Testosterone induces Ca<sup>2+</sup> influx via non‐genomic surface receptors in activated T cells

Benten, W. Peter M.; Lieberherr, Michèle; Sékeris, Constantin E.; Wunderlich, Frank

doi:10.1016/s0014-5793(97)00346-3

Cited by 123 publications

(75 citation statements)

References 28 publications

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“…These actions do not involve the classic androgen receptor pathway but, rather, suggest the participation of a signal-generating membrane surface receptor. In particular, rapid testosterone-induced intracellular Ca 2ϩ elevations have been observed in a variety of cell types, including rat Sertoli cells, human prostatic cells (LNCaP and PC3) (22), rat heart myocytes (26), male (but not female) rat osteoblasts (27), and mouse T cells lacking the functional AR protein (28,29). However, the molecular identity of the hypothesized membrane testosterone receptor remained unknown.…”

Section: Discussionmentioning

confidence: 99%

The TRPM8 Protein Is a Testosterone Receptor

Asuthkar

Demirkhanyan

Sun

et al. 2015

Journal of Biological Chemistry

107

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Section: Discussionmentioning

confidence: 99%

The TRPM8 Protein Is a Testosterone Receptor

Asuthkar

Demirkhanyan

Sun

et al. 2015

Journal of Biological Chemistry

107

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“…Alternatively, the effects of androgens that are important to the inflammatory response to LPS may be nongenomic, similar to the detrimental effects ascribed to androgens in ischemic renal inflammation and injury (21). These effects may potentially be mediated through the recently described plasma membrane androgen receptor, which has been identified on various cell types including T cells (23) and macrophages (24) and the activation of which increases intracellular Ca 2ϩ levels. However, its expression in the lung and potential involvement in LPS-induced lung inflammatory responses are unknown at present.…”

Section: Discussionmentioning

confidence: 99%

Gender Differences in Murine Airway Responsiveness and Lipopolysaccharide-Induced Inflammation

Card

Carey

Bradbury

et al. 2006

The Journal of Immunology

189

147

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The roles of gender and sex hormones in lung function and disease are complex and not completely understood. The present study examined the influence of gender on lung function and respiratory mechanics in naive mice and on acute airway inflammation and hyperresponsiveness induced by intratracheal LPS administration. Basal lung function characteristics did not differ between naive males and females, but males demonstrated significantly greater airway responsiveness than females following aerosolized methacholine challenge as evidenced by increased respiratory system resistance and elastance (p < 0.05). Following LPS administration, males developed more severe hypothermia and greater airway hyperresponsiveness than females (p < 0.05). Inflammatory indices including bronchoalveolar lavage fluid total cells, neutrophils, and TNF-α content were greater in males than in females 6 h following LPS administration (p < 0.05), whereas whole-lung TLR-4 protein levels did not differ among treatment groups, suggesting that differential expression of TLR-4 before or after LPS exposure did not underlie the observed inflammatory outcomes. Gonadectomy decreased airway inflammation in males but did not alter inflammation in females, whereas administration of exogenous testosterone to intact females increased their inflammatory responses to levels observed in intact males. LPS-induced airway hyperresponsiveness was also decreased in castrated males and was increased in females administered exogenous testosterone. Collectively, these data indicate that airway responsiveness in naive mice is influenced by gender, and that male mice have exaggerated airway inflammatory and functional responses to LPS compared with females. These gender differences are mediated, at least in part, by effects of androgens.

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“…It is also possible that the effects of androgens on the immune system are mediated through plasma membrane-bound receptors that may not directly affect gene transcription. 30 Alternatively, androgens may be indirectly inhibiting autoimmune processes by affecting transcription in non-immune cells or at other time points. Still, Csf3-r and Histhlc were identified as candidate genes that may contribute to androgen-mediated inhibition of lupus.…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate genes that influence sex hormone-dependent disease phenotypes in mouse lupus

2007

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Ninety percent of systemic lupus erythematosus patients are female, and gender differences in lupus susceptibility are also observed in (New Zealand Black Â New Zealand White)F1 (BWF1) lupus-prone mice. We followed orchiectomized, intact male and female BWF1 mice for lupus-like disease for 1 year. A comparative gene expression analysis was then used to identify candidate genes potentially responsible for gender-dependent differences in lupus susceptibility. Seven genes encoded on the sex chromosomes and 77 probe sets, including 14 immunoglobulin genes, encoded on the autosomal chromosomes were identified as differentially expressed in male versus female BWF1 splenocytes prior to disease onset. Five genes were determined to be regulated by either estradiol or dihydrotestosterone in an in vivo system and most of them were preferentially expressed in antigen-presenting cells. Gender differences in the expression of Csf3-r, Histh1c, Serpinb2, Slc6a4 and Cd22 in BWF1 mice are the result of transcriptional modification by sex hormones and warrant further investigation. The identification of candidate genes and their expression patterns in splenocyte sub-populations provide new information regarding the mechanisms by which sex hormones influence the development of mouse lupus.

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Testosterone induces Ca²⁺ influx via non‐genomic surface receptors in activated T cells

Cited by 123 publications

References 28 publications

The TRPM8 Protein Is a Testosterone Receptor

The TRPM8 Protein Is a Testosterone Receptor

Gender Differences in Murine Airway Responsiveness and Lipopolysaccharide-Induced Inflammation

Identification of candidate genes that influence sex hormone-dependent disease phenotypes in mouse lupus

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Testosterone induces Ca2+ influx via non‐genomic surface receptors in activated T cells

Cited by 123 publications

References 28 publications

The TRPM8 Protein Is a Testosterone Receptor

The TRPM8 Protein Is a Testosterone Receptor

Gender Differences in Murine Airway Responsiveness and Lipopolysaccharide-Induced Inflammation

Identification of candidate genes that influence sex hormone-dependent disease phenotypes in mouse lupus

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Resources

About

Testosterone induces Ca²⁺ influx via non‐genomic surface receptors in activated T cells