Restoration of responsiveness to gonadotropin releasing hormone (GnRH) in calcium-depleted rat pituitary cells

Conn, P. Michael; Rogers, Deloris C.

doi:10.1016/0024-3205(79)90456-9

Cited by 21 publications

(5 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ionized extracellular calcium is required for stimulated but not basal secretion from both normal and tumor cells (Table I; 19,30,54,60). Basal secretion from many other peptide-secreting tissues is also independent of ionized extracellular calcium (6,58,59,63). Interestingly, AtT-20/Dlbv cells are capable of exhibiting regenerative changes in membrane potential which have pharmacological properties similar to calcium action potentials .…”

Section: Discussionmentioning

confidence: 99%

Coordinate, equimolar secretion of smaller peptide products derived from pro-ACTH/endorphin by mouse pituitary tumor cells.

Mains¹,

Eipper²

1981

The Journal of Cell Biology

102

View full text Add to dashboard Cite

The secretion of peptide products derived from pro-ACTH/endorphin was examined with several radioimmunoassays and with polyacrylamide gel analyses of immunoprecipitates of radioactively labeled peptides . In studies using a mouse pituitary tumor cell line the accumulation of each of the four molecular forms of adrenocorticotropic hormone (ACTH) in tissue culture medium was shown to be a linear function of time . No evidence for selfinhibition of secretion by accumulated, secreted peptides (i .e ., ultra-short feedback) was found . Furthermore, synthetic human ACTH and synthetic camel /3-endorphin did not alter secretion of peptides when added to the culture medium at levels up to 10,000 times physiological . Stimulation of the release of ACTH-, endorphin-, lipotropin-, and 16k fragment immunoreactive material by norepinephrine was fully blocked by cobalt ; by this criterion, stimulated release was calcium dependent. All the smaller molecules derived from the pro-ACTH/endorphin common precursor were secreted in equimolar amounts under all circumstances tested, within the precision of these studies (±11%) . Norepinephrine and cobalt did not significantly alter the secretion of pro-ACTH/endorphin and ACTH biosynthetic intermediate . The stimulation of secretion by norephinephrine and inhibition of secretion by cobalt was restricted to the lower molecular weight products derived from pro-ACTH/endorphin : glycosylated and nonglycosylated ACTH(1-39) ; a-lipotropin,,-endorphin, and y-lipotropin ; and 16k fragment .The AtT-20/D-16v mouse pituitary tumor cell line, which was derived from anterior pituitary tissue, provided the first system in which the common precursor to adrenocorticotropic hormone (ACTH)' and /3-lipotropin (#LPH)/,B-endorphin was demonstrated (38) . There is now considerable support for the existence of a similar common precursor to ACTH-related and endorphin-related peptides (pro-ACTH/endorphin) in many species and in several different tissues (reviewed in references 5, 16, and 22). The ACTH/endorphin biosynthetic pathway that operates in AtT20/D-16v cells is summarized in Fig. 1 . 'Abbreviations used in thispaper: ACTH, adrenocorticotropic hormone or corticotropin; 8LPH, /3-lipotropin; yLPH, y-lipotropin or roughly the NH 2-terminal two-thirds of /8LPH; aMSH ; a-melanotropin or Nacetyl-ACTH(1-13)NH2 ; CLIP, corticotropin-like intermediate lobe peptide or ACTH(18-39) ; 16k fragment, the NH2-terminal non-ACTH, non-/3LPH region of pro-ACTH/endorphin, containing a melanotropin-like region called yMSH; 31k, 16k, etc., molecules with apparent molecular weights of 31,000, 16,000, etc., when determined by SDS polyacrylamide gel electrophoresis using a borate/acetate buffer system.

show abstract

Section: Discussionmentioning

confidence: 99%

Coordinate, equimolar secretion of smaller peptide products derived from pro-ACTH/endorphin by mouse pituitary tumor cells.

Mains¹,

Eipper²

1981

The Journal of Cell Biology

102

View full text Add to dashboard Cite

show abstract

“…However, elevation of cGMP is not obligatory for LH release, since GnRH-stimulated LH release is not blocked by inhibitors of cGMP synthesis, and LH is not released when intracellular cGMP levels are elevated (75). The role of Ca 2+ in the stimulus-secretion coupling process has received considerable attention, and an obligatory requirement for this cation has been demonstrated for GnRH action (76)(77)(78)(79). However, GnRHreceptor binding is not dependent upon Ca 2+ , indicating that Ca 2+ action is at a locus beyond the ligand-receptor interaction (79).…”

Section: ) Cellular Receptors and Mechanism Of Action Of Gnrhmentioning

confidence: 99%

Gonadotropin-Releasing Hormone Receptors: Characterization, Physiological Regulation, and Relationship to Reproductive Function

1981

View full text Add to dashboard Cite

“…However, other studies have shown that LH release and cyclic AMP production can be uncoupled (6)(7)(8)(9). Recently, a line of evidence has developed which suggests that calcium may play a central role in GnRH stimulation of gonadotropin release from cultured rat pituitary cells (10)(11)(12)(13) and that the specific requirement for Ca2+ occurs at a postreceptor step (14). Nevertheless, the effect of GnRH on cellular receptor distribution is not known.…”

mentioning

confidence: 99%

Receptor-mediated internalization of fluorescent gonadotropin-releasing hormone by pituitary gonadotropes.

Hazum¹,

Cuatrecasas²,

Marian³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

160

View full text Add to dashboard Cite

show abstract

Restoration of responsiveness to gonadotropin releasing hormone (GnRH) in calcium-depleted rat pituitary cells

Cited by 21 publications

References 11 publications

Coordinate, equimolar secretion of smaller peptide products derived from pro-ACTH/endorphin by mouse pituitary tumor cells.

Coordinate, equimolar secretion of smaller peptide products derived from pro-ACTH/endorphin by mouse pituitary tumor cells.

Gonadotropin-Releasing Hormone Receptors: Characterization, Physiological Regulation, and Relationship to Reproductive Function

Receptor-mediated internalization of fluorescent gonadotropin-releasing hormone by pituitary gonadotropes.

Contact Info

Product

Resources

About