Nitric oxide protects anterior pituitary cells from cadmium-induced apoptosis

2004 ◽  
Vol 37 (9) ◽  
pp. 1463-1471 ◽  
Author(s):  
Ariel H.B. Poliandri ◽  
Miguel O. Velardez ◽  
Jimena P. Cabilla ◽  
Cristian C.A. Bodo ◽  
Leticia I. Machiavelli ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Induced Apoptosis

Nitric oxide protects the mitochondria of anterior pituitary cells and prevents cadmium-induced cell death by reducing oxidative stress

2006 ◽  
Vol 40 (4) ◽  
pp. 679-688 ◽  
Author(s):  
Ariel H.B. Poliandri ◽  
Leticia I. Machiavelli ◽  
Alnilan F. Quinteros ◽  
Jimena P. Cabilla ◽  
Beatriz H. Duvilanski
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cell Death ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells

Estrogens exert a rapid apoptotic action in anterior pituitary cells

2009 ◽  
Vol 296 (4) ◽  
pp. E664-E671 ◽  
Author(s):  
S. Zárate ◽  
G. Jaita ◽  
V. Zaldivar ◽  
D. B. Radl ◽  
G. Eijo ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Primary Cultures ◽  
Ovariectomized Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Steroid Signaling ◽  
A Cell ◽  
17Β Estradiol ◽  
Induced Apoptosis ◽  
Classical Mechanism

It is now accepted that estrogens not only stimulate lactotrope proliferation but also sensitize anterior pituitary cells to proapoptotic stimuli. In addition to their classical mechanism of action through binding to intracellular estrogen receptors (ERs), there is increasing evidence that estrogens exert rapid actions mediated by cell membrane-localized ERs (mERs). In the present study, we examined the involvement of membrane-initiated steroid signaling in the proapoptotic action of estradiol in primary cultures of anterior pituitary cells from ovariectomized rats by using estren, a synthetic estrogen with no effect on classical transcription and a cell-impermeable 17β-estradiol conjugate (E2-BSA). Both compounds induced cell death of anterior pituitary cells after 60 min of incubation as assessed by flow cytometry and the [3-(4,5-dimethylthiazol-2-yl)]-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Estren, E2, and E2-BSA induced apoptosis of lactotropes and somatotropes as evaluated by the deoxynucleotidyltransferase-mediated dUTP nick end-labeling assay and immunodetection of prolactin (PRL) and growth hormone (GH). The proapoptotic effect of E2-BSA was abrogated by ICI-182,780, an antagonist of ERs. The expression of membrane-associated ERα was observed in PRL- and GH-bearing cells. Our results indicate that estradiol is able to exert a rapid apoptotic action in anterior pituitary cells, especially lactotropes and somatotropes, by a mechanism triggered by mERs. This mechanism could be involved in anterior pituitary cell turnover.

scholarly journals Long-Term Treatment of Anterior Pituitary Cells with Nitric Oxide Induces Programmed Cell Death

Endocrinology ◽  
2004 ◽  
Vol 145 (4) ◽  
pp. 2064-2070 ◽  
Author(s):  
Miguel Omar Velardez ◽  
Ariel Hernán Poliandri ◽  
Jimena Paula Cabilla ◽  
Cristian Carlos Armando Bodo ◽  
Leticia Inés Machiavelli ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Anterior Pituitary ◽  
Term Treatment ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Long Term Treatment

Nitric oxide donors modify free intracellular calcium levels in rat anterior pituitary cells

1998 ◽  
Vol 146 (1-2) ◽  
pp. 19-26 ◽  
Author(s):  
Beatriz H. Duvilanski ◽  
Miguel O. Velardez ◽  
Arturo Gonzalez Iglesias ◽  
Susana Theas ◽  
Adriana Seilicovich ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Intracellular Calcium ◽  
Anterior Pituitary ◽  
Nitric Oxide Donors ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Free Intracellular Calcium

scholarly journals Nitric oxide decreases the production of inositol phosphates stimulated by angiotensin II and thyrotropin-releasing hormone in anterior pituitary cells

2003 ◽  
pp. 89-97 ◽  
Author(s):  
MO Velardez ◽  
AH Benitez ◽  
JP Cabilla ◽  
CC Bodo ◽  
BH Duvilanski
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Guanylyl Cyclase ◽  
Anterior Pituitary ◽  
Inositol Phosphates ◽  
Soluble Guanylyl Cyclase ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Deta Nonoate

OBJECTIVE: Nitric oxide (NO) affects the synthesis of several second messengers, such as cyclic nucleotides, arachidonic acid metabolites and the intracellular calcium concentration, involved in the anterior pituitary hormone release. The present study was performed to investigate the effect of NO on phosphoinositide metabolism. METHODS: The synthesis of inositol phosphates (IPs) was studied in primary cultures of anterior pituitary cells from Wistar male rats. IPs (mono, bis and tris phosphates) were determined by ionic exchange chromatography. RESULTS: Sodium nitroprusside and DETA NONOate (DETA/NO) significantly decreased IP synthesis and prolactin release stimulated by angiotensin II (AngII) and thyrotropin-releasing hormone (TRH). These effects were not observed with decayed DETA NONOate (unable to release NO). LY-83583, a guanylyl cyclase inhibitor, completely reversed the inhibitory effect of DETA/NO on AngII-induced IP production. However, BAY 41-2272, a novel stimulator of the soluble guanylyl cyclase, did not mimic the effect of NO donors. Likewise, neither 8-Bromine-cyclic GMP (8-Br-cGMP), an analog of cGMP, nor Sp-8-pCPT-cGMPS triethylamine, a cGMP-dependent protein kinase (PKG) stimulator, decreased IP synthesis stimulated by AngII. In addition, Rp-8-pCPT-cGMPS triethylamine, a PKG inhibitor, did not block the effect of NO. The decrease of IPs induced by DETA/NO was fully reversed by guanosine 5'-O-(3-thiotriphosphate) tetralithium salt, a non-hydrolyzable analog of GTP. CONCLUSIONS: The present work indicated that NO decreases IP synthesis stimulated by Ang II and TRH in anterior pituitary cells by a soluble guanylyl cyclase/cGMP/PKG-independent pathway, and suggested that NO affects some regulatory factor located between the plasma membrane receptor and G-protein.

Reactive oxygen species are key mediators of the nitric oxide apoptotic pathway in anterior pituitary cells

Nitric Oxide ◽  
2007 ◽  
Vol 16 (2) ◽  
pp. 237-246 ◽  
Author(s):  
Leticia I. Machiavelli ◽  
Ariel H. Poliandri ◽  
Fernanda A. Quinteros ◽  
Jimena P. Cabilla ◽  
Beatriz H. Duvilanski
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Anterior Pituitary ◽  
Reactive Oxygen ◽  
Pituitary Cells ◽  
Oxygen Species ◽  
Apoptotic Pathway ◽  
Anterior Pituitary Cells

Mechanisms of chromium (VI)-induced apoptosis in anterior pituitary cells

Toxicology ◽  
2008 ◽  
Vol 249 (2-3) ◽  
pp. 109-115 ◽  
Author(s):  
Fernanda A. Quinteros ◽  
Leticia I. Machiavelli ◽  
Eliana A. Miler ◽  
Jimena P. Cabilla ◽  
Beatriz H. Duvilanski
Keyword(s):  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Chromium Vi ◽  
Anterior Pituitary Cells ◽  
Induced Apoptosis

scholarly journals Estrogens Up-Regulate the Fas/FasL Apoptotic Pathway in Lactotropes

Endocrinology ◽  
2005 ◽  
Vol 146 (11) ◽  
pp. 4737-4744 ◽  
Author(s):  
G. Jaita ◽  
M. Candolfi ◽  
V. Zaldivar ◽  
S. Zárate ◽  
L. Ferrari ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Cell Types ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Pituitary Cells ◽  
Cell Renewal ◽  
Apoptotic Pathway ◽  
Anterior Pituitary Cells ◽  
Ovx Rats ◽  
17Β Estradiol ◽  
Induced Apoptosis

The Fas/FasL system provides the major apoptotic mechanism for many cell types, participating in cell turnover in hormone-dependent tissues. In the present study, we localized both Fas and FasL in anterior pituitary cells, mainly in lactotropes and somatotropes. The percentage of anterior pituitary cells showing immunoreactivity for Fas or FasL was higher in cells from rats killed in proestrus than in diestrus. Also, the proportion of pituitary cells from ovariectomized (OVX) rats expressing Fas or FasL increased in the presence of 17β-estradiol (10−9m). This steroid increased the percentage of lactotropes with immunoreactivity for Fas or FasL and the percentage of somatotropes expressing Fas. Activation of Fas by an agonist anti-Fas antibody (Mab-Fas) decreased the vi-ability—3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT assay)—of anterior pituitary cells from OVX rats cultured in the presence of 17β-estradiol. Also, membrane-bound FasL decreased cell viability—[3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] assay (MTS assay)—only when anterior pituitary cells from OVX rats were incubated with 17β-estradiol. Moreover, FasL increased the percentage of hypodiploid anterior pituitary cells (flow cytometry). Mab-Fas increased the percentage of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL)-positive pituitary cells and lactotropes from OVX rats only when cells were incubated in the presence of 17β-estradiol. Also, Mab-Fas triggered apoptosis of anterior pituitary cells from rats killed at proestrus but not at diestrus. Our results show that 17β-estradiol up-regulates the expression of the Fas/FasL system in anterior pituitary cells and increases Fas-induced apoptosis in lactotropes, suggesting that Fas-induced apoptosis could be involved in the pituitary cell renewal during the estrous cycle.

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