PMID- 29391264
OWN - NLM
STAT- MEDLINE
DCOM- 20180918
LR  - 20180918
IS  - 1879-3177 (Electronic)
IS  - 0887-2333 (Linking)
VI  - 48
DP  - 2018 Apr
TI  - Genome-wide gene expression changes associated with exposure of rat liver, heart, 
      and kidney cells to endosulfan.
PG  - 244-254
LID - S0887-2333(18)30024-9 [pii]
LID - 10.1016/j.tiv.2018.01.022 [doi]
AB  - Endosulfan was once the most commonly used pesticide in agriculture and 
      horticulture. It is an environmentally persistent organochlorine compound with 
      the potential to bioaccumulate as it progresses through the food chain. Its acute 
      and chronic toxicity to mammals, including humans, is well known, but the 
      molecular mechanisms of its toxicity are not fully understood. To gain insight to 
      these mechanisms, we examined genome-wide gene expression changes of rat liver, 
      heart, and kidney cells induced by endosulfan exposure. We found that among the 
      cell types examined, kidney and liver cells were the most sensitive and most 
      resilient, respectively, to endosulfan insult. We acquired RNA sequencing 
      information from cells exposed to endosulfan to identify differentially expressed 
      genes, which we further examined to determine the cellular pathways that were 
      affected. In kidney cells, exposure to endosulfan was uniquely associated with 
      altered expression levels of genes constituting the hypoxia-inducible factor-1 
      (HIF-1) signaling pathway. In heart and liver cells, exposure to endosulfan 
      altered the expression levels of genes for many members of the extracellular 
      matrix (ECM)-receptor interaction pathway. Because both HIF-1 signaling and 
      ECM-receptor interaction pathways directly or indirectly control cell growth, 
      differentiation, proliferation, and apoptosis, our findings suggest that 
      dysregulation of these pathways is responsible for endosulfan-induced cell death.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Liu, Ruifeng
AU  - Liu R
AD  - Department of Defense Biotechnology High Performance Computing Software 
      Applications Institute, Telemedicine and Advanced Technology Research Center, US 
      Army Medical Research and Materiel Command, Fort Detrick, MD 21702, USA.
FAU - Printz, Richard L
AU  - Printz RL
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University School 
      of Medicine, Nashville, TN 37232, USA.
FAU - Jenkins, Erin C
AU  - Jenkins EC
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University School 
      of Medicine, Nashville, TN 37232, USA.
FAU - O'Brien, Tracy P
AU  - O'Brien TP
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University School 
      of Medicine, Nashville, TN 37232, USA.
FAU - Te, Jerez A
AU  - Te JA
AD  - Department of Defense Biotechnology High Performance Computing Software 
      Applications Institute, Telemedicine and Advanced Technology Research Center, US 
      Army Medical Research and Materiel Command, Fort Detrick, MD 21702, USA.
FAU - Shiota, Masakazu
AU  - Shiota M
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University School 
      of Medicine, Nashville, TN 37232, USA.
FAU - Wallqvist, Anders
AU  - Wallqvist A
AD  - Department of Defense Biotechnology High Performance Computing Software 
      Applications Institute, Telemedicine and Advanced Technology Research Center, US 
      Army Medical Research and Materiel Command, Fort Detrick, MD 21702, USA. 
      Electronic address: sven.a.wallqvist.civ@mail.mil.
LA  - eng
PT  - Journal Article
DEP - 20180131
PL  - England
TA  - Toxicol In Vitro
JT  - Toxicology in vitro : an international journal published in association with 
      BIBRA
JID - 8712158
RN  - 0 (Hif1a protein, rat)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Insecticides)
RN  - OKA6A6ZD4K (Endosulfan)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Endosulfan/*toxicity
MH  - Extracellular Matrix/drug effects
MH  - Gene Expression/*drug effects
MH  - Genome-Wide Association Study
MH  - Hepatocytes/*drug effects
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis/drug effects
MH  - Insecticides/*toxicity
MH  - Kidney/*cytology/*drug effects
MH  - Myocytes, Cardiac/*drug effects
MH  - Primary Cell Culture
MH  - Rats
MH  - Signal Transduction/drug effects
OTO - NOTNLM
OT  - Cytotoxicity
OT  - Endosulfan
OT  - Extracellular matrix-receptor interaction
OT  - Hypoxia-inducible factor-1
OT  - RNA-seq
EDAT- 2018/02/03 06:00
MHDA- 2018/09/19 06:00
CRDT- 2018/02/03 06:00
PHST- 2017/06/01 00:00 [received]
PHST- 2018/01/25 00:00 [revised]
PHST- 2018/01/27 00:00 [accepted]
PHST- 2018/02/03 06:00 [pubmed]
PHST- 2018/09/19 06:00 [medline]
PHST- 2018/02/03 06:00 [entrez]
AID - S0887-2333(18)30024-9 [pii]
AID - 10.1016/j.tiv.2018.01.022 [doi]
PST - ppublish
SO  - Toxicol In Vitro. 2018 Apr;48:244-254. doi: 10.1016/j.tiv.2018.01.022. Epub 2018 
      Jan 31.