Characteristics of steroid hormone receptors in cultured MC3T3-E1 osteoblastic cells and effect of steroid hormones on cell proliferation

1992 ◽  
Vol 51 (5) ◽  
pp. 376-381 ◽  
Author(s):  
Akihiro Masuyama ◽  
Yasuyoshi Ouchi ◽  
Fumiyasu Sato ◽  
Takyauki Hosoi ◽  
Tetsuro Nakamura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Steroid Hormones ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Steroid Hormone Receptors ◽  
Osteoblastic Cells

scholarly journals Differential Responses to Steroid Hormones in Fibroblasts From the Vocal Fold, Trachea, and Esophagus

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 1000-1009 ◽  
Author(s):  
Shigeyuki Mukudai ◽  
Ken Ichi Matsuda ◽  
Takeshi Nishio ◽  
Yoichiro Sugiyama ◽  
Hideki Bando ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Steroid Hormones ◽  
Vocal Fold ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Vocal Folds ◽  
Steroid Hormone Receptors ◽  
Male Rats ◽  
Target Cells ◽  
Cultured Fibroblasts

Abstract There is accumulating evidence that fibroblasts are target cells for steroids such as sex hormones and corticoids. The characteristics of fibroblasts vary among tissues and organs. Our aim in this study is to examine differences in responses to steroid hormones among fibroblasts from different cervicothoracic regions. We compared the actions of steroid hormones on cultured fibroblasts from the vocal folds, which are considered to be the primary target of steroid hormones, and the trachea and esophagus in adult male rats. Expression of steroid hormone receptors (androgen receptor, estrogen receptor α, and glucocorticoid receptor) was identified by immunofluorescence histochemistry. Androgen receptor was much more frequently expressed in fibroblasts from the vocal fold than in those from the trachea and esophagus. Cell proliferation analysis showed that administration of testosterone, estradiol, or corticosterone suppressed growth of all 3 types of fibroblasts. However, mRNA expression for extracellular matrix–associated genes, including procollagen I and III and elastin, and hyaluronic acid synthase I was elevated only by addition of testosterone to fibroblasts from the vocal fold. These results indicate that each steroid hormone exerts region-specific effects on cervicothoracic fibroblasts with different properties through binding to specific receptors.

Protein p53 expression, cell proliferation and steroid hormone receptors in ductal carcinoma in situ of the breast

1997 ◽  
Vol 29 (3) ◽  
pp. 126-131
Author(s):  
Angelika Reiner ◽  
Margaretha Rudas ◽  
Renate Neumayer ◽  
M. F. X. Gnant ◽  
Martina Mittlböck ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Ductal Carcinoma In Situ ◽  
Carcinoma In Situ ◽  
Hormone Receptors ◽  
Ductal Carcinoma ◽  
Steroid Hormone ◽  
Steroid Hormone Receptors ◽  
P53 Expression ◽  
Protein P53

Physical exercise on the rat ventral prostate: Steroid hormone receptors, apoptosis and cell proliferation

2012 ◽  
Vol 22 (5) ◽  
pp. e86-e92 ◽  
Author(s):  
G. R. Teixeira ◽  
W. J. Fávaro ◽  
P. F. F. Pinheiro ◽  
L. G. A. Chuffa ◽  
J. P. A. Amorim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Physical Exercise ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Steroid Hormone Receptors ◽  
Ventral Prostate ◽  
Rat Ventral Prostate

scholarly journals Historical Perspectives: An abridged history of sex steroid hormone receptor action

2001 ◽  
Vol 91 (4) ◽  
pp. 1854-1859 ◽  
Author(s):  
Stacey A. Fannon ◽  
Regina M. Vidaver ◽  
Sherry A. Marts
Keyword(s):  
Human Health ◽  
Steroid Hormones ◽  
Hormone Receptor ◽  
Hormone Receptors ◽  
Steroid Hormone ◽  
Steroid Hormone Receptors ◽  
Future Research ◽  
Steroid Hormone Receptor ◽  
Historical Perspectives ◽  
Receptor Action

The field of steroid hormone action is well established, although it is barely more than four decades old. Pivotal experiments in the late 1950s and 1960s showed that hormone-binding components exist within nuclei of target tissues and that steroid hormones act by regulating gene expression, rather than directly influencing enzymatic processes. The understanding that steroid hormone receptors interact with the general transcription machinery and alter chromatin structure came in the 1970s and 1980s, and details of this mechanism continue to be elucidated. In addition, the discovery of rapid cellular responses to steroid hormones has led to the identification of putative membrane-bound steroid receptors that act without affecting gene transcription. As noted in the recent Institute of Medicine report Exploring the Biological Contributions to Human Health: Does Sex Matter?, the effects of steroid hormones and defects in steroid hormone receptor action have a profound impact on human health and disease. Future research directives include the development of potent, selective steroid receptor modulators, the elucidation of nongenomic steroid hormone effects, and further exploration of hormone-genome interactions.

scholarly journals Non-genomic actions of sex steroid hormones

2003 ◽  
Vol 148 (3) ◽  
pp. 281-292 ◽  
Author(s):  
T Simoncini ◽  
AR Genazzani
Keyword(s):  
Cell Membrane ◽  
Steroid Hormones ◽  
Hormone Receptors ◽  
Nuclear Translocation ◽  
Steroid Hormone ◽  
Regulation Of Gene Expression ◽  
Steroid Hormone Receptors ◽  
Target Cells ◽  
Specific Response ◽  
Receptor Modulation

Steroid hormone receptors have been traditionally considered to act via the regulation of transcriptional processes, involving nuclear translocation and binding to specific response elements, and ultimately leading to regulation of gene expression. However, novel non-transcriptional mechanisms of signal transduction through steroid hormone receptors have been identified. These so-called 'non-genomic' effects do not depend on gene transcription or protein synthesis and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Several relevant biological actions of steroids have been associated with this kind of signaling. Ubiquitous regulatory cascades such as mitogen-activated protein kinases, the phosphatidylinositol 3-OH kinase and tyrosine kinases are modulated through non-transcriptional mechanisms by steroid hormones. Furthermore, steroid hormone receptor modulation of cell membrane-associated molecules such as ion channels and G-protein-coupled receptors has been shown. TIssues traditionally considered as 'non-targets' for classical steroid actions are instead found to be vividly regulated by non-genomic mechanisms. To this aim, the cardiovascular and the central nervous system provide excellent examples, where steroid hormones induce rapid vasodilatation and neuronal survival via non-genomic mechanisms, leading to relevant pathophysiological consequences. The evidence collected in the past Years indicates that target cells and organs are regulated by a complex interplay of genomic and non-genomic signaling mechanisms of steroid hormones, and the integrated action of these machineries has important functional roles in a variety of pathophysiological processes. The understanding of the molecular basis of the rapid effects of steroids is therefore important, and may in the future turn out to be of relevance for clinical purposes.

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