TNF-α Induces Apoptosis of Lactotropes from Female Rats

Candolfi, Marianela; Zaldivar, V.; Laurentiis, Andrea De; Jaita, Gabriela; Pisera, Daniel; Seilicovich, Adriana

doi:10.1210/en.2002-220377

Cited by 37 publications

(76 citation statements)

References 47 publications

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“…TNF-␣-induced cellular shrinkage and atypical structure of nuclei in MCF7 cells as has been described previously for fibroblast (Luschen et al, 2000) and neuronal cells (Candolfi et al, 2002). It was difficult to observe the chromatin clumping (typical for apoptosis) in TNF-␣-treated cells due to shrinkage of the nuclei as opposed to this feature readily apparent in paclitaxel-treated cells (our unpublished data).…”

Section: Inhibition Of Bad Is a Critical Event In Estradiol-induced Asupporting

confidence: 59%

“…We have previously validated the coexpression of plasmid constructs in MCF7 cells (Foster, 2003). Morphological changes in the nuclei were analyzed and condensed/shrunk nuclei were counted as apoptotic as opposed to normal round nuclei (Candolfi et al, 2002).…”

Section: Transient Transfection Microscopic Analysis Of Nuclear Morpmentioning

confidence: 99%

“…Two hundred cells expressing EGFP were randomly selected from each slide, and nuclear morphology was analyzed. Round nuclei with clear periphery were considered as live and shrunk nuclei were considered as dead (Candolfi et al, 2002). The percentage of apoptotic nuclei in the transfected population is shown on the y-axis.…”

Section: Estradiol-induced Bad Phosphorylation Requires Rasactivated mentioning

confidence: 99%

See 2 more Smart Citations

Estradiol Abrogates Apoptosis in Breast Cancer Cells through Inactivation of BAD: Ras-dependent Nongenomic Pathways Requiring Signaling through ERK and Akt

Fernando

Wimalasena

2004

MBoC

113

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Estrogens such as 17-β estradiol (E2) play a critical role in sporadic breast cancer progression and decrease apoptosis in breast cancer cells. Our studies using estrogen receptor-positive MCF7 cells show that E2 abrogates apoptosis possibly through phosphorylation/inactivation of the proapoptotic protein BAD, which was rapidly phosphorylated at S112 and S136. Inhibition of BAD protein expression with specific antisense oligonucleotides reduced the effectiveness of tumor necrosis factor-α, H2O2, and serum starvation in causing apoptosis. Furthermore, the ability of E2 to prevent tumor necrosis factor-α-induced apoptosis was blocked by overexpression of the BAD S112A/S136A mutant but not the wild-type BAD. BAD S112A/S136A, which lacks phosphorylation sites for p90RSK1 and Akt, was not phosphorylated in response to E2 in vitro. E2 treatment rapidly activated phosphatidylinositol 3-kinase (PI-3K)/Akt and p90RSK1 to an extent similar to insulin-like growth factor-1 treatment. In agreement with p90RSK1 activation, E2 also rapidly activated extracellular signal-regulated kinase, and this activity was down-regulated by chemical and biological inhibition of PI-3K suggestive of cross talk between signaling pathways responding to E2. Dominant negative Ras blocked E2-induced BAD phosphorylation and the Raf-activator RasV12T35S induced BAD phosphorylation as well as enhanced E2-induced phosphorylation at S112. Chemical inhibition of PI-3K and mitogen-activated protein kinase kinase 1 inhibited E2-induced BAD phosphorylation at S112 and S136 and expression of dominant negative Ras-induced apoptosis in proliferating cells. Together, these data demonstrate a new nongenomic mechanism by which E2 prevents apoptosis.

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Section: Inhibition Of Bad Is a Critical Event In Estradiol-induced Asupporting

confidence: 59%

Section: Transient Transfection Microscopic Analysis Of Nuclear Morpmentioning

confidence: 99%

Section: Estradiol-induced Bad Phosphorylation Requires Rasactivated mentioning

confidence: 99%

See 1 more Smart Citation

Estradiol Abrogates Apoptosis in Breast Cancer Cells through Inactivation of BAD: Ras-dependent Nongenomic Pathways Requiring Signaling through ERK and Akt

Fernando

Wimalasena

2004

MBoC

113

View full text Add to dashboard Cite

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“…Interestingly, Candolfi et al had reported that Fas activation induces apoptosis of anterior pituitary cells from female rats, suggesting that FasL is involved in the maintenance of tissue homeostasis in the anterior pituitary gland and could have potential benefits for the treatment of pituitary adenomas (18)(19)(20)(21). In the present study, we detected the expressions of Fas and DcR3 on 3 pituitary adenoma cell lines.…”

Section: Introductionsupporting

confidence: 50%

RGD-FasL Induces Apoptosis of Pituitary Adenoma Cells

Chen

Zhuang

et al. 2008

Cell Mol Immunol

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“…We have previously reported that TNFR1 and Fas activation induce apoptosis of anterior pituitary cells from female rats (Candolfi et al 2002, Jaita et al 2005b suggesting that TNF-and FasL are involved in the maintenance of tissue homeostasis in the anterior pituitary gland and could have potential benefits for the treatment of pituitary diseases. Although major advances have been made in the therapy of pituitary tumors, only partial success has been possible and novel therapies are needed.…”

Section: Introductionmentioning

confidence: 99%

Adenoviral vectors encoding tumor necrosis factor-α and FasL induce apoptosis of normal and tumoral anterior pituitary cells

Candolfi

Jaita

Pisera

et al. 2006

Journal of Endocrinology

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Our previous work showed that tumor necrosis factor (TNF)-and FasL induce apoptosis of anterior pituitary cells. To further analyze the effect of these proapoptotic factors, we infected primary cultures from rat anterior pituitary, GH3 and AtT20 cells with first-generation adenoviral vectors encoding TNF-, FasL or, as a control, -galactosidase ( -Gal), under the control of the human cytomegalovirus promoter. Successful expression of the encoded transgenes was determined by immunocytochemistry. Although we observed basal expression of TNF-and FasL in control cultures of anterior pituitary cells, fluorescence-activated cell sorting (FACS) cell cycle analysis showed that the overexpression of TNF-or FasL increases the percentage of hypodiploid lactotropes and somatotropes. Nuclear morphology and TUNEL staining revealed that the cells undergo an apoptotic death process. We detected strong immunoreactivity for TNFR1 and Fas in the somatolactotrope cell line GH3. TNF-, but not FasL, was expressed in control cultures of GH3 cells. The infection of GH3 cells with adenovirus encoding TNF-or FasL increased the percentages of hypodiploid and TUNEL-positive cells. TNF-or FasL immunoreactivity was not observed in the corticotrope cell line AtT20. However, adenovirus encoding TNF-or FasL efficiently transduced these cells and increased the percentages of hypodiploid and TUNEL-positive cells. The expression of -Gal was detected in all these cultures but did not affect cell viability. In conclusion, these results suggest that death signaling cascades triggered by TNF receptor 1 (TNFR1) and Fas are present in both normal and tumoral pituitary cells. Therefore, overexpression of proapoptotic factors could be a useful tool in the therapy of pituitary adenomas.

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TNF-α Induces Apoptosis of Lactotropes from Female Rats

Cited by 37 publications

References 47 publications

Estradiol Abrogates Apoptosis in Breast Cancer Cells through Inactivation of BAD: Ras-dependent Nongenomic Pathways Requiring Signaling through ERK and Akt

Estradiol Abrogates Apoptosis in Breast Cancer Cells through Inactivation of BAD: Ras-dependent Nongenomic Pathways Requiring Signaling through ERK and Akt

RGD-FasL Induces Apoptosis of Pituitary Adenoma Cells

Adenoviral vectors encoding tumor necrosis factor-α and FasL induce apoptosis of normal and tumoral anterior pituitary cells

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