Isolation and characterization of 5′‐regulatory region of mouse activin ßa subunit gene

Yoshida, Eisaku; Tanimoto, Keiji; Murakami, Kazuo; Fukamizu, Akiyoshi

doi:10.1080/15216549800201342

Cited by 3 publications

(3 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is important to recognise that the sampling duration of 72 h and resulting overlap of sampling time-points means that the placement of some events, such as the exact timing of the commencement of the activin A surge and its subsequent decline, are approximations. (Tanimoto et al 1996, Ardekani et al 1998, Yoshida et al 1998. The data also suggest that the reciprocal relationship between the actions of IL-1 and FSH on Sertoli cell, activin A and inhibin B, secretion is modified by the presence of developing spermatogenic cells, consistent with previous observations (Clifton et al 2002).…”

Section: Discussionsupporting

confidence: 80%

Regulated production of activin A and inhibin B throughout the cycle of the seminiferous epithelium in the rat

Okuma

O’Connor

Hayashi

et al. 2006

Journal of Endocrinology

View full text Add to dashboard Cite

Production and regulation of activin A and inhibin B during the cycle of the seminiferous epithelium were investigated in adult rats. Immunohistochemistry localised the activin b Asubunit to the Sertoli cell cytoplasm, with much weaker expression in spermatocytes and spermatids. Both activin A and inhibin B, measured by ELISA were secreted by, seminiferous tubule fragments over 72 h in culture. Activin A was secreted in a cyclic manner with peak secretion from tubules isolated at stage VIII. Tubules collected during stage VI produced the least activin A. Inhibin B secretion was highest from stage IX-I tubules and lowest from stage VII tubules. Addition of interleukin-1b (IL-1b) had relatively little effect on activin A or inhibin B secretion in culture. In contrast, the peak secretion of activin A by stage VIII tubules was blocked by co-incubation with an excess of human recombinant IL-1 receptor antagonist, whereas inhibin B secretion increased slightly. Dibutyryl cAMP stimulated activin A secretion by late stage VII and VIII tubules and stimulated inhibin B across all stages. These data indicate that activin A and inhibin B are cyclically regulated within the seminiferous epithelium, with endogenous IL-1 (presumably IL-1a produced by the Sertoli cells), responsible for a peak of activin A production subsequent to sperm release at stage VIII. These data provide direct evidence that production of activin A and inhibin B by the Sertoli cell is locally modulated by IL-1a, in addition to FSH/cAMP, under the influence of the developing spermatogenic cells.

show abstract

Section: Discussionsupporting

confidence: 80%

Regulated production of activin A and inhibin B throughout the cycle of the seminiferous epithelium in the rat

Okuma

O’Connor

Hayashi

et al. 2006

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…In contrast to the A subunit, regulation of the and B subunits principally involves cAMP response elements (CRE) and the transcription factors SP1, AP-2 and GATA (Feng et al 1989, Dykema & Mayo 1994, Thompson et al 1994, Feng et al 2000. In the rat and mouse, the A subunit promoter also contains a CRE or CRE-like sequence (Ardekani et al 1998, Yoshida et al 1998, which may account for the small stimulatory effect of maximal doses of dbcAMP on baseline activin A production in some experiments. Nonetheless, while differences in the promoters partially help to understand the differential regulation of activin A and inhibin B by LPS/IL-1 and FSH/cAMP, it is clear that the complexity of this interaction requires considerably more study.…”

Section: Discussionmentioning

confidence: 99%

“…In turn, the MAP kinases activate multiple downstream events, including production of the transcription factor AP-1 via the c-jun N-terminal kinase, Jnk. The activin A subunit promoter in the human (Tanimoto et al 1996), rat (Ardekani et al 1998), bovine (Thompson et al 1994) and mouse (Yoshida et al 1998) contains multiple AP-1 responsive elements, indicating that the stimulation of activin A synthesis by both LPS and IL-1 involves this transcription factor. In fact, the regulation may be even more complex than this since IL-1, and to a lesser degree LPS, also signals via bioactive lipid intermediates produced through the action of sphingomyelinase (the ceramide pathway), phospholipase A 2 (the arachidonic acid metabolite pathway) and phosphoinositide-specific phospholipase C (the diacyglycerol and inositol trisphosphate pathways) (Dinarello 1996).…”

Section: Discussionmentioning

confidence: 99%

Regulation of activin A and inhibin B secretion by inflammatory mediators in adult rat Sertoli cell cultures

Okuma¹,

O’Connor²,

Muir³

et al. 2005

Journal of Endocrinology

View full text Add to dashboard Cite

The regulation of Sertoli cell activin A and inhibin B secretion during inflammation was investigated in vitro. Adult rat Sertoli cells were incubated with the inflammatory mediators, lipopolysaccharide (LPS), interleukin-1 (IL-1 ), IL-6 and the IL-1 receptor antagonist (IL-1ra) over 48 h in culture. Activin A, inhibin B and IL-1 were measured in the culture medium by specific two-site ELISAs. Both IL-1 -and LPS-stimulated activin A and inhibited inhibin B secretion. LPS also stimulated the production of IL-1 in the cultures. In contrast to IL-1 , IL-6 had no effect on activin A, although it did have a significant inhibitory effect on inhibin B secretion. Ovine follicle-stimulating hormone (FSH) and the cAMP analogue dibutyryl cAMP opposed the actions of IL-1 and LPS by suppressing activin A and IL-1 secretion and by stimulating inhibin B. Blocking IL-1 activity in the cultures by addition of an excess of IL-1ra completely prevented the response of activin A to exogenous IL-1 , and reduced the response to LPS by 50%. In the presence of IL-1ra, basal secretion of inhibin B was increased, but IL-1ra was unable to reverse the suppression of inhibin B by LPS. These data indicate the importance of both IL-1 isoforms in regulating secretion of activin A and inhibin B by mature Sertoli cells during inflammation. The data also establish that inflammation exerts its effects on activin A and inhibin B secretion via other pathways in addition to those mediated by IL-1, and that hormonal stimulation by FSH and cAMP moderates the Sertoli cell response to inflammation. Interference with the complex interactions between these cytokines and hormones may contribute to the disruption of reproductive function that can accompany infection and illness in men.

show abstract

Molecular Mechanisms in Spermatogenesis

Cheng¹

2008

Advances in Experimental Medicine and Biology

View full text Add to dashboard Cite

Isolation and characterization of 5′‐regulatory region of mouse activin ßa subunit gene

Cited by 3 publications

References 15 publications

Regulated production of activin A and inhibin B throughout the cycle of the seminiferous epithelium in the rat

Regulated production of activin A and inhibin B throughout the cycle of the seminiferous epithelium in the rat

Regulation of activin A and inhibin B secretion by inflammatory mediators in adult rat Sertoli cell cultures

Molecular Mechanisms in Spermatogenesis

Contact Info

Product

Resources

About