PMID- 34060109
OWN - NLM
STAT- MEDLINE
DCOM- 20220128
LR  - 20220128
IS  - 1440-1681 (Electronic)
IS  - 0305-1870 (Linking)
VI  - 48
IP  - 9
DP  - 2021 Sep
TI  - Substance P ameliorates TNF-alpha-mediated impairment of human aortic vascular cells 
      in vitro.
PG  - 1288-1297
LID - 10.1111/1440-1681.13533 [doi]
AB  - Vascular diseases are caused by endothelial dysfunction due to inflammation. On 
      endothelial injury, the expression of extracellular matrix (ECM) is enhanced and 
      nitric oxide (NO) bioavailability becomes deficient. This condition affects 
      endothelial metabolism and leads to vascular destruction. The aim of this 
      investigation was to determine whether substance P (SP) is able to protect the 
      endothelium against inflammatory stress. To this end, aortic endothelial cells 
      were pre-treated with SP, followed by tumour necrosis factor alpha (TNF-alpha), and 
      cellular responses were evaluated using a combination of cell biology and 
      quantification assays, as well as western blot analyses. Our results show that 
      TNF-alpha enhanced ECM expression and reduced NO production within 4 hours, promoting 
      immune cell adhesion to the endothelium and monocyte chemoattractant protein-1 
      (MCP-1) secretion from aortic smooth muscle cells. However, SP treatment 
      ameliorated TNF-alpha-induced endothelial impairment by maintaining low ECM levels. 
      Our data suggest that this protective effect is mediated by Akt activation and 
      NO-enriched conditions. The inhibition of aortic endothelial cell injury by SP 
      also reduced MCP-1 production in aortic smooth muscle cells. Together, our data 
      indicate that SP can protect aortic endothelial and smooth muscle cells from 
      inflammatory injury, which suggests that SP may prevent cardiovascular disease.
CI  - (c) 2021 John Wiley & Sons Australia, Ltd.
FAU - Kim, Do Young
AU  - Kim DY
AD  - Department of Biomedical Science and Technology, Graduate School, Kyung Hee 
      University, Seoul, South Korea.
FAU - Piao, Jiyuan
AU  - Piao J
AD  - Department of Genetic Engineering, College of Life Science and Graduate School of 
      Biotechnology, Kyung Hee University, Seoul, South Korea.
FAU - Park, Jeong Seop
AU  - Park JS
AD  - Department of Biomedical Science and Technology, Graduate School, Kyung Hee 
      University, Seoul, South Korea.
FAU - Lee, Dahyeon
AU  - Lee D
AD  - Department of Biomedical Science and Technology, Graduate School, Kyung Hee 
      University, Seoul, South Korea.
FAU - Hong, Hyun Sook
AU  - Hong HS
AD  - Department of Biomedical Science and Technology, Graduate School, Kyung Hee 
      University, Seoul, South Korea.
AD  - East-West Medical Research Institute, Kyung Hee University, Seoul, South Korea.
AD  - Kyung Hee Institute of Regenerative Medicine (KIRM), Medical Science Research 
      institute, Kyung Hee University Medical Center, Seoul, South Korea.
LA  - eng
GR  - HI18C1492/Korean Health Technology R&D Project grant from the Ministry of 
      Health and Welfare (Sejong, Republic of Korea)/
GR  - 2018R1D1A1B0704104813/Basic Science Research Program through the National 
      Research Foundation of Korea (NRF) funded by the Ministry of Education/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210624
PL  - Australia
TA  - Clin Exp Pharmacol Physiol
JT  - Clinical and experimental pharmacology & physiology
JID - 0425076
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - *Tumor Necrosis Factor-alpha
OTO - NOTNLM
OT  - aortic endothelial cell
OT  - aortic smooth muscle cells
OT  - inflammation
OT  - substance P
EDAT- 2021/06/02 06:00
MHDA- 2022/01/29 06:00
CRDT- 2021/06/01 06:48
PHST- 2021/05/24 00:00 [revised]
PHST- 2021/04/09 00:00 [received]
PHST- 2021/05/28 00:00 [accepted]
PHST- 2021/06/02 06:00 [pubmed]
PHST- 2022/01/29 06:00 [medline]
PHST- 2021/06/01 06:48 [entrez]
AID - 10.1111/1440-1681.13533 [doi]
PST - ppublish
SO  - Clin Exp Pharmacol Physiol. 2021 Sep;48(9):1288-1297. doi: 
      10.1111/1440-1681.13533. Epub 2021 Jun 24.