Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas

Paola Luciani, Stefania Gelmini, Emanuele Ferrante, Andrea Lania, Susanna Benvenuti, Silvana Baglioni, Giovanna Mantovani, Ilaria Cellai, Franco Ammannati, Anna Spada, Mario Serio, Alessandro Peri

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Context: Seladin-1 (from selective Alzheimer's disease indicator-1) is a recently discovered gene that has been found to be down-regulated in brain regions affected by Alzheimer's disease. Seladin-1 effectively protects neurons against β-amyloid-mediated toxicity and prevents apoptosis via inhibition of the activation of caspase-3, a key mediator of the apoptotic cascade. Although seladin-1 is expressed in the pituitary gland, no study addressed the expression or the function of this gene in pituitary adenomas. Objective: The aim of the present study was to determine the expression level of the seladin-1 gene in pituitary tumors, i.e. GH-secreting and nonfunctioning pituitary adenomas (NFPA), and to determine whether differential expression might be associated with different somatostatin (sst)-induced apoptosis. Results: We found by quantitative real-time RT-PCR that the expression level of seladin-1 was significantly higher in NFPA (n = 21) than in GH-secreting adenomas (n = 30; mean ± SE, 25.69 ± 6.39 vs. 8.02 ± 2.68 pg/μg total RNA; P = 0.006). Although the amount of activated caspase-3 did not differ between the two groups of tumors, in primary cell cultures, octreotide was able to increase apoptosis, evaluated by the level of cleaved cytokeratin 18 and the presence of apoptotic nuclei, in GH-secreting adenomas, but not in NFPA. This different response was not attributable to differences in the amount of transcript of sst receptors 2 and 5, which was similar in the two groups of tumors. Conclusions: Our results suggest that differential seladin-1 expression in pituitary adenomas may be associated with a different apoptotic response to sst analogs.

Original languageEnglish
Pages (from-to)6156-6161
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume90
Issue number11
DOIs
Publication statusPublished - Nov 2005

Fingerprint

Growth Hormone-Secreting Pituitary Adenoma
Octreotide
Pituitary Neoplasms
Growth Hormone
Tumors
Genes
Apoptosis
Somatostatin
Gene Expression
Caspase 3
Keratin-18
Silicone Elastomers
Adenoma
Cell culture
Amyloid
Neurons
Toxicity
Brain
Chemical activation
Primary Cell Culture

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas. / Luciani, Paola; Gelmini, Stefania; Ferrante, Emanuele; Lania, Andrea; Benvenuti, Susanna; Baglioni, Silvana; Mantovani, Giovanna; Cellai, Ilaria; Ammannati, Franco; Spada, Anna; Serio, Mario; Peri, Alessandro.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 90, No. 11, 11.2005, p. 6156-6161.

Research output: Contribution to journalArticle

Luciani, Paola ; Gelmini, Stefania ; Ferrante, Emanuele ; Lania, Andrea ; Benvenuti, Susanna ; Baglioni, Silvana ; Mantovani, Giovanna ; Cellai, Ilaria ; Ammannati, Franco ; Spada, Anna ; Serio, Mario ; Peri, Alessandro. / Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas. In: Journal of Clinical Endocrinology and Metabolism. 2005 ; Vol. 90, No. 11. pp. 6156-6161.
@article{304abf3a3d0844669739a70885be5304,
title = "Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas",
abstract = "Context: Seladin-1 (from selective Alzheimer's disease indicator-1) is a recently discovered gene that has been found to be down-regulated in brain regions affected by Alzheimer's disease. Seladin-1 effectively protects neurons against β-amyloid-mediated toxicity and prevents apoptosis via inhibition of the activation of caspase-3, a key mediator of the apoptotic cascade. Although seladin-1 is expressed in the pituitary gland, no study addressed the expression or the function of this gene in pituitary adenomas. Objective: The aim of the present study was to determine the expression level of the seladin-1 gene in pituitary tumors, i.e. GH-secreting and nonfunctioning pituitary adenomas (NFPA), and to determine whether differential expression might be associated with different somatostatin (sst)-induced apoptosis. Results: We found by quantitative real-time RT-PCR that the expression level of seladin-1 was significantly higher in NFPA (n = 21) than in GH-secreting adenomas (n = 30; mean ± SE, 25.69 ± 6.39 vs. 8.02 ± 2.68 pg/μg total RNA; P = 0.006). Although the amount of activated caspase-3 did not differ between the two groups of tumors, in primary cell cultures, octreotide was able to increase apoptosis, evaluated by the level of cleaved cytokeratin 18 and the presence of apoptotic nuclei, in GH-secreting adenomas, but not in NFPA. This different response was not attributable to differences in the amount of transcript of sst receptors 2 and 5, which was similar in the two groups of tumors. Conclusions: Our results suggest that differential seladin-1 expression in pituitary adenomas may be associated with a different apoptotic response to sst analogs.",
author = "Paola Luciani and Stefania Gelmini and Emanuele Ferrante and Andrea Lania and Susanna Benvenuti and Silvana Baglioni and Giovanna Mantovani and Ilaria Cellai and Franco Ammannati and Anna Spada and Mario Serio and Alessandro Peri",
year = "2005",
month = "11",
doi = "10.1210/jc.2005-0633",
language = "English",
volume = "90",
pages = "6156--6161",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "11",

}

TY - JOUR

T1 - Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas

AU - Luciani, Paola

AU - Gelmini, Stefania

AU - Ferrante, Emanuele

AU - Lania, Andrea

AU - Benvenuti, Susanna

AU - Baglioni, Silvana

AU - Mantovani, Giovanna

AU - Cellai, Ilaria

AU - Ammannati, Franco

AU - Spada, Anna

AU - Serio, Mario

AU - Peri, Alessandro

PY - 2005/11

Y1 - 2005/11

N2 - Context: Seladin-1 (from selective Alzheimer's disease indicator-1) is a recently discovered gene that has been found to be down-regulated in brain regions affected by Alzheimer's disease. Seladin-1 effectively protects neurons against β-amyloid-mediated toxicity and prevents apoptosis via inhibition of the activation of caspase-3, a key mediator of the apoptotic cascade. Although seladin-1 is expressed in the pituitary gland, no study addressed the expression or the function of this gene in pituitary adenomas. Objective: The aim of the present study was to determine the expression level of the seladin-1 gene in pituitary tumors, i.e. GH-secreting and nonfunctioning pituitary adenomas (NFPA), and to determine whether differential expression might be associated with different somatostatin (sst)-induced apoptosis. Results: We found by quantitative real-time RT-PCR that the expression level of seladin-1 was significantly higher in NFPA (n = 21) than in GH-secreting adenomas (n = 30; mean ± SE, 25.69 ± 6.39 vs. 8.02 ± 2.68 pg/μg total RNA; P = 0.006). Although the amount of activated caspase-3 did not differ between the two groups of tumors, in primary cell cultures, octreotide was able to increase apoptosis, evaluated by the level of cleaved cytokeratin 18 and the presence of apoptotic nuclei, in GH-secreting adenomas, but not in NFPA. This different response was not attributable to differences in the amount of transcript of sst receptors 2 and 5, which was similar in the two groups of tumors. Conclusions: Our results suggest that differential seladin-1 expression in pituitary adenomas may be associated with a different apoptotic response to sst analogs.

AB - Context: Seladin-1 (from selective Alzheimer's disease indicator-1) is a recently discovered gene that has been found to be down-regulated in brain regions affected by Alzheimer's disease. Seladin-1 effectively protects neurons against β-amyloid-mediated toxicity and prevents apoptosis via inhibition of the activation of caspase-3, a key mediator of the apoptotic cascade. Although seladin-1 is expressed in the pituitary gland, no study addressed the expression or the function of this gene in pituitary adenomas. Objective: The aim of the present study was to determine the expression level of the seladin-1 gene in pituitary tumors, i.e. GH-secreting and nonfunctioning pituitary adenomas (NFPA), and to determine whether differential expression might be associated with different somatostatin (sst)-induced apoptosis. Results: We found by quantitative real-time RT-PCR that the expression level of seladin-1 was significantly higher in NFPA (n = 21) than in GH-secreting adenomas (n = 30; mean ± SE, 25.69 ± 6.39 vs. 8.02 ± 2.68 pg/μg total RNA; P = 0.006). Although the amount of activated caspase-3 did not differ between the two groups of tumors, in primary cell cultures, octreotide was able to increase apoptosis, evaluated by the level of cleaved cytokeratin 18 and the presence of apoptotic nuclei, in GH-secreting adenomas, but not in NFPA. This different response was not attributable to differences in the amount of transcript of sst receptors 2 and 5, which was similar in the two groups of tumors. Conclusions: Our results suggest that differential seladin-1 expression in pituitary adenomas may be associated with a different apoptotic response to sst analogs.

UR - http://www.scopus.com/inward/record.url?scp=27744470577&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=27744470577&partnerID=8YFLogxK

U2 - 10.1210/jc.2005-0633

DO - 10.1210/jc.2005-0633

M3 - Article

VL - 90

SP - 6156

EP - 6161

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 11

ER -