PMID- 30417274
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1873-9601 (Print)
IS  - 1873-961X (Electronic)
IS  - 1873-9601 (Linking)
VI  - 13
IP  - 2
DP  - 2019 Jun
TI  - Transforming growth factor-beta1 mediated CHST11 and CHSY1 mRNA expression is ROS 
      dependent in vascular smooth muscle cells.
PG  - 225-233
LID - 10.1007/s12079-018-0495-x [doi]
AB  - Transforming growth factor (TGF)-beta1 mediates glycosaminoglycan (GAG) chain 
      hyperelongation on secreted proteoglycans and these modifications are associated 
      with increased lipid binding in the vessel wall and the development of 
      atherosclerosis. In vascular smooth muscle cells (VSMCs), TGF-beta1 regulated GAG 
      elongation via extracellular signal-regulated kinase (ERK) and p38 as well as 
      Smad2 linker region phosphorylation. In this study, our aim was to identify the 
      TGF-beta1 mediated signalling pathway involving reactive oxygen species (ROS) and 
      Smad2 linker region phosphorylation that regulate the mRNA expression of GAG 
      synthesizing enzymes, chondroitin 4-O-sulfotransferase 1 (CHST11) and chondroitin 
      sulfate synthase 1 (CHSY1) which are the rate limiting enzymes involved in GAG 
      chain elongation. Signalling molecules were assessed by western blotting, 
      quantitative real-time PCR was used for analysis of gene expression and 
      intracellular ROS level was measured by a fluorescence based assay. TGF-beta1 
      induced ROS production in VSMCs. Nicotinamide adenine dinucleotide phosphate 
      oxidase (Nox) inhibitors, diphenyleneiodonium (DPI) and apocynin blocked TGF-beta1 
      mediated Smad2 linker region phosphorylation. TGF-beta1 treatment increased the mRNA 
      levels of CHST11 and CHSY1. Pharmacological inhibition of Nox blocked TGF-beta1 
      mediated mitogen activated protein kinases (MAPKs) phosphorylation and TGF-beta1 
      stimulated CHST11 and CHSY1 mRNA expression. These findings demonstrated that 
      TGF-beta1 mediated expression of CHST11 and CHSY1 can occur via Nox-dependent 
      pathways and Smad2 linker region phosphorylation.
FAU - Mohamed, Raafat
AU  - Mohamed R
AD  - Pharmacy Australia Centre of Excellence, School of Pharmacy, The University of 
      Queensland, 20 Cornwall St, Woolloongabba, QLD, 4102, Australia.
AD  - Department of Basic Sciences, College of Dentistry, University of Mosul, Mosul, 
      Iraq.
FAU - Dayati, Parisa
AU  - Dayati P
AD  - Hyperlipidemia Research Center, Department of Clinical Biochemistry, Faculty of 
      Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
FAU - Mehr, Reyhaneh Niayesh
AU  - Mehr RN
AD  - Hyperlipidemia Research Center, Department of Clinical Biochemistry, Faculty of 
      Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
FAU - Kamato, Danielle
AU  - Kamato D
AD  - Pharmacy Australia Centre of Excellence, School of Pharmacy, The University of 
      Queensland, 20 Cornwall St, Woolloongabba, QLD, 4102, Australia.
AD  - Department of Pharmacy, Xinhua College of Sun Yat-sen University, Tianhe 
      District, Guangzhou, 510520, Guangdong Pr., China.
FAU - Seif, Faezeh
AU  - Seif F
AD  - Hyperlipidemia Research Center, Department of Clinical Biochemistry, Faculty of 
      Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
FAU - Babaahmadi-Rezaei, Hossein
AU  - Babaahmadi-Rezaei H
AD  - Hyperlipidemia Research Center, Department of Clinical Biochemistry, Faculty of 
      Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 
      babaahmadi-h@ajums.ac.ir.
FAU - Little, Peter J
AU  - Little PJ
AD  - Pharmacy Australia Centre of Excellence, School of Pharmacy, The University of 
      Queensland, 20 Cornwall St, Woolloongabba, QLD, 4102, Australia. 
      p.little@uq.edu.au.
AD  - Department of Pharmacy, Xinhua College of Sun Yat-sen University, Tianhe 
      District, Guangzhou, 510520, Guangdong Pr., China. p.little@uq.edu.au.
LA  - eng
PT  - Journal Article
DEP - 20181111
PL  - Netherlands
TA  - J Cell Commun Signal
JT  - Journal of cell communication and signaling
JID - 101308338
PMC - PMC6498334
OTO - NOTNLM
OT  - Atherosclerosis
OT  - Glycosaminoglycan
OT  - Mitogen activated protein kinases
OT  - Nox
OT  - Reactive oxygen species
EDAT- 2018/11/13 06:00
MHDA- 2018/11/13 06:01
PMCR- 2019/06/01
CRDT- 2018/11/13 06:00
PHST- 2018/09/07 00:00 [received]
PHST- 2018/11/01 00:00 [accepted]
PHST- 2018/11/13 06:00 [pubmed]
PHST- 2018/11/13 06:01 [medline]
PHST- 2018/11/13 06:00 [entrez]
PHST- 2019/06/01 00:00 [pmc-release]
AID - 10.1007/s12079-018-0495-x [pii]
AID - 495 [pii]
AID - 10.1007/s12079-018-0495-x [doi]
PST - ppublish
SO  - J Cell Commun Signal. 2019 Jun;13(2):225-233. doi: 10.1007/s12079-018-0495-x. 
      Epub 2018 Nov 11.