scholarly journals Effects of low-dose ionising radiation on pituitary adenoma: is there a role for L-type calcium channel?

2005 ◽  
Vol 48 (spe2) ◽  
pp. 185-190
Author(s):  
Marcella Araugio Soares ◽  
Raquel Gouvêa dos Santos
Keyword(s):  
Pituitary Adenoma ◽  
Pituitary Adenomas ◽  
Low Dose ◽  
Calcium Influx ◽  
Calcium Currents ◽  
Gh3 Cells ◽  
Live Cells ◽  
Radiation Induced ◽  
Induced Apoptosis

Pituitary adenomas constitute about 6-18% of brain tumours in adults. Activation of voltage gated calcium currents can account for growth hormone oversecretion in some GH-secreting pituitary adenomas that produce an acromegaly appearance and increase mortality. Ca2+ ions, as mediators of intracellular signalling, are crucial for the development of apoptosis. However, the role of [Ca2+] in the development of apoptosis is ambiguous. In this study, the effects of low-dose ionising gamma radiation (60Co) on rat pituitary adenoma cells survival and proliferation and the role of calcium channels on the apoptosis radio-induced were evaluated. Doses as low as 3 Gy were found to inhibit GH3 cell proliferation. Even though there was a significant number of live cells,168 hours following irradiation, they were not able to proliferate. The results indicate that the blockade of extracellular calcium influx through these channels does not interfere in the radiation-induced apoptosis in GH3 cells.

PTTG has a Dual Role of Promotion-Inhibition in the Development of Pituitary Adenomas

2019 ◽  
Vol 26 (11) ◽  
pp. 800-818
Author(s):  
Zujian Xiong ◽  
Xuejun Li ◽  
Qi Yang
Keyword(s):  
Cell Cycle ◽  
Pituitary Adenoma ◽  
Pituitary Adenomas ◽  
Cell Cycle Progression ◽  
Key Factors ◽  
Cycle Progression ◽  
Sister Chromatids ◽  
Regulation Of Cell Cycle ◽  
Late Stages

Pituitary Tumor Transforming Gene (PTTG) of human is known as a checkpoint gene in the middle and late stages of mitosis, and is also a proto-oncogene that promotes cell cycle progression. In the nucleus, PTTG works as securin in controlling the mid-term segregation of sister chromatids. Overexpression of PTTG, entering the nucleus with the help of PBF in pituitary adenomas, participates in the regulation of cell cycle, interferes with DNA repair, induces genetic instability, transactivates FGF-2 and VEGF and promotes angiogenesis and tumor invasion. Simultaneously, overexpression of PTTG induces tumor cell senescence through the DNA damage pathway, making pituitary adenoma possessing the potential self-limiting ability. To elucidate the mechanism of PTTG in the regulation of pituitary adenomas, we focus on both the positive and negative function of PTTG and find out key factors interacted with PTTG in pituitary adenomas. Furthermore, we discuss other possible mechanisms correlate with PTTG in pituitary adenoma initiation and development and the potential value of PTTG in clinical treatment.

scholarly journals HIF-1α Inhibition Sensitized Pituitary Adenoma Cells to Temozolomide by Regulating Presenilin 1 Expression and Autophagy

2016 ◽  
Vol 15 (6) ◽  
pp. NP95-NP104 ◽  
Author(s):  
Zhang kun ◽  
Yang yuling ◽  
Wang dongchun ◽  
Xie bingbing ◽  
Li xiaoli ◽  
...  
Keyword(s):  
Pituitary Adenoma ◽  
Pituitary Adenomas ◽  
Ph Value ◽  
Hypoxia Inducible Factor ◽  
Presenilin 1 ◽  
Gh3 Cells ◽  
Lysosomal Ph ◽  
Hypoxia Inducible Factor 1Α ◽  
Anticancer Effects ◽  
Autophagy Induction

Pituitary adenomas usually develop temozolomide resistance, which could compromise the anticancer effects of temozolomide. Suppression of hypoxia-inducible factor 1α has been shown to sensitize glioblastoma cells to temozolomide treatment according to previous reports. However, whether and how the suppression of hypoxia-inducible factor 1α could sensitize pituitary adenomas to temozolomide treatment are still poorly understood. In the present study, using hypoxia-inducible factor 1α knockdown strategy, we demonstrated for the first time that hypoxia-inducible factor 1α knockdown could inhibit temozolomide-induced autophagy in rat pituitary adenoma GH3 cells and thus increase antitumor efficacy of temozolomide. Furthermore, we found hypoxia-inducible factor 1α knockdown could block autophagy process through neutralizing lysosomal pH value but not inhibiting autophagy induction. Finally, we found hypoxia-inducible factor 1α could regulate lysosomal pH value through regulating full length presenilin 1 expression, and exogenous reexpression of presenilin 1could restore lysosome acidic levels. Our data indicated hypoxia-inducible factor 1α knockdown could be a potential approach to improve the efficacy of temozolomide therapy for pituitary adenomas.

scholarly journals Oxidized Cell-Free DNA Is a Factor of Stress Signaling in Radiation-Induced Bystander Effects in Different Types of Human Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Marina S. Konkova ◽  
Andrew A. Kaliyanov ◽  
Vasilina A. Sergeeva ◽  
Margarita S. Abramova ◽  
Svetlana V. Kostyuk
Keyword(s):  
Low Dose ◽  
Bystander Effect ◽  
Biological Properties ◽  
Stress Signaling ◽  
Cell Free Dna ◽  
Free Dna ◽  
Cytokine Levels ◽  
Different Types ◽  
Radiation Induced

In pathology or under damaging conditions, the properties of cell-free DNA (cfDNA) change. An example of such change is GC enrichment, which drastically alters the biological properties of cfDNA. GC-rich cfDNA is a factor of stress signaling, whereas genomic cfDNA is biologically inactive. GC-rich cfDNA stimulates TLR9-MyD88-NF-κB signaling cascade, leading to an increase in proinflammatory cytokine levels in the organism. In addition, GC-rich DNA is prone to oxidation and oxidized cfDNA can stimulate secondary oxidative stress. This article is a review of works dedicated to the investigation of a low-dose ionizing radiation effect, a bystander effect, and the role of cfDNA in both of these processes.

The role of the stress-activated protein kinase (SAPK/JNK) signaling pathway in radiation-induced apoptosis

1998 ◽  
Vol 47 (3) ◽  
pp. 225-232 ◽  
Author(s):  
Marcel Verheij ◽  
Gerald A Ruiter ◽  
Shuraila F Zerp ◽  
Wim J van Blitterswijk ◽  
Zvi Fuks ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Jnk Signaling ◽  
Radiation Induced ◽  
Jnk Signaling Pathway ◽  
Induced Apoptosis

The efficacy of dopamine agonist therapy in a young man with a giant prolactinoma: case report

2017 ◽  
Vol 63 (4) ◽  
pp. 231-235
Author(s):  
Alexandr I. Tsiberkin ◽  
Tatiana L. Karonova ◽  
Anna B. Dalmatova ◽  
Elena N. Grineva
Keyword(s):  
Pituitary Adenoma ◽  
Pituitary Adenomas ◽  
Young Patients ◽  
Young Male ◽  
Serum Prolactin ◽  
Agonist Therapy ◽  
Giant Prolactinoma ◽  
Dopamine Agonist Therapy ◽  
History Of

Prolactinomas are the most common of hormone secreting pituitary adenomas. Patients with prolactinomas generally have a benign prognosis. An algorithm is currently available for managing of this disease. Giant prolactinoma larger than 40 mm with severe invasive growth account for about 2—3% of the prolactin-secreting pituitary adenomas and evidence about management of such patients is limited. This case illustrates progress of a giant prolactin-secreting pituitary adenoma up to 70 mm in young male with a family history of prolactinomas in the absence of the adequate therapy for 8 years after initial diagnosis. After evaluation, it was decided to prescribe medical treatment. Cabergoline therapy started after evaluation appeared to be effective and had lead to significant decrease of serum prolactin level and shrinkage of pituitary adenoma. Described case emphasize the crucial role of identification of hyperprolactinemia among young patients on early stages of the disease. Our observation implies that treatment with dopamine agonists might be effective even in cases with giant prolactinomas.

scholarly journals DR5 Knockout Mice Are Compromised in Radiation-Induced Apoptosis

2005 ◽  
Vol 25 (5) ◽  
pp. 2000-2013 ◽  
Author(s):  
Niklas Finnberg ◽  
Joshua J. Gruber ◽  
Peiwen Fei ◽  
Dorothea Rudolph ◽  
Anka Bric ◽  
...  
Keyword(s):  
Cell Death ◽  
Null Mouse ◽  
Organ Specific ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
The Brain ◽  
Necrosis Factor

ABSTRACT DR5 (also called TRAIL receptor 2 and KILLER) is an apoptosis-inducing membrane receptor for tumor necrosis factor-related apoptosis-inducing ligand (also called TRAIL and Apo2 ligand). DR5 is a transcriptional target of p53, and its overexpression induces cell death in vitro. However, the in vivo biology of DR5 has remained largely unexplored. To better understand the role of DR5 in development and in adult tissues, we have created a knockout mouse lacking DR5. This mouse is viable and develops normally with the exception of having an enlarged thymus. We show that DR5 is not expressed in developing embryos but is present in the decidua and chorion early in development. DR5-null mouse embryo fibroblasts expressing E1A are resistant to treatment with TRAIL, suggesting that DR5 may be the primary proapoptotic receptor for TRAIL in the mouse. When exposed to ionizing radiation, DR5-null tissues exhibit reduced amounts of apoptosis compared to wild-type thymus, spleen, Peyer's patches, and the white matter of the brain. In the ileum, colon, and stomach, DR5 deficiency was associated with a subtle phenotype of radiation-induced cell death. These results indicate that DR5 has a limited role during embryogenesis and early stages of development but plays an organ-specific role in the response to DNA-damaging stimuli.

scholarly journals Low-dose radiation-induced apoptosis in human leukemia K562 cells through mitochondrial pathways

2014 ◽  
Vol 10 (3) ◽  
pp. 1569-1575 ◽  
Author(s):  
YONG XIN ◽  
HAI-BIN ZHANG ◽  
TIAN-YOU TANG ◽  
GUI-HONG LIU ◽  
JIAN-SHE WANG ◽  
...  
Keyword(s):  
Low Dose ◽  
K562 Cells ◽  
Human Leukemia ◽  
Low Dose Radiation ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
Dose Radiation ◽  
Human Leukemia K562 Cells
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