schaller and Ingo M{\"u}ller and Masayuki Amagai and Rupert Handgretinger and Martin R{\"o}cken",
note = "Copyright {\textcopyright} 2017 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2018",
month = may,
doi = "10.1016/j.jid.2017.10.035",
language = "English",
volume = "138",
pages = "1157--1165",
journal = "J INVEST DERMATOL",
issn = "0022-202X",
publisher = "NATURE PUBLISHING GROUP",
number = "5",

}

RIS

TY - JOUR

T1 - Bone Marrow-Derived Stem Cells Migrate into Intraepidermal Skin Defects of a Desmoglein-3 Knockout Mouse Model but Preserve their Mesodermal Differentiation

AU - Hünefeld, Christian

AU - Mezger, Markus

AU - Müller-Hermelink, Eva

AU - Schaller, Martin

AU - Müller, Ingo

AU - Amagai, Masayuki

AU - Handgretinger, Rupert

AU - Röcken, Martin

N1 - Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2018/5

Y1 - 2018/5

N2 - Inherited forms of epidermolysis bullosa are blistering diseases of the skin and mucosa resulting from various gene mutations. Transplantation of bone marrow-derived stem cells might be a promising systemic treatment for severe dystrophic or junctional epidermolysis bullosa, but many key questions remain unresolved. Two open questions of clinical interest are whether systemically transplanted bone marrow-derived stem cells of mesodermal origin might be able to transdifferentiate into keratinocytes with an ectodermal phenotype and whether these cells are also capable of repairing a specific intraepidermal gene defect. To address these questions, we transplanted bone marrow-derived stem cells into mice with a blistering disease exclusively localized to the epidermis resulting from a functional knockout of desmoglein-3 (Dsg3). We found that Dsg3+ donor-derived cells migrate into the recipient epidermis. However, these cells failed to restore the missing Dsg3 mRNA and DSG3 protein expression in the transplanted Dsg3-/- mice. The donor-derived cells found in the epidermis preserved their CD45+ hematopoietic origin, and no transdifferentiation into integrin α6+ keratinocytes or integrin α6+/CD34+ epidermal stem cells occurred. Our results indicate that bone marrow-derived stem cells preserve their mesodermal fate after systemic transplantation and are not capable of treating patients with epidermolysis bullosa with an intraepidermal skin defect.

AB - Inherited forms of epidermolysis bullosa are blistering diseases of the skin and mucosa resulting from various gene mutations. Transplantation of bone marrow-derived stem cells might be a promising systemic treatment for severe dystrophic or junctional epidermolysis bullosa, but many key questions remain unresolved. Two open questions of clinical interest are whether systemically transplanted bone marrow-derived stem cells of mesodermal origin might be able to transdifferentiate into keratinocytes with an ectodermal phenotype and whether these cells are also capable of repairing a specific intraepidermal gene defect. To address these questions, we transplanted bone marrow-derived stem cells into mice with a blistering disease exclusively localized to the epidermis resulting from a functional knockout of desmoglein-3 (Dsg3). We found that Dsg3+ donor-derived cells migrate into the recipient epidermis. However, these cells failed to restore the missing Dsg3 mRNA and DSG3 protein expression in the transplanted Dsg3-/- mice. The donor-derived cells found in the epidermis preserved their CD45+ hematopoietic origin, and no transdifferentiation into integrin α6+ keratinocytes or integrin α6+/CD34+ epidermal stem cells occurred. Our results indicate that bone marrow-derived stem cells preserve their mesodermal fate after systemic transplantation and are not capable of treating patients with epidermolysis bullosa with an intraepidermal skin defect.

KW - Journal Article

U2 - 10.1016/j.jid.2017.10.035

DO - 10.1016/j.jid.2017.10.035

M3 - SCORING: Journal article

C2 - 29203359

VL - 138

SP - 1157

EP - 1165

JO - J INVEST DERMATOL

JF - J INVEST DERMATOL

SN - 0022-202X

IS - 5

ER -