PMID- 29491215
OWN - NLM
STAT- MEDLINE
DCOM- 20180829
LR  - 20231213
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 41
IP  - 3
DP  - 2018
TI  - Cigarette Smoke Extract Disrupts Transcriptional Activities Mediated by Thyroid 
      Hormones and Its Receptors.
PG  - 383-393
LID - 10.1248/bpb.b17-00735 [doi]
AB  - Cigarette smoke contains over 4800 compounds, including at least 200 toxicants or 
      endocrine disruptors. Currently, effects of cigarette smoke on thyroid hormone 
      (TH) levels remains to be clarified. Here, we demonstrate that cigarette smoke 
      extract (CSE) possesses thyroid hormone properties and acts synergistically as a 
      partial agonist for thyroid hormone receptors (TRs) in the presence of TH. In 
      transient gene expression experiments, CSE stimulated transcriptional activity 
      with TH in a dose-dependent manner. Stimulatory effects were observed with 
      physiological TH concentrations, although CSE did not activate TRs without TH. 
      CSE (5%) dissolved in phosphate-buffered saline (PBS) supplemented with 1 nM TH 
      was approximately comparable to 3.2+/-0.1 and 2.3+/-0.2 nM of TRalpha1 and TRbeta1, 
      respectively. To illustrate probable mechanisms of the CSE agonistic activity, 
      effects on TR mediated transcriptional functions with cofactors were 
      investigated. With a mammalian two-hybrid assay, CSE recruited the nuclear 
      coactivators glucocorticoid receptor interacting protein 1 (GRIP1) and steroid 
      receptor coactivator 1 (SRC1) to the TR. Unsaturated carbonyl compounds, 
      acrolein, crotonaldehyde, and methyl vinyl ketone, representative constituents of 
      CSE, retained such agonistic properties and possibly contributed to stimulatory 
      effects. The results suggest that CSE recruits a transcriptional activator and 
      may reinforce TH binding to the TR additively, resulting in gene expression. CSE 
      partially agonizes TH action and may disturb the function of various nuclear 
      hormone receptor types and their cofactors to disrupt the physiological 
      processes.
FAU - Hayashi, Misa
AU  - Hayashi M
AD  - Department of Medicine and Clinical Science, Graduate School of Pharmaceutical 
      Sciences, Mukogawa Women's University.
FAU - Futawaka, Kumi
AU  - Futawaka K
AD  - Department of Medicine and Clinical Science, Graduate School of Pharmaceutical 
      Sciences, Mukogawa Women's University.
FAU - Matsushita, Midori
AU  - Matsushita M
AD  - Department of Medicine and Clinical Science, Graduate School of Pharmaceutical 
      Sciences, Mukogawa Women's University.
FAU - Hatai, Mayuko
AU  - Hatai M
AD  - Department of Medicine and Clinical Science, Graduate School of Pharmaceutical 
      Sciences, Mukogawa Women's University.
FAU - Yoshikawa, Noriko
AU  - Yoshikawa N
AD  - Department of Medicine and Clinical Science, Graduate School of Pharmaceutical 
      Sciences, Mukogawa Women's University.
FAU - Nakamura, Kazuki
AU  - Nakamura K
AD  - Department of Medicine and Clinical Science, Graduate School of Pharmaceutical 
      Sciences, Mukogawa Women's University.
FAU - Tagami, Tetsuya
AU  - Tagami T
AD  - Division of Endocrinology, Metabolism and Hypertension, Clinical Research 
      Institute, Kyoto Medical Center, National Hospital Organization.
FAU - Moriyama, Kenji
AU  - Moriyama K
AD  - Department of Medicine and Clinical Science, Graduate School of Pharmaceutical 
      Sciences, Mukogawa Women's University.
AD  - Division of Endocrinology, Metabolism and Hypertension, Clinical Research 
      Institute, Kyoto Medical Center, National Hospital Organization.
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Carrier Proteins)
RN  - 0 (GRIP1 protein, human)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 0 (Smoke)
RN  - 0 (Thyroid Hormone Receptors alpha)
RN  - 0 (Thyroid Hormone Receptors beta)
RN  - 0 (Thyroid Hormones)
RN  - EC 1.1.1.37 (Malate Dehydrogenase)
RN  - EC 1.1.1.39 (malate dehydrogenase (decarboxylating))
RN  - EC 2.3.1.48 (NCOA1 protein, human)
RN  - EC 2.3.1.48 (Nuclear Receptor Coactivator 1)
SB  - IM
MH  - Carrier Proteins/drug effects
MH  - Gene Expression Regulation/drug effects
MH  - HEK293 Cells
MH  - Humans
MH  - Malate Dehydrogenase/biosynthesis
MH  - Nerve Tissue Proteins/drug effects
MH  - Nuclear Receptor Coactivator 1/genetics
MH  - Receptors, Thyroid Hormone/*drug effects/genetics
MH  - Smoke/*adverse effects/analysis
MH  - Thyroid Hormone Receptors alpha/drug effects/genetics
MH  - Thyroid Hormone Receptors beta/drug effects/genetics
MH  - Thyroid Hormones/*pharmacology
MH  - Nicotiana/*adverse effects/chemistry
MH  - Transcription, Genetic/*drug effects
OTO - NOTNLM
OT  - endocrine disruptor
OT  - signal transduction
OT  - thyroid hormone receptor
EDAT- 2018/03/02 06:00
MHDA- 2018/08/30 06:00
CRDT- 2018/03/02 06:00
PHST- 2018/03/02 06:00 [entrez]
PHST- 2018/03/02 06:00 [pubmed]
PHST- 2018/08/30 06:00 [medline]
AID - 10.1248/bpb.b17-00735 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2018;41(3):383-393. doi: 10.1248/bpb.b17-00735.