PMID- 29343424
OWN - NLM
STAT- MEDLINE
DCOM- 20180724
LR  - 20180724
IS  - 1096-0333 (Electronic)
IS  - 0041-008X (Linking)
VI  - 341
DP  - 2018 Feb 15
TI  - IGF1/MAPK/ERK signaling pathway-mediated programming alterations of adrenal 
      cortex cell proliferation by prenatal caffeine exposure in male offspring rats.
PG  - 64-76
LID - S0041-008X(18)30008-5 [pii]
LID - 10.1016/j.taap.2018.01.008 [doi]
AB  - Our previous study proposed a glucocorticoid-insulin-like growth factor 1 
      (GC-IGF1) axis programming mechanism for prenatal caffeine exposure (PCE)-induced 
      adrenal developmental dysfunction. Here, we focused on PCE-induced cell 
      proliferation changes of the adrenal cortex in male offspring rats before and 
      after birth and clarified the intrauterine programming mechanism. On gestational 
      day (GD) 20, the PCE group had an elevated serum corticosterone level reduced 
      fetal bodyweight, maximum adrenal sectional area, and elevated adrenal 
      corticosterone and aldosterone contents. However, in postnatal week (PW) 6, the 
      serum corticosterone level was decreased, and the bodyweight, with catch-up 
      growth, adrenal cortex maximum cross-sectional area and aldosterone content were 
      relatively increased, while the adrenal corticosterone content was lower. On 
      GD20, the expression of adrenal IGF1, IGF1R and proliferating cell nuclear 
      antigen (PCNA) were decreased, while the expression of these factors at PW6 were 
      increased in the PCE group. Fetal adrenal gene chip analysis suggested that the 
      mitogen-activated protein kinase/extracellular regulated protein kinase 
      (MAPK/ERK) signal pathway was suppressed in the PCE group. Moreover, in the rat 
      primary adrenal cells, corticosterone (rather than caffeine) was shown to 
      significantly inhibit cell proliferation, IGF1 and PCNA expression, and ERK 
      phosphorylation, which could be reversed by exogenous IGF1. Meanwhile, the 
      effects of exogenous IGF1 were reversed by the ERK pathway inhibitor (PD184161). 
      In conclusion, PCE could induce programming alterations in adrenal cortical cell 
      proliferation before and after birth in male offspring rats. The underlying 
      mechanism is associated with the inhibition of fetal adrenal IGF1-related 
      MAPK/ERK signaling pathway caused by high glucocorticoid levels.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Chen, Guanghui
AU  - Chen G
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China.
FAU - Yuan, Chao
AU  - Yuan C
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China.
FAU - Duan, Fangfang
AU  - Duan F
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China.
FAU - Liu, Yanyan
AU  - Liu Y
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China.
FAU - Zhang, Jinzhi
AU  - Zhang J
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China.
FAU - He, Zheng
AU  - He Z
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China.
FAU - Huang, Hegui
AU  - Huang H
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China.
FAU - He, Chunjiang
AU  - He C
AD  - Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan 
      430071, China.
FAU - Wang, Hui
AU  - Wang H
AD  - Department of Pharmacology, Basic Medical School of Wuhan University, Wuhan 
      430071, China; Hubei Provincial Key Laboratory of Developmentally Originated 
      Disease, Wuhan 430071, China. Electronic address: wanghui19@whu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180116
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (insulin-like growth factor-1, rat)
RN  - 3G6A5W338E (Caffeine)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
SB  - IM
MH  - Adrenal Cortex/cytology/drug effects/*metabolism
MH  - Animals
MH  - Body Weight/drug effects/physiology
MH  - Caffeine/administration & dosage/*toxicity
MH  - Cell Proliferation/drug effects/*physiology
MH  - Cells, Cultured
MH  - Cellular Reprogramming/drug effects/physiology
MH  - Dose-Response Relationship, Drug
MH  - Female
MH  - Insulin-Like Growth Factor I/antagonists & inhibitors/*metabolism
MH  - MAP Kinase Signaling System/drug effects/*physiology
MH  - Male
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/chemically induced/*metabolism
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
OTO - NOTNLM
OT  - Adrenal cell proliferation
OT  - Glucocorticoid
OT  - Insulin-like growth factor 1
OT  - Mitogen-activated protein kinase/extracellular signal-regulated kinase
OT  - Prenatal caffeine exposure
EDAT- 2018/01/19 06:00
MHDA- 2018/07/25 06:00
CRDT- 2018/01/19 06:00
PHST- 2017/08/25 00:00 [received]
PHST- 2018/01/01 00:00 [revised]
PHST- 2018/01/12 00:00 [accepted]
PHST- 2018/01/19 06:00 [pubmed]
PHST- 2018/07/25 06:00 [medline]
PHST- 2018/01/19 06:00 [entrez]
AID - S0041-008X(18)30008-5 [pii]
AID - 10.1016/j.taap.2018.01.008 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 2018 Feb 15;341:64-76. doi: 10.1016/j.taap.2018.01.008. 
      Epub 2018 Jan 16.