PACAP 38 regulates prolactin (PRL) and growth hormone (GH) secretion and gene expression in cultured rat pituitary cells

We report here an examination of the effect of thioredoxin (TRX) on the secretion of growth hormone (GH) from rat anterior pituitary cells in vitro. Treatment of rat pituitary cells with growth hormone-releasing factor (GRF), but not GH, led to a significant increase in intracellular TRX protein levels. GRF, recombinant human TRX (rhTRX), and a combination thereof were all shown to induce immediate GH secretion from pituitary cells, as evidenced by perifusion experiments. RhTRX, but not other reducing agents such as β-mercaptoethanol and N-acetyl-l-cysteine, augmented GRF-stimulated and -unstimulated GH secretion from rat pituitary cells in a dose-dependent manner. RhTRX did not significantly affect the GH mRNA expression of pituitary cells stimulated in the presence or absence of GRF. In addition, rhTRX-augmented GH secretion was not significantly affected by the presence of cycloheximide. Collectively, these findings suggest that TRX is induced by stimulation with GRF and plays a regulatory role in GH secretion from rat anterior pituitary cells by enhancing the secretion of stored GH, rather than by the synthesis of GH.

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Desensitization studies using perifused rat pituitary cells show that growth hormone-releasing hormone and His-d-Trp-Ala-Trp-d-Phe-Lys-NH2 stimulate growth hormone release through distinct receptor sites

Journal of Endocrinology ◽

10.1677/joe.0.1290011 ◽

1991 ◽

Vol 129 (1) ◽

pp. 11-19 ◽

Cited By ~ 89

Author(s):

A. D. Blake ◽

R. G. Smith

Keyword(s):

Growth Hormone ◽

Culture Medium ◽

Pituitary Cells ◽

Hormone Release ◽

Culture Studies ◽

Gh Secretion ◽

Receptor Sites ◽

Rat Pituitary ◽

Second Messenger Pathways ◽

Rat Pituitary Cells

ABSTRACT The hexapeptide His-d-Trp-Ala-Trp-d-Phe-Lys-NH2 (GHRP-6) and GH-releasing factor (GHRH) produced a rapid release of GH upon perifusion of dispersed rat pituitary cells. In contrast to the native hormone GHRH, GHRP-6 elicited a response of short duration. When perifusion of each secretagogue was continued until the cells no longer released GH, a challenge by the alternative secretagogue immediately resulted in a secondary release of GH. These results are consistent with each secretagogue causing desensitization of discrete receptor-linked second messenger pathways. Cells which were perifused for 1 min with GHRP-6 required continued perifusion with culture medium alone for 60 min before they completely regained responsiveness to a subsequent challenge with GHRP-6. Somatostatin (SRIF) was able to inhibit the action of either secretagogue completely. However, when both GHRH and GHRP-6 were perifused together, SRIF attenuated but did not block GH secretion. These perifusion data add support to conclusions derived from static cell culture studies, that GHRH and GHRP-6 act through different receptor sites and that through discrete signalling pathways their individual effects on GH release are amplified Journal of Endocrinology (1991) 129, 11–19

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Stimulatory effect of retinoic acid on GH gene expression: the interaction of retinoic acid and tri-iodothyronine in rat pituitary cells

Journal of Endocrinology ◽

10.1677/joe.0.1250251 ◽

1990 ◽

Vol 125 (2) ◽

pp. 251-256 ◽

Cited By ~ 11

Author(s):

S. Morita ◽

K. Matsuo ◽

M. Tsuruta ◽

S. Leng ◽

S. Yamashita ◽

...

Keyword(s):

Gene Expression ◽

Retinoic Acid ◽

Thyroid Hormone ◽

Specific Gene ◽

Pituitary Cells ◽

Mrna Levels ◽

Gh Secretion ◽

Rat Pituitary ◽

Gh Gene ◽

Rat Pituitary Cells

ABSTRACT We have previously demonstrated that retinoic acid (RA) as well as thyroid hormone stimulates GH gene expression. To clarify the relationship between the action of RA and thyroid hormone, pituitary-specific gene expression was investigated further in rat pituitary cells. Rat clonal pituitary cells, GH3, were treated with RA with or without tri-iodothyronine (T3) for up to 3 days. After treatment with 10–1000 nmol RA/1 with or without 0·1–10 nmol T3/1, medium was collected for radioimmunoassay and cells were subjected to RNA extraction, and GH and prolactin gene expression was analysed using 32P-labelled rat GH and rat prolactin cDNA probes respectively. The data demonstrated the dose–responsive manner of the stimulatory effects of RA and T3 on GH secretion with T3-depleted media. The action of RA was additive to that of T3 for GH secretion when maximum effective doses of RA or T3 were used. Using dot blot and Northern gel analysis, it was shown that RA increased GH mRNA levels in T3-depleted media, and that this action of RA was additive to that of T3 on the induction of GH mRNA levels. In contrast, neither RA nor T3 stimulated the secretion of prolactin and prolactin mRNA levels in these cells. Our results indicate that RA stimulates GH mRNA increment and GH secretion in T3-depleted media, and that the stimulatory effect of RA is additive to the maximum effective dose of T3. Journal of Endocrinology (1990) 125, 251–256

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Regulation by calcium of prolactin and growth hormone mRNA sequences in primary cultures of rat pituitary cells.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(17)39653-9 ◽

1985 ◽

Vol 260 (12) ◽

pp. 7614-7618 ◽

Cited By ~ 2

Author(s):

G G Gick ◽

C Bancroft

Keyword(s):

Growth Hormone ◽

Primary Cultures ◽

Pituitary Cells ◽

Growth Hormone Mrna ◽

Rat Pituitary ◽

Rat Pituitary Cells

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CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells

Animals ◽

10.3390/ani11020558 ◽

2021 ◽

Vol 11 (2) ◽

pp. 558

Author(s):

ZeWen Yu ◽

WenZhi Ren ◽

Tian Wang ◽

WeiDi Zhang ◽

ChangJiang Wang ◽

...

Keyword(s):

Pituitary Gland ◽

Inhibitory Effect ◽

Pituitary Cells ◽

Sequencing Analysis ◽

Hormone Regulation ◽

Gh Secretion ◽

Qrt Pcr ◽

Rat Pituitary ◽

Rat Pituitary Cells

CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT–PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT–PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT–PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.

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