17β-Estradiol Enhances the Production of Nerve Growth Factor in THP-1-Derived Macrophages or Peripheral Blood Monocyte-Derived Macrophages

Kanda, Naoko; Watanabe, Shinichi

doi:10.1046/j.1523-1747.2003.12487.x

Cited by 78 publications

(50 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For this, the early expression of c-FOS has been considered has an earlier marker of estrogenic response through GPER, although it can also be induced by ERa activation (58). Moreover, the induction of c-FOS has been related with the activation of the cAMP/PKA signaling pathway (59). Similarly, we observed that GPER is functional in AGs, as shown by the significant induction on cfos mRNA levels after G1 treatment.…”

Section: Discussionsupporting

confidence: 61%

Estrogen Signaling through the G Protein–Coupled Estrogen Receptor Regulates Granulocyte Activation in Fish

Cabas

Rodenas

Abellán

et al. 2013

The Journal of Immunology

View full text Add to dashboard Cite

Neutrophils are major participants in innate host responses. It is well known that estrogens have an immune-modulatory role, and some evidence exists that neutrophil physiology can be altered by these molecules. Traditionally, estrogens act via classical nuclear estrogen receptors, but the identification of a G protein–coupled estrogen receptor (GPER), a membrane estrogen receptor that binds estradiol and other estrogens, has opened up the possibility of exploring additional estrogen-mediated effects. However, information on the importance of GPER for immunity, especially, in neutrophils is scant. In this study, we report that gilthead seabream (Sparus aurata L.) acidophilic granulocytes, which are the functional equivalent of mammalian neutrophils, express GPER at both mRNA and protein levels. By using a GPER selective agonist, G1, it was found that GPER activation in vitro slightly reduced the respiratory burst of acidophilic granulocytes and drastically altered the expression profile of several genes encoding major pro- and anti-inflammatory mediators. In addition, GPER signaling in vivo modulated adaptive immunity. Finally, a cAMP analog mimicked the effects of G1 in the induction of the gene coding for PG-endoperoxide synthase 2 and in the induction of CREB phosphorylation, whereas pharmacological inhibition of protein kinase A superinduced PG-endoperoxide synthase 2. Taken together, our results demonstrate for the first time, to our knowledge, that estrogens are able to modulate vertebrate granulocyte functions through a GPER/cAMP/protein kinase A/CREB signaling pathway and could establish therapeutic targets for several immune disorders in which estrogens play a prominent role.

show abstract

Section: Discussionsupporting

confidence: 61%

Estrogen Signaling through the G Protein–Coupled Estrogen Receptor Regulates Granulocyte Activation in Fish

Cabas

Rodenas

Abellán

et al. 2013

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…We recently found that E 2 induced a PI-PLC/PKC-␣/MEK1/ERK signaling pathway via undefined membrane G protein-coupled receptor(s) (33) or induced a cAMP/PKA pathway via membrane G proteincoupled receptor GPR30 in keratinocytes (32). It is reported that E 2 transactivates EGF receptor via membrane G proteincoupled receptors in MCF-7 breast carcinoma cells (23,49).…”

Section: Resultsmentioning

confidence: 99%

“…Cutaneous wound healing requires a variety of growth factors, and the application of a single growth factor is not always effective (29). In addition to HB-EGF production in keratinocytes, E 2 induces production of multiple growth factors in multiple cell types, including nerve growth factor and vascular endothelial growth factor production in macrophages (31,33), leading to reinnervation and angiogenesis in the wound. E 2 stimulates transforming growth factor-␤1 production in fibroblasts (6), related to granulation tissue formation.…”

Section: Discussionmentioning

confidence: 99%

17β-Estradiol enhances heparin-binding epidermal growth factor-like growth factor production in human keratinocytes

Kanda¹,

Watanabe²

2005

American Journal of Physiology-Cell Physiology

Self Cite

View full text Add to dashboard Cite

Heparin-binding epidermal growth factor-like growth factor (HB-EGF) enhances reepithelialization in wounds. Estrogen is known to promote cutaneous wound repair. We examined the in vitro effects of 17β-estradiol (E2) on HB-EGF production by human keratinocytes. E2 or membrane-impermeable BSA-conjugated E2 (E2-BSA) increased HB-EGF secretion, mRNA level, and promoter activity in keratinocytes. E2 or E2-BSA enhanced in vitro wound closure in keratinocytes, and the closure was suppressed by anti-HB-EGF antibody. Activator protein-1 (AP-1) and specificity protein 1 (Sp1) sites on HB-EGF promoter were responsible for the E2- or E2-BSA-induced transactivation. Antisense oligonucleotides against c-Fos, c-Jun, and Sp1 blocked E2- or E2-BSA-induced HB-EGF transactivation. E2 or E2-BSA enhanced DNA binding and transcriptional activity of AP-1 and generated c-Fos/c-Jun heterodimers by inducing c-Fos expression. E2 or E2-BSA enhanced DNA binding and transcriptional activity of Sp1 in parallel with the enhancement of Sp1 phosphorylation. These effects of E2 or E2-BSA were not blocked by the nuclear estrogen receptor antagonist ICI-182,780 or anti-estrogen receptor-α or -β antibodies but were blocked by inhibitors of G protein, phosphatidylinositol-specific PLC, PKC-α, and MEK1. These results suggest that E2 or E2-BSA may enhance HB-EGF production via activation of AP-1 and Sp1. These effects of E2 or E2-BSA may be dependent on membrane G protein-coupled receptors different from nuclear estrogen receptors and on the receptor-mediated activities of phosphatidylinositol-specific PLC, PKC-α, and MEK1. E2 may enhance wound reepithelialization by promoting HB-EGF production in keratinocytes.

show abstract

“…Kanda & Watanabe established this link with macrophages and keratinocytes. The elevated levels of cAMP that GPR30 signaling triggers lead to the induced expression of c-fos in macrophages (Kanda & Watanabe 2003a) and activation of the transcription factor CREB in keratinocytes (Kanda & Watanabe 2003b). These in turn activate the expression of target genes such as nerve growth factor in macrophages and cyclin D2 and BCL2 in keratinocytes.…”

Section: Signal Transduction Pathwaysmentioning

confidence: 99%

The unfolding stories of GPR30, a new membrane-bound estrogen receptor

Maggiolini¹,

Picard²

2009

Journal of Endocrinology

320

264

View full text Add to dashboard Cite

Steroid hormones such as estrogens are known to signal through ligand-regulated transcription factors of the nuclear receptor superfamily. In addition, they elicit rapid nongenomic responses from membrane-associated receptors. One of these receptors belongs to an entirely different family of proteins. The G protein-coupled and seventransmembrane receptor, GPR30, is now widely recognized as an estrogen receptor (ER), hence its official new acronym GPER. It appears to mediate a wide range of responses to estrogen in a large variety of cell types. Its functions are clearly distinct from those of the classical nuclear ERs, although these pathways may overlap and interact in some cases. Here, we review the history of the discovery of this new ER, the evidence for the claim that it is an ER, its signal transduction, and its potential functions in physiology and disease.

show abstract

17β-Estradiol Enhances the Production of Nerve Growth Factor in THP-1-Derived Macrophages or Peripheral Blood Monocyte-Derived Macrophages

Cited by 78 publications

References 70 publications

Estrogen Signaling through the G Protein–Coupled Estrogen Receptor Regulates Granulocyte Activation in Fish

Estrogen Signaling through the G Protein–Coupled Estrogen Receptor Regulates Granulocyte Activation in Fish

17β-Estradiol enhances heparin-binding epidermal growth factor-like growth factor production in human keratinocytes

The unfolding stories of GPR30, a new membrane-bound estrogen receptor

Contact Info

Product

Resources

About