CFTR expression is regulated during both the cycle of the seminiferous epithelium and the oestrous cycle of rodents

Trezise, A. E. O.; Linder, C.; Grieger, David M.; Thompson, Erik W.; Meunier, Hélène; Griswold, Michael D.; Buchwald, M.

doi:10.1038/ng0293-157

Cited by 125 publications

(94 citation statements)

References 43 publications

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“…Such a proposition is not untenable in view of the recent reports that germ cells in vitro activate the phosphatidyl inositol pathway (probably through ATP release) in rat Sertoli cells (Welsh & Ireland, 1992). Furthermore, the detection of cystic fibrosis transmembrane conductance (CFTR) gene expression in germ cells in vivo (Trezise et al 1993) gives added weight to this hypothesis, for there is now a growing body of evidence that CFTR mediates ATP efflux in a number of cell systems (Rotoli et al 1996;Cantiello et al 1997). Alternatively, ATP may be released by the Sertoli cells in the testis and act on the same or adjacent Sertoli cells to control fluid secretion.…”

Section: Discussionmentioning

confidence: 99%

Regulated anion secretion in cultured epithelia from Sertoli cells of immature rats

Chan

Chew

et al. 1998

The Journal of Physiology

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Cultured epithelia of Sertoli cells from prepubertal rats were grown on Matrigel‐coated millipore filters for short‐circuit current (Isc) measurements. Under basal conditions, these epithelia exhibited a ‘zero’ transepithelial potential difference, a ‘zero’ short‐circuit current and a transepithelial resistance of 60 Ω cm2. Forskolin (100 μm) and 8‐(4‐chlorophenylthio)‐cAMP (cpt‐cAMP) (100 μm) added to the apical side stimulated the Isc (forskolin, peak ΔIsc= 1.32 ± 0.16 μA cm−1; cpt‐cAMP, peak ΔIsc= 0.88 ± 0.16 μA cm−2). ATP (100 μm) added apically elicited a Isc response (peak ΔIsc= 6.45 ± 0.28 μA cm−2) which was similar in magnitude to that of 1 μm thapsigargin (peak ΔIsc= 6.09 ± 0.44 μA cm−2). The potency of the responses to other nucleotides: UTP ≥ ATP > ADP >> AMP = adenosine indicates the involvement of a mixture of P2Y receptors. Removal of extracellular Cl− and HCO3− reduced the Isc response to ATP by 70 % and 40 %, respectively. Removal of K+ had no effect, whereas removal of Na+ attenuated the Isc response. The response to ATP was insensitive to agents known to block anion secretion (except apical diphenylamine‐2‐carboxylate (DPC) and DIDS). The resistance to perturbation by pharmacological agents may be a unique property of the seminiferous epithelium. Whole‐cell current recordings in cultured rat Sertoli cells demonstrated a DIDS‐sensitive outwardly rectifying Cl− conductance with activating and inactivating characteristics at depolarizing and hyperpolarizing voltages, respectively. The stimulation of electrogenic ion transport by ATP may be part of a complex mechanism regulating fluid secretion by the testis. Cultured Sertoli cell epithelia are shown to provide a useful model to investigate transepithelial transport in the seminiferous epithelium.

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Section: Discussionmentioning

confidence: 99%

Regulated anion secretion in cultured epithelia from Sertoli cells of immature rats

Chan

Chew

et al. 1998

The Journal of Physiology

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“…However, the presence of CFTR in the vas deferens has been controversial. Using in situ hybridization, Trezise et al (1993) did not detect Cftr mRNA in the rat vas deferens, whereas Patrizio & Salameh (1998) reported a strong signal in the human vas deferens. Pietrement et al (2008) reported that CFTR co-localized with aquaporin 9 and NHERF1 in the apical membrane of rat epididymis and vas deferens, but they only show results for the epididymis.…”

Section: Discussionmentioning

confidence: 99%

Locally produced relaxin may affect testis and vas deferens function in rats

Cardoso¹,

Nascimento²,

Royer³

et al. 2010

Reproduction

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We have previously shown that the rat testis and vas deferens contain high levels of the relaxin receptor, RXFP1. The present study was undertaken to determine the expression of relaxin in these tissues, and the effect of exogenous relaxin on Sertoli cell proliferation and on the mRNA levels of some proteins that may contribute to epithelial secretion and tissue reorganization in the vas deferens. Relaxin mRNA levels in testis and vas deferens were much lower than in the prostate. Sertoli cells seem to be an important source of relaxin mRNA in testis. Relaxin immunoreactivity was detected in the seminiferous epithelium but not in the interstitial compartment. The relaxin precursor was expressed in the vas deferens, and relaxin immunoreactivity was detected in apical cells of the vas deferens. Castration, but not treatment with the anti-estrogen ICI 182,780, dramatically reduced relaxin mRNA levels in the prostate and vas deferens, and this effect was prevented by testosterone. Rxfp1 mRNA levels in the vas deferens and prostate were not affected by castration or treatment with ICI 182,780. Exogenous relaxin increased the incorporation of 3 H-thymidine in cultured Sertoli cells, and treatment of the vas deferens with 100 ng/ml relaxin increased the mRNA levels for the cystic fibrosis chloride channel (cystic fibrosis transmembrane regulator) about three times, and doubled mRNA levels for the inducible form of nitric oxide synthase and metalloproteinase 7. These results suggest that locally produced relaxin acts as an autocrine or paracrine agent in the testis and vas deferens to affect spermatogenesis and seminal fluid composition.

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“…These included consensus sites in PR3 for C\EBP, and in PR4 for CRE, AP-1 and ER. CFTR is known to show hormonal regulation of expression during the oestrous cycle of rodents [10]. However, the ER site in 164 was a single half-site, with no sites in the adjacent DNA ; it was therefore thought unlikely to be important and was not investigated further.…”

Section: Discussionmentioning

confidence: 99%

“…Analysis of rodent tissues by in situ hybridization have shown gradients of CFTR expression in the intestine along both the crypt-villus and proximal-distal axes [9]. CFTR expression is also hormonally regulated in the rodent uterus and shows stage-specific expression during spermatogenesis [10]. Hence the CFTR gene exhibits a complex, tightly regulated pattern of expression, yet relatively little is known of the complex mechanisms underlying this.…”

Section: Introductionmentioning

confidence: 99%

Analysis of DNase-I-hypersensitive sites at the 3′ end of the cystic fibrosis transmembrane conductance regulator gene (CFTR)

Nuthall

Moulin

Huxley

et al. 1999

Biochemical Journal

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The cystic fibrosis transmembrane conductance regulator gene (CFTR) exhibits a complex pattern of expression that shows temporal and spatial regulation, although the control mechanisms are not fully known. We have mapped DNase-I-hypersensitive sites (DHSs) flanking the CFTR gene with the aim of identifying potential regulatory elements. We previously characterized DHSs at -79.5 and -20.9 kb with respect to the CFTR translational start site and a regulatory element in the first intron of the gene at 185+10 kb. We have now mapped five DHSs lying 3′ to the CFTR gene at 4574+5.4, +6.8, +7.0, +7.4 and +15.6 kb that show some degree of tissue specificity. The DHSs are seen in chromatin extracted from human primary epithelial cells and cell lines; the presence of the +15.6 kb site is tissue-specific in transgenic mice carrying a human CFTR yeast artificial chromosome. Further analysis of the 4574+15.6 kb DHS implicates the involvement of CCAAT-enhancer-binding protein (C/EBP), cAMP-response-element-binding protein (CREB)/activating transcription factor (ATF) and activator protein 1 (AP-1) family transcription factors at this regulatory element.

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CFTR expression is regulated during both the cycle of the seminiferous epithelium and the oestrous cycle of rodents

Cited by 125 publications

References 43 publications

Regulated anion secretion in cultured epithelia from Sertoli cells of immature rats

Regulated anion secretion in cultured epithelia from Sertoli cells of immature rats

Locally produced relaxin may affect testis and vas deferens function in rats

Analysis of DNase-I-hypersensitive sites at the 3′ end of the cystic fibrosis transmembrane conductance regulator gene (CFTR)

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