scholarly journals The role of nuclear hormone receptors in cutaneous wound repair

2014 ◽  
Vol 33 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Sandra Rieger ◽  
Hengguang Zhao ◽  
Paige Martin ◽  
Koichiro Abe ◽  
Thomas S. Lisse
Keyword(s):  
Wound Repair ◽  
Hormone Receptors ◽  
Nuclear Hormone Receptors ◽  
Cutaneous Wound

Role of nuclear hormone receptors in butyrate-mediated up-regulation of the antimicrobial peptide cathelicidin in epithelial colorectal cells

2007 ◽  
Vol 44 (8) ◽  
pp. 2107-2114 ◽  
Author(s):  
Markus Schwab ◽  
Veerle Reynders ◽  
Yogesh Shastri ◽  
Stefan Loitsch ◽  
Jürgen Stein ◽  
...  
Keyword(s):  
Antimicrobial Peptide ◽  
Hormone Receptors ◽  
Nuclear Hormone Receptors

A crucial role of β1 integrins for keratinocyte migration in vitro and during cutaneous wound repair

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2303-2315 ◽  
Author(s):  
Richard Grose ◽  
Caroline Hutter ◽  
Wilhelm Bloch ◽  
Irmgard Thorey ◽  
Fiona M. Watt ◽  
...  
Keyword(s):  
Crucial Role ◽  
Wound Repair ◽  
Proliferation Rate ◽  
Cutaneous Wound ◽  
Keratinocyte Migration ◽  
Β1 Integrins ◽  
Cell Matrix Interactions

Integrins are ubiquitous transmembrane receptors that play crucial roles in cell-cell and cell-matrix interactions. In this study, we have determined the effects of the loss of β1 integrins in keratinocytes in vitro and during cutaneous wound repair. Flow cytometry of cultured β1-deficient keratinocytes confirmed the absence of β1 integrins and showed downregulation of α6β4 but not of αv integrins. β1-null keratinocytes were characterised by poor adhesion to various substrates, by a reduced proliferation rate and by a strongly impaired migratory capacity. In vivo, the loss of β1 integrins in keratinocytes caused a severe defect in wound healing. β1-null keratinocytes showed impaired migration and were more densely packed in the hyperproliferative epithelium. Surprisingly, their proliferation rate was not reduced in early wounds and even increased in late wounds. The failure in re-epithelialisation resulted in a prolonged inflammatory response, leading to dramatic alterations in the expression of important wound-regulated genes. Ultimately, β1-deficient epidermis did cover the wound bed, but the epithelial architecture was abnormal. These findings demonstrate a crucial role of β1 integrins in keratinocyte migration and wound re-epithelialisation. Movies available on-line

scholarly journals Involvement of Histone Methylation and Phosphorylation in Regulation of Transcription by Thyroid Hormone Receptor

2002 ◽  
Vol 22 (16) ◽  
pp. 5688-5697 ◽  
Author(s):  
Jiwen Li ◽  
Qiushi Lin ◽  
Ho-Geun Yoon ◽  
Zhi-Qing Huang ◽  
Brian D. Strahl ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Histone Acetylation ◽  
Histone Methylation ◽  
Hormone Receptor ◽  
Transcriptional Control ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Nuclear Hormone Receptors ◽  
Regulation Of Transcription

ABSTRACT Previous studies have established an important role of histone acetylation in transcriptional control by nuclear hormone receptors. With chromatin immunoprecipitation assays, we have now investigated whether histone methylation and phosphorylation are also involved in transcriptional regulation by thyroid hormone receptor (TR). We found that repression by unliganded TR is associated with a substantial increase in methylation of H3 lysine 9 (H3-K9) and a decrease in methylation of H3 lysine 4 (H3-K4), methylation of H3 arginine 17 (H3-R17), and a dual modification of phosphorylation of H3 serine 10 and acetylation of lysine 14 (pS10/acK14). On the other hand, transcriptional activation by liganded TR is coupled with a substantial decrease in both H3-K4 and H3-K9 methylation and a robust increase in H3-R17 methylation and the dual modification of pS10/acK14. Trichostatin A treatment results in not only histone hyperacetylation but also an increase in methylation of H3-K4, increase in dual modification of pS10/acK14, and reduction in methylation of H3-K9, revealing an extensive interplay between histone acetylation, methylation, and phosphorylation. In an effort to understand the underlying mechanism for an increase in H3-K9 methylation during repression by unliganded TR, we demonstrated that TR interacts in vitro with an H3-K9-specific histone methyltransferase (HMT), SUV39H1. Functional analysis indicates that SUV39H1 can facilitate repression by unliganded TR and in so doing requires its HMT activity. Together, our data uncover a novel role of H3-K9 methylation in repression by unliganded TR and provide strong evidence for the involvement of multiple distinct histone covalent modifications (acetylation, methylation, and phosphorylation) in transcriptional control by nuclear hormone receptors.

Gene repression by nuclear hormone receptors

2004 ◽  
Vol 40 ◽  
pp. 89-104 ◽  
Author(s):  
Udo Moehren ◽  
Maren Eckey ◽  
Aria Baniahmad
Keyword(s):  
Hormone Receptors ◽  
Chromatin Modification ◽  
Chromatin Accessibility ◽  
Nuclear Hormone Receptors ◽  
Comprehensive Overview ◽  
Cancer Proliferation ◽  
Response Elements ◽  
Breast And Prostate Cancer ◽  
Basal Transcription Factors

Repression by nuclear hormone receptors (NHRs) plays an important role in development, immune response and cellular function. We review mechanisms of how NHRs act as repressors of gene transcription either by direct contact with basal transcription factors or through recruitment of cofactors and enzymic activities that modulate chromatin accessibility. We describe also the role and biochemical mechanism of the cognate hormone that switches a NHR from a transcriptional silencer into an activator. This includes data from crystal structure, functional receptor domain analyses and the role of co-repressors in chromatin modification and remodelling. Furthermore, the comparison of negative response elements with classical response elements unravels the role of co-repressors in this context. We also describe the inhibition of the nuclear factor kappaB and Jun/Fos pathway by NHRs, as well as the molecular mechanism of anti-hormone therapies. Anti-hormones are commonly used in breast and prostate cancer therapy to inhibit cancer proliferation through repression of the oestrogen or androgen receptor, respectively. Here we provide a comprehensive overview of the various mechanism of NHR repression.

Nuclear Hormone Receptors and Adipogenesis

1998 ◽  
Vol 8 (2) ◽  
pp. 141-168 ◽  
Author(s):  
Jeffrey M. Gimble ◽  
Claudius E. Robinson ◽  
Stephen L. Clarke ◽  
Molly R. Hill
Keyword(s):  
Hormone Receptors ◽  
Nuclear Hormone Receptors
Sign in / Sign up

Export Citation Format

Share Document