PubMed Health⌕ Search

Biomedical subjects

L Heckert

Publications and source records attributed to L Heckert.

5 recordsLinked to original sources
PubMed1995

The molecular biology of the FSH receptor.

The actions of follicle stimulating hormone (FSH) mediated through its receptor are necessary for the proper functioning of mammalian gonads. The FSH receptor is localized on granulosa cells of the ovary and Sertoli cells of the testis. The expression of the FSH receptor (FSHR) in Sertoli cells varies in vivo as a function of the stage of the cycle of the seminiferous epithelium and in culture as a result of the addition of exogenous hormones. The gene for the FSH receptor is large and has been shown to be related in structure to the genes for luteinizing hormone (LH) receptor and thyroid stimulating hormone (TSH) receptor. The promoter region of the gene for FSHR does not contain a TATA box and has multiple transcriptional start sites. Less than 280 bp of the promoter are sufficient in transient transfection assays to direct expression of the chloramphenicol acetyl transferase gene (CAT) in a number of different cell types including non-gonadal cells. However, the promoter does direct the expression of a marker gene only into testis and ovary of transgenic mice.

Female↗
PubMed1993

Expression of the FSH receptor in the testis.

FSH has multiple and changing roles in the regulation of spermatogenesis. The first function of FSH is to increase the number of Sertoli cells by stimulation of their mitotic activity. During the prepubertal phase of development, FSH is important for the maturation of the Sertoli cells. Hormonal stimulation of tight junction formation and specific protein secretion are essential. In the adult rat, some of the functions carried out by FSH in prepubertal animals are assumed by testosterone. However, there is evidence that even in the adult rat, FSH is important for quantitatively normal spermatogenesis. The gene for the FSH receptor is large (greater than 85 kb) and complex (10 introns) and is structurally similar to the genes for the LH and TSH receptor. The promoter region of the FSHR gene has been identified and is active in the expression of transgenes in transfected Sertoli cells. We have shown that the FSH receptor mRNA is present in the testes of the adult rat and that the levels of this mRNA are changing during the cycle of the seminiferous epithelium. The presence of relatively high levels of FSHR mRNA in stages XIV-II of the cycle and the relatively low levels in stages VII-VIII suggest that the FSH receptor is carefully regulated in adult rats and presumably has an important function in spermatogenesis. The levels of FSHR mRNA in cultured Sertoli cells are immediately reduced in the presence of FSH or phorbol esters, but the levels soon return to normal.

Animals↗
PubMed1990

Pleiotypic actions of the seminiferous growth factor on two testicular cell lines: comparisons with acidic and basic fibroblast growth factors.

Bovine seminiferous growth factor (SGF) stimulated different pleiotypic responses in TM3 Leydig and TM4 Sertoli cells from those obtained with bovine acidic and basic fibroblast growth factors (aFGF, bFGF). First, the three growth factors had distinct mitogenic effects. SGF increased TM3 and TM4 cell numbers, whereas aFGF was mitogenic only for TM3 cells, and bFGF was inactive on both cell lines. Second, only SGF and bFGF stimulated TM4 cells to produce 3- and 2-fold, respectively, greater levels of extracellular, sulfated glycoprotein-1. By Northern analyses, SGF increased the steady-state levels of sulfated glycoprotein-1 mRNA approximately 1.34-fold relative to those of actin mRNA during a 48-hr period. Third, the cell lines secreted different [35S]methionine-labeled proteins. With TM3 cells, some proteins were secreted specifically, whereas other were up- or down-regulated differentially in response to SGF, aFGF, or bFGF. Likewise, with TM4 cells, the three growth factors induced qualitative and quantitative changes in the secretion of specific proteins. On immunoblots, SGF did not bind antibodies specific for an internal domain of aFGF or FGF-5, nor those directed against N-terminal, internal, and C-terminal regions of bFGF. These data suggest SGF, aFGF, and bFGF acted on TM3 Leydig and TM4 Sertoli cells through different receptors and/or diverging pathways of signal transduction to induce different pleiotypic effects.

Animals↗