Human cultured skin fibroblasts express estrogen receptor α and β

Haczyński, Józef; Tarkowski, Rafał; Jarząbek, Katarzyna; Słomczyńska, Maria; Wołczyński, Sławomir; Magoffin, Denis A.; Jakowicki, J; Jakimiuk, Artur

doi:10.3892/ijmm.10.2.149

Cited by 55 publications

(54 citation statements)

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“…Despite the obvious effect of estrogen on dermal collagen content (220 -222), the underlying molecular mechanisms are still poorly understood. However, it has been demonstrated that both ER␣ and ER␤ are expressed in human dermal fibroblasts, which is in line with the concept that E2 effects in the dermis may occur, at least in part, through direct regulation of ER-mediated fibroblast functions (239).…”

Section: Immunohistochemistry 28mentioning

confidence: 76%

The Hair Follicle as an Estrogen Target and Source

et al. 2006

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For many decades, androgens have dominated endocrine research in hair growth control. Androgen metabolism and the androgen receptor currently are the key targets for systemic, pharmacological hair growth control in clinical medicine. However, it has long been known that estrogens also profoundly alter hair follicle growth and cycling by binding to locally expressed high-affinity estrogen receptors (ERs). Besides altering the transcription of genes with estrogen-responsive elements, 17␤-estradiol (E2) also modifies androgen metabolism within distinct subunits of the pilosebaceous unit (i.e., hair follicle and sebaceous gland). The latter displays prominent aromatase activity, the key enzyme for androgen conversion to E2, and is both an estrogen source and target.Here, we chart the recent renaissance of estrogen research in hair research; explain why the hair follicle offers an ideal, clinically relevant test system for studying the role of sex steroids, their receptors, and interactions in neuroectodermal-mesodermal interaction systems in general; and illustrate how it can be exploited to identify novel functions and signaling cross talks of ER-mediated signaling. Emphasizing the long-underestimated complexity and species-, gender-, and site-dependence of E2-induced biological effects on the hair follicle, we explore targets for pharmacological intervention in clinically relevant hair cycle manipulation, ranging from androgenetic alopecia and hirsutism via telogen effluvium to chemotherapy-induced alopecia. While defining major open questions, unsolved clinical challenges, and particularly promising research avenues in this area, we argue that the time has come to pay estrogen-mediated signaling the full attention it deserves in future endocrinological therapy of common hair growth disorders. (Endocrine Reviews 27: 677-706, 2006)

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Section: Immunohistochemistry 28mentioning

confidence: 76%

The Hair Follicle as an Estrogen Target and Source

et al. 2006

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“…It has been shown that both E2R␣ and -␤ are expressed in the skin and specifically in skin fibroblasts (21). However, considerable variability appears with respect to the ratio of both ER subtypes in various organs, ages, and species (37,38). Therefore, the expression of E2R␣ and -␤ was determined by real time PCR in hairless skh-1 mice.…”

Section: Discussionmentioning

confidence: 99%

Estradiol Protects Dermal Hyaluronan/Versican Matrix during Photoaging by Release of Epidermal Growth Factor from Keratinocytes

Röck

Meusch

Fuchs

et al. 2012

Journal of Biological Chemistry

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Background: Skin aging involves UVB-induced degeneration of the dermal extracellular matrix. Results: Estrogen induces epidermal growth factor expression in keratinocytes thereby stimulating hyaluronan synthase 3 and versican expression in dermal fibroblasts of UVB-irradiated skin. Conclusion: Paracrine release of epidermal growth factor in response to estrogen maintains hyaluronan and versican-rich extracellular matrix. Significance: Estrogen prevents specific aging responses in the hyaluronan matrix of photoaged skin.

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“…Samples from MCF7 cells were used as experimental internal positive controls. 30 Secondly, we preincubated cells with graded concentrations of E-17-b (ranging from 0.2 to 30 nM) for 12, 24 and 48 h before TRAIL treatment. We found that E-17-b was significantly protected from TRAIL-induced cell death both in concentration-(data not shown) and time-dependent modes.…”

Section: Trail Receptors Are Expressed By Human Oligodendrocytic Cellmentioning

confidence: 99%

Protective effects of estradiol on TRAIL-induced apoptosis in a human oligodendrocytic cell line: evidence for multiple sites of interactions

et al. 2004

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Demyelinating diseases are high impact neurological disorders. Steroids are regarded as protective molecules in the susceptibility to these diseases. Here, we studied the interactions between tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), a potent proapoptotic molecule toxic to oligodendrocytes, and 17-b-estradiol (E-17-b), in human oligodendrocytic MO3.13 cells. Exposure of cells to TRAIL resulted in the upregulation of both death receptors DR4 and DR5 and apoptosis, as well as the activation of caspase-8 and -3, increased phosphorylation of Jun-Nterminal kinase and p38 kinase, and the reduction of bcl-2 and bcl-xL proteins. TRAIL-mediated MO3.13 cell apoptosis was abrogated by the dominant-negative form of the adaptor protein FADD and by caspase inhibitors. Preincubation with E-17-b completely prevented both TRAIL-induced DR4 and DR5 upregulation and apoptosis. Estrogen-induced cytoprotection was time and concentration dependent and reverted by antiestrogens. Estrogen treatment per se reduced kinase phosphorylation, and upregulated bcl-2 and bcl-xL proteins.In conclusion, our data show that the detrimental role of TRAIL on oligodendrocytes can be effectively counteracted by estrogens, thus suggesting that the underlying molecular interactions can be of potential relevance in characterizing novel targets for therapy of demyelinating disorders.

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Human cultured skin fibroblasts express estrogen receptor α and β

Cited by 55 publications

References 0 publications

The Hair Follicle as an Estrogen Target and Source

The Hair Follicle as an Estrogen Target and Source

Estradiol Protects Dermal Hyaluronan/Versican Matrix during Photoaging by Release of Epidermal Growth Factor from Keratinocytes

Protective effects of estradiol on TRAIL-induced apoptosis in a human oligodendrocytic cell line: evidence for multiple sites of interactions

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