Universität zu Köln

Vidali, Silvia ORCID: 0000-0003-1981-8833, Cheret, Jeremy, Giesen, Melanie, Haeger, Swantje, Alam, Majid ORCID: 0000-0002-5783-6605, Watson, Rachel E. B., Langton, Abigail K., Klinger, Matthias, Knuever, Jana, Funk, Wolfgang, Kofler, Barbara ORCID: 0000-0002-1198-4776 and Paus, Ralf (2016). Thyroid Hormones Enhance Mitochondrial Function in Human Epidermis. J. Invest. Dermatol., 136 (10). S. 2003 - 2013. NEW YORK: ELSEVIER SCIENCE INC. ISSN 1523-1747

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Abstract

Since it is unknown whether thyroid hormones (THs) regulate mitochondrial function in human epidermis, we treated organ-cultured human skin, or isolated cultured human epidermal keratinocytes, with triiodothyronine (100 pmol/L) or thyroxine (100 nmol/L). Both THs significantly increased protein expression of the mitochondrially encoded cytochrome C oxidase I (MTCO1), complex I activity, and the number of perinuclear mitochondria. Triiodothyronine also increased mitochondrial transcription factor A (TFAM) protein expression, and thyroxine stimulated complex II/IV activity. Increased mitochondrial function can correlate with increased reactive oxygen species production, DNA damage, and accelerated tissue aging. However, THs neither raised reactive oxygen species production or matrix metalloproteinase-1, -2 and -9 activity nor decreased sirtuin1 (Sirt1) immunoreactivity. Instead, triiodothyronine increased sirtuin-1, fibrillin-1, proliferator-activated receptor-gamma 1-alpha (PGC1 alpha), collagen I and III transcription, and thyroxine decreased cyclin-dependent kinase inhibitor 2A (p16(ink4)) expression in organ-cultured human skin. Moreover, TH treatment increased intracutaneous fibrillin-rich microfibril and collagen III deposition and decreased mammalian target of rapamycin (mTORC1/2) expression ex vivo. This identifies THs as potent endocrine stimulators of mitochondrial function in human epidermis, which down-regulates rather than enhance the expression of skin aging-related biomarkers ex vivo. Therefore, topically applied THs deserve further exploration as candidate agents for treating skin conditions characterized by reduced mitochondrial function.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Vidali, Silvia UNSPECIFIED orcid.org/0000-0003-1981-8833 UNSPECIFIED Cheret, Jeremy UNSPECIFIED UNSPECIFIED UNSPECIFIED Giesen, Melanie UNSPECIFIED UNSPECIFIED UNSPECIFIED Haeger, Swantje UNSPECIFIED UNSPECIFIED UNSPECIFIED Alam, Majid UNSPECIFIED orcid.org/0000-0002-5783-6605 UNSPECIFIED Watson, Rachel E. B. UNSPECIFIED UNSPECIFIED UNSPECIFIED Langton, Abigail K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Klinger, Matthias UNSPECIFIED UNSPECIFIED UNSPECIFIED Knuever, Jana UNSPECIFIED UNSPECIFIED UNSPECIFIED Funk, Wolfgang UNSPECIFIED UNSPECIFIED UNSPECIFIED Kofler, Barbara UNSPECIFIED orcid.org/0000-0002-1198-4776 UNSPECIFIED Paus, Ralf UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-261624
DOI:	10.1016/j.jid.2016.05.118
Journal or Publication Title:	J. Invest. Dermatol.
Volume:	136
Number:	10
Page Range:	S. 2003 - 2013
Date:	2016
Publisher:	ELSEVIER SCIENCE INC
Place of Publication:	NEW YORK
ISSN:	1523-1747
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language MATRIX METALLOPROTEINASE-1; PHOTOAGED SKIN; TRANSCRIPTION INITIATION; MOLECULAR ASPECTS; GENE-EXPRESSION; BIOGENESIS; PROLIFERATION; DEGRADATION; COLLAGEN; COMPLEX Multiple languages Dermatology Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/26162