LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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CHAPTER 3 RESULTS Fig.3.4.4b DNA damage in EL-4 cells cultured for 2 h in presence of different conditioned media was measured using single cell gel electrophoresis (‘comet assay’) and expressed as tail length. Key: Lane 1, control EL-4 cells; Lane 2, EL-4 cells receiving medium from LPSstimulated (500ng/ml) and γ irradiated RAW 264.7 cells; Lane 3, EL-4 cells receiving medium from γ irradiated RAW 264.7 cells without LPS-stimulation; Lane 4, EL-4 cells receiving medium from LPS-stimulated RAW 264.7 cells; Lane 5, EL-4 cells receiving medium from unirradiated RAW 264.7 cells. Data represents means ± SE of three independent 3.4.5 Effect of L-NAME and cPTIO on Bystander response. Since the expressions of NF-κB and iNOS gene were significantly upregulated in irradiated as well as in bystander cells (Fig.3.4.5a, Lane 2 and 3), it was of interest to determine which 181
CHAPTER 3 RESULTS signaling factors were involved in bystander response. The response was looked at in the presence of cPTIO or L-NAME. L-NAME was washed out before irradiation so that the bystander cells are not exposed to L-NAME and iNOS is inhibited only in the irradiated cells. The addition of cPTIO, which scavenges the NO released in the medium, did not affect the expression of iNOS gene if the bystanding cell was of same origin, although NF-κB was somewhat inhibited (Fig.3.4.5a, Compare Lane 5 and Lane 3). The addition of L-NAME, which inhibits the iNOS in the irradiated cells, completely inhibited the bystander response in the EL-4 cells (Fig.3.4.5a, Compare Lane 4 and Lane 3). However both L-NAME and cPTIO inhibited the expression of NF-κB and iNOS in the bystander EL-4 cells if the medium was from LPS stimulated and irradiated RAW 264.7 cells (Fig.3.4.5a, Lane 6 and 7) i.e. the cell type was different, indicating that the bystander response was dependent on the cells type and the state of stimulation of the irradiated cells. The DNA damage was significantly higher in irradiated as well as in bystander cells (Fig.3.4.5b, Lane 2 and 3) as compared to the unirradiated control. However, the unirradiated EL-4 cells that had received medium either from L-NAME treated and irradiated EL-4 cells or from LPS stimulated, L-NAME treated and irradiated RAW 264.7 cells did not show any increase in DNA damage as compared to that in unirradiated control (Fig.3.4.5b, Lane 4 and 6). Similarly the unirradiated EL-4 cells that had received medium either from cPTIO treated and irradiated EL-4 cells or from LPS stimulated, cPTIO treated and irradiated RAW 264.7 cells did not show any increase in DNA damage as compared to that in unirradiated control (Fig.3.4.5b, Lane 5 and 7). Neither L-NAME nor cPTIO itself had any effect on DNA damage in EL-4 cells (Fig.3.4.5b, Lane 8 and 9). 182
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RADIATION INDUCED SIGNALING IN MAMM
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DECLARATION I, hereby declare that
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CONTENTS Page No. SYNOPSIS………
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2.11 Measurement of NO production
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PREAMBLE SYNOPSIS Ionising radiatio
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SYNOPSIS Aims and Objectives: To St
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SYNOPSIS 2.6 Immunofluorescence sta
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SYNOPSIS ATM gene expression, which
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SYNOPSIS Percentage Survival 100 80
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SYNOPSIS Ratio of Rad52 to Actin Ra
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Relative Phosphorylation 45 40 35 3
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SYNOPSIS Fig. 3.3A Clonogenic Cell
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SYNOPSIS (A) Av No. of phospho BRCA
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SYNOPSIS Percentage Survival 120 10
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SYNOPSIS Fig.3.4B. Existance of cro
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SYNOPSIS Fig. 3.4EDNA damage in EL-
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SYNOPSIS subsequent cytotoxicity ca
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SYNOPSIS [4] Hall, E. J. Radiobiolo
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CHAPTER 1 INTRODUCTION INTRODUCTION
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CHAPTER 1 INTRODUCTION 15.8% 9.56%
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CHAPTER 1 INTRODUCTION far apart an
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CHAPTER 1 INTRODUCTION and are more
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CHAPTER 1 INTRODUCTION 1.3 DNA dama
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CHAPTER 1 INTRODUCTION associates w
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CHAPTER 1 INTRODUCTION are unable t
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CHAPTER 1 INTRODUCTION Perhaps one
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CHAPTER 1 INTRODUCTION occurs at DS
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CHAPTER 1 INTRODUCTION related prot
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CHAPTER 1 INTRODUCTION damage must
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CHAPTER 1 INTRODUCTION At the prese
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CHAPTER 1 INTRODUCTION predominant
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CHAPTER 1 INTRODUCTION provide a me
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CHAPTER 1 INTRODUCTION hypersensiti
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CHAPTER 1 INTRODUCTION cycle-specif
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CHAPTER 1 INTRODUCTION 1.4 Overview
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CHAPTER 1 INTRODUCTION 1.4.1 Radiat
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CHAPTER 1 INTRODUCTION interaction
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CHAPTER 1 INTRODUCTION p90S6 kinase
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CHAPTER 1 INTRODUCTION CD4 (formerl
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CHAPTER 1 INTRODUCTION unrepaired d
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CHAPTER 1 INTRODUCTION well to the
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CHAPTER 1 INTRODUCTION 1.6 Radiatio
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CHAPTER 1 INTRODUCTION becomes pote
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CHAPTER 2 MATERIALS AND METHODS MAT
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CHAPTER 2 MATERIALS AND METHODS 2.2
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CHAPTER 2 MATERIALS AND METHODS res
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CHAPTER 2 MATERIALS AND METHODS Arr
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CHAPTER 2 MATERIALS AND METHODS PBS
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CHAPTER 2 MATERIALS AND METHODS the
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CHAPTER 2 MATERIALS AND METHODS 2.1
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CHAPTER 3 RESULTS RESULTS 93
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CHAPTER 3 RESULTS fractionated regi
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CHAPTER 3 RESULTS On comparison of
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CHAPTER 3 RESULTS Table 3.1.2A List
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CHAPTER 3 RESULTS 80 NM_002185 IL7R
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CHAPTER 3 RESULTS SAA2 149 AU134977
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CHAPTER 3 RESULTS 221 LOC643167 RNA
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CHAPTER 3 RESULTS 299 BF244402 FBXO
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CHAPTER 3 RESULTS CDK4) 57 AU152107
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CHAPTER 3 RESULTS 134 AL045793 METT
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CHAPTER 3 RESULTS 58 AF237813 ABAT
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CHAPTER 3 RESULTS 127 AI809749 ORMD
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CHAPTER 3 RESULTS 31 BE615699 UNC84
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CHAPTER 3 RESULTS 47 AF026303 SULT1
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CHAPTER 3 RESULTS 117 BF062193 CYor
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CHAPTER 3 RESULTS 187 AL036662 ---
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CHAPTER 3 RESULTS 52 AV686514 EMP2
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CHAPTER 3 RESULTS exposed to 10 Gy
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CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
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Page 142 and 143: CHAPTER 3 RESULTS Fig. 3.1.7 Transl
Page 144 and 145: CHAPTER 3 RESULTS 3.1.9 Stabilizati
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Page 148 and 149: CHAPTER 3 RESULTS whereas only the
Page 150 and 151: CHAPTER 3 RESULTS Fig.3.2.2 Gene ex
Page 152 and 153: CHAPTER 3 RESULTS Fig.3.2.4 Gene ex
Page 154 and 155: CHAPTER 3 RESULTS with equal doses
Page 156 and 157: CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
Page 158 and 159: CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
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Page 164 and 165: CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
Page 166 and 167: CHAPTER 3 RESULTS 3.3.2 Oxygen beam
Page 168 and 169: CHAPTER 3 RESULTS in all the cells.
Page 170 and 171: CHAPTER 3 RESULTS 3.3.2.3 Radiation
Page 176 and 177: CHAPTER 3 RESULTS Fig.3.3.2.7 Apopt
Page 178 and 179: CHAPTER 3 RESULTS PMA stimulated U9
Page 180 and 181: CHAPTER 3 RESULTS Fig.3.4.2. Exista
Page 182 and 183: CHAPTER 3 RESULTS up-regulation of
Page 184 and 185: CHAPTER 3 RESULTS Fig.3.4.3.2 NO pr
Page 186 and 187: CHAPTER 3 RESULTS 3.4.3.4 Apoptotic
Page 188 and 189: CHAPTER 3 RESULTS 3.4.4 Bystander e
Page 192 and 193: CHAPTER 3 RESULTS Fig.3.4.5a Gene e
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Page 196 and 197: CHAPTER 4 DISCUSSION directly expos
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Page 220 and 221: CHAPTER 4 DISCUSSION The survival o
Page 222 and 223: CHAPTER 5 REFERENCES [1] Khan, F. T
Page 224 and 225: CHAPTER 5 REFERENCES [19] Woo, R. A
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Page 232 and 233: CHAPTER 5 REFERENCES [84] Uziel, T.
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CHAPTER 5 REFERENCES [141] Pierce,
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CHAPTER 5 REFERENCES [156] Roots, R
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CHAPTER 5 REFERENCES [171] Xia, Z.;
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CHAPTER 5 REFERENCES (MAP) kinase c
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CHAPTER 5 REFERENCES phosphorylatio
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CHAPTER 5 REFERENCES [211] Anderson
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CHAPTER 5 REFERENCES [229] Konca, K
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CHAPTER 5 REFERENCES [245] Kastan,
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CHAPTER 5 REFERENCES [261] Miralbel
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CHAPTER 5 REFERENCES [278] Weizman,
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CHAPTER 5 REFERENCES [294] Zhou, H.
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PUBLICATIONS AND PRESENTATIONS Publ
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Mutation Research 729 (2012) 61-72
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S. Ghosh, M. Krishna / Mutation Res
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1568 I. J. Radiation Oncology d Bio
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