Cellular damage in vitro

2009 ◽  
Vol 48 (05) ◽  
pp. 208-214 ◽  
Author(s):  
J. Drechsel ◽  
R. Freudenberg ◽  
R. Runge ◽  
G. Wunderlich ◽  
J. Kotzerke ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Survival ◽  
Cell Line ◽  
Cellular Damage ◽  
Thyroid Cell ◽  
Response Curves ◽  
Beta Emitters ◽  
Thyroid Cell Line ◽  
Clonogenic Cell ◽  
Radionuclide Uptake

Summary Aim: The cellular damage of ionising radiation depends on dose, physical radiation quality (e. g. LET) and intracellular radionuclide uptake. The influence of two beta emitters (188Re and 131I) on the thyroid cell line PC Cl3 was studied. Furthermore, we analysed the effect of intracellular accumulation. Methods: The thyroid cell line PC Cl3 was irradiated with 188Re-perrhenate or 131I-sodium iodide in presence or absence of perchlorate. The initial DNA-damage was measured in the comet assay as olive tail moment (OTM). The colony forming assay detects the clonogenic cell survival as surviving fraction. Additional the intracellular radionuclide uptake was quantified. Results: Dose response curves were established for irradiation with 188Re-perrhenate or 131I-iodine under various extra- and intracellular activity distribution conditions. In the presence of perchlorate DNA-damage and clonogenic cell survival for both radionuclides were comparable. In the absence of perchlorat radionuclide uptake of 1.39% (131I) and 4.14% (188Re) were measured causing twofold higher radiotoxicity. Although 131I uptake was lower than 188Re uptake the OTM values were higher und surviving fractions were lower. Conclusions: 131I, compared to 188Re, has lower mean beta energy and a higher LET, and therefore, it induced a higher DNA-damage even at lower intracellular uptake. An additional explanation for the higher radiotoxicity of 131I could be the higher dose exposition caused by crossfire through neighborhood cells.

Regulation of major histocompatibility complex class II antigen expression by the FRTL-5 rat thyroid cell line

1987 ◽  
Vol 115 (3) ◽  
pp. 481-487 ◽  
Author(s):  
A. P. Weetman ◽  
C. Green ◽  
L. K. Borysiewicz
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Line ◽  
Antigen Expression ◽  
Class Ii ◽  
Thyroid Cell ◽  
Histocompatibility Complex ◽  
Thyroid Cell Line ◽  
Rat Thyroid ◽  
Class Ii Antigen ◽  
Γ Interferon

ABSTRACT We have used the continuously growing FRTL-5 rat thyroid cell line to examine the regulation of major histocompatibility complex (MHC) class II (or la) antigen expression. Of the various stimuli investigated, only the supernatant from activated T cells or recombinant γ-interferon induced Ia expression. All Ia-inducing activity was removed from the T cell supernatant by acid dialysis, suggesting that γ-interferon is the single critical mediator for class II antigen expression. Its action was not TSH dependent but expression of class II antigens increased from the G0-G1 to the S and G2 phases of the cell cycle, so that TSH enhanced Ia expression by its action on cell division. Other agents including lectins, hormones, epidermal growth factor, a calcium ionophore and a phorbol ester did not induce Ia expression. Substances known to inhibit murine macrophage Ia expression (cortisol, prostaglandin E2 and 5-hydroxytryptamine) had no effect on FRTL-5 Ia expression. The use of this thyroid cell line has permitted direct examination of modulators in the absence of any possible effects from contaminating non-thyroid cells present in primary cultures and the results suggest that, of the agents tested, only γ-interferon has significance in the context of Ia antigen expression by the thyroid. J. Endocr. (1987) 115, 481–487

Adhesion molecule expression by the FRTL-5 rat thyroid cell line

1991 ◽  
Vol 130 (3) ◽  
pp. 451-456 ◽  
Author(s):  
N. Tandon ◽  
C. Dinsdale ◽  
T. Tamatani ◽  
M. Miyasaka ◽  
A. P. Weetman
Keyword(s):  
Cell Line ◽  
Adhesion Molecule ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Thyroid Cell ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Thyroid Cells ◽  
Thyroid Cell Line ◽  
Rat Thyroid

ABSTRACT We have examined the expression and function of rat CD54, a homologue of human intercellular adhesion molecule-1 (ICAM-1), by the continuously growing rat thyroid cell line FRTL-5. Approximately 10% of FRTL-5 cells express CD54 under basal conditions and this is not influenced by thyrotrophin. Expression of CD54 is increased by cytokines (γ-interferon, tumour necrosis factor, interleukin-1) and by an activator of C-kinase, phorbol 12-myristate 13-acetate. Blocking ICAM-1 with a monoclonal antibody directed against this molecule significantly (P <0·01) reduced the binding of splenic lymphocytes to FRTL-5 cells but inhibition was consistently greater (P <0·01) in the presence of antibodies against a rat homologue of lymphocyte function-associated antigen-1, the receptor on T cells for ICAM-1. In no case was complete blocking of cluster formation observed. These results show that a pure line of rat thyroid cells can express an ICAM-1 homologue and this is directly enhanced by cytokines. Expression of this homologue is partially responsible for lymphocyte adhesion to thyroid cells, which is likely to be a major event in T cell recognition of thyroid antigens in autoimmune thyroiditis. Journal of Endocrinology (1991) 130, 451–456

Persistent Infection of a Carcinoma Thyroid Cell Line with Coxsackievirus B

Thyroid ◽  
2009 ◽  
Vol 19 (4) ◽  
pp. 369-374 ◽  
Author(s):  
Rachel Desailloud ◽  
Famara Sané ◽  
Delphine Caloone ◽  
Didier Hober
Keyword(s):  
Cell Line ◽  
Persistent Infection ◽  
Thyroid Cell ◽  
Thyroid Cell Line ◽  
Coxsackievirus B

High-efficient Nonviral Transfection of the Rat Thyroid Cell Line FRTL-5

2010 ◽  
Vol 42 (12) ◽  
pp. 897-899 ◽  
Author(s):  
A. Klagge ◽  
K. Krause ◽  
K. Müller ◽  
J. Haag ◽  
D. Fuhrer
Keyword(s):  
Cell Line ◽  
Thyroid Cell ◽  
Thyroid Cell Line ◽  
High Efficient ◽  
Nonviral Transfection ◽  
Rat Thyroid

Differential response of prostate cancer cells to ionizing radiation: The RB status.

2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 106-106
Author(s):  
Robert Benjamin Den ◽  
Steve Ciment ◽  
Ankur Sharma ◽  
Hestia Mellert ◽  
Steven McMahon ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Dna Damage ◽  
Dna Repair ◽  
Ionizing Radiation ◽  
Cell Survival ◽  
Hormone Sensitive ◽  
Clonogenic Cell ◽  
Castrate Resistant

106 Background: Prostate cancer is the most frequently diagnosed malignancy and the second leading cause of cancer death in U.S. men. The retinoblastoma tumor suppressor protein, RB, plays a critical role in cell cycle regulation and loss of RB has been observed in 25-30% of prostate cancers. We have previously shown that RB loss results in a castrate resistant phenotype, however the consequences of RB status with regard to radiation response are unknown. We hypothesized that RB loss would downregulate the G1-S cell cycle checkpoint arrest normally induced by irradiation, inhibit DNA repair, and subsequently sensitize cells to ionizing radiation. Methods: Experimental work was performed with multiple isogenic prostate cancer cell lines (hormone sensitive: LNCaP and LAP-C4 cells and hormone resistant C42, 22Rv1 cells; stable knockdown of RB using shRNA). Gamma H2AX assays were used to quantitate DNA damage and PARP cleavage and Caspase 3 were used to quantitate apoptosis. FACS analysis with BrdU was used to assess the cell cycle. Cell survival was measured using the clonogenic cell survival assay. In vivo work was performed in nude mice with tumor xenografts. Results: We observed that loss of RB increased radioresponsiveness in both transient and clonogenic cell survival assays in both hormone sensitive and castrate resistant cell lines (p<0.05). Cell death was not mediated through increased apoptosis nor was perturbations in cell cycle noted. However, loss of RB effected DNA repair as measured by gamma H2AX staining as well as cellular senescence. In vivo xenografts of the RB deficient tumors exhibited diminished tumor mass, lower PSA kinetics and decreased tumor growth after treatment with single fraction of ionizing radiation in comparison to RB intact tumors (p<0.05). Conclusions: Loss of RB results in a differential response to ionizing radiation. Isogenic cells with RB knockdown are more sensitive to DNA damage and result in reduced cell survival. The underlying mechanism appears to be related to DNA damage repair and cellular senescence.

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