Stanniocalcin 1 as a pleiotropic factor in mammals

Yoshiko, Yuji; Aubin, Jane E.

doi:10.1016/j.peptides.2004.04.015

Cited by 78 publications

(63 citation statements)

References 57 publications

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“…For instance, the expression level of the stanniocalcin 1 (Stc1) gene was upregulated (2-to 3-fold) following DEHP treatment, while a gene similar to ankyrin repeat domain 6 (Ard6) showed significant downregulation. It has been reported that Stc1, an important gene in the process of stimulating osteoblast differentiation, is considered to be a pleiotropic factor in mammals [40]. In addition, induction of Stc1 expression by dexamethasone (DEX, 100 nM) has been observed in a rat primary Sertoli cell culture, suggesting that it responds to environmental chemicals in the male reproductive system [41].…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Flutamide and Di-(2-ethylhexyl) phthalate on Male Reproductive Organs in a Rat Model

Jung

Dang

et al. 2009

J. Reprod. Dev.

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Abstract. Endocrine disruptors (EDs) with androgenic and anti-androgenic effects may alter reproductive function by binding to androgenic receptors (AR) and inducing or modulating AR-dependent responses in the male reproductive system. However, the molecular mechanism(s) underlying these events remains unclear. In the present study, pregnant Sprague Dawley (SD) rats were treated with testosterone propionate (TP), flutamide (Flu) and di-(2-ethylhexyl) phthalate (DEHP) from gestation days (GD) 11 to 21. Interestingly, maternal exposure to Flu or DEHP caused fluctuations in the neonatal levels of serum testosterone (T) and luteinizing hormone (LH). Serum testosterone and LH were upregulated by Flu, but these hormones were down-regulated by DEHP. The anogenital distances (AGD) of male newborns were determined at post-neonatal days (PND) 1, 21 and 63. Male rats treated prenatally with DEHP (100 mg/kg mother's body weight) or Flu showed an AGD shorter than that of control rats. At PND 63, sperm concentration, viability and motility were reduced in the maternal DEHP and Flu-treated groups. The numbers of seminiferous tubules were reduced in the Flu and DEHP-treated offspring when compared with the vehicle-and TPtreated groups, and the tubules of the testes at PND 63 were disrupted by a high dose of Flu. In addition, we found differential gene expression patterns by microarray analysis following ED exposure, particularly in sex determinationrelated genes. Although Flu and DEHP are considered to be identical with regard to their anti-androgenic effects, their effects on developing male reproductive organs were distinct, suggesting that Flu competes with endogenous T, while DEHP influences a different step in androgenesis. Key words: Flutamide, Male reproduction, Phthalate (J. Reprod. Dev. 55: [400][401][402][403][404][405][406][407][408][409][410][411] 2009) ecently, environmental, anti-androgenic compounds have been recognized as endocrine disruptors (EDs) because of their hormone-like activities. Anti-androgenic chemicals have the potential to interfere with male reproductive development and function in humans and animals. The EDs are thought to act via many mechanisms, such as by decreasing androgen synthesis, exerting effects on the pituitary-gonadal axis and/or blocking the androgen receptor (AR) [1,2]. The consequences of these actions may cause abnormal hormonal regulation and gene expression.It has been demonstrated that the AR plays a critical role in control of male sexual differentiation. During mammalian sex differentiation, the androgens, testosterone (T) and its metabolite dihydrotestosterone (DHT), produced by the fetal/neonatal male during sexual differentiation are critical factors in the male phenotype [3]. Sex development continues postnatally with the onset of secondary sexual characteristics at puberty and the acquisition of reproductive capacity. In addition, the differentiation of the Wolffian structures (e.g., the epididymis, vas deferens and seminal vesicles) appears to be T-mediated, while ma...

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Section: Discussionmentioning

confidence: 99%

Differential Effects of Flutamide and Di-(2-ethylhexyl) phthalate on Male Reproductive Organs in a Rat Model

Jung

Dang

et al. 2009

J. Reprod. Dev.

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“…97,99 Calcitonin (CT) is certainly expressed in fish, and fish CT is even more potent in humans than mammalian CT. The physiologic role of CT in fish is, however, disputed as some studies could not reveal an effect on calcium homeostasis whereas others found the expected hypocalcemic effects.…”

Section: Pth Sibling Proteinsmentioning

confidence: 99%

Vitamin D: calcium and bone homeostasis during evolution

2014

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Vitamin D 3 is already found early in the evolution of life but essentially as inactive end products of the photochemical reaction of 7-dehydrocholestol with ultraviolet light B. A full vitamin D (refers to vitamin D 2 and D 3 ) endocrine system, characterized by a specific VDR (vitamin D receptor, member of the nuclear receptor family), specific vitamin D metabolizing CYP450 enzymes regulated by calciotropic hormones and a dedicated plasma transport-protein is only found in vertebrates. In the earliest vertebrates (lamprey), vitamin D metabolism and VDR may well have originated from a duplication of a common PRX/VDR ancestor gene as part of a xenobiotic detoxification pathway. The vitamin D endocrine system, however, subsequently became an important regulator of calcium supply for an extensive calcified skeleton. Vitamin D is essential for normal calcium and bone homeostasis as shown by rickets in vitamin D-deficient growing amphibians, reptiles, birds and mammals. From amphibians onward, bone is gradually more dynamic with regulated bone resorption, mainly by combined action of PTH and 1a, (1,25(OH) 2 D 3 ) on the generation and function of multinucleated osteoclasts. Therefore, bone functions as a large internal calcium reservoir, under the control of osteoclasts. Osteocytes also display a remarkable spectrum of activities, including mechanical sensing and regulating mineral homeostasis, but also have an important role in global nutritional and energy homeostasis. Mineralization from reptiles onward is under the control of well-regulated SIBLING proteins and associated enzymes, nearly all under the control of 1,25(OH) 2 D 3 . The vitamin D story thus started as inert molecule but gained an essential role for calcium and bone homeostasis in terrestrial animals to cope with the challenge of higher gravity and calcium-poor environment.

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“…Moreover, there is no solid evidence to illustrate that mammalian STC1 plays an important role in this aspect. With increasing evidence to demonstrate the local actions of STC1, the focus of STC1 research has been moved from serum Ca 2C /P i homeostasis to cellular inflammation and carcinogenesis (Wagner et al 1997, Madsen et al 1998, Chang et al 2003, Yoshiko & Aubin 2004, Ellard et al 2007, Re & Cook 2010, Sheikh-Hamad 2010.…”

Section: Introductionmentioning

confidence: 99%

Synergistic effect of p53 on TSA-induced stanniocalcin 1 expression in human nasopharyngeal carcinoma cells, CNE2

Ching

Yeung

Wong³

2012

Journal of Molecular Endocrinology

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Human stanniocalcin 1 (STC1) has recently been identified as a putative protein factor involved in cellular apoptosis. The use of histone deacetylase inhibitor (i.e. trichostatin A (TSA)) and doxorubicin (Dox) is one of the common treatment methods to induce apoptosis in human cancer cells. A study on TSA and Dox-mediated apoptosis may shed light on the regulation and function of STC1 in cancer treatment. In this study, TSA and Dox cotreatment in human nasopharyngeal carcinoma cells (CNE2) elicited synergistic effects on STC1 gene expression and cellular apoptosis. An activation of p53 (TP53) transcriptional activity in Dox-or DoxCTSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities. To elucidate the possible involvement of p53 in STC1 gene transcription, a vector expressing wild-type or dominant negative (DN) p53 was transiently transfected into the cells. Both STC1 promoter luciferase constructs and chromatin immunoprecipitation assays did not support the direct role of p53 in STC1 gene transactivation. However, the synergistic effects of p53 on the induction of NF-kB phosphorylation and the recruitment of acetylated histone H3 in STC1 promoter were observed in TSA-cotreated cells. The overexpression of exogenous STC1 sensitized apoptosis in Dox-treated cells. Taken together, this study provides data to show the cross talk of NF-kB, p53, and histone protein in the regulation of STC1 expression and function.

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Stanniocalcin 1 as a pleiotropic factor in mammals

Cited by 78 publications

References 57 publications

Differential Effects of Flutamide and Di-(2-ethylhexyl) phthalate on Male Reproductive Organs in a Rat Model

Differential Effects of Flutamide and Di-(2-ethylhexyl) phthalate on Male Reproductive Organs in a Rat Model

Vitamin D: calcium and bone homeostasis during evolution

Synergistic effect of p53 on TSA-induced stanniocalcin 1 expression in human nasopharyngeal carcinoma cells, CNE2

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