PMID- 32190663
OWN - NLM
STAT- MEDLINE
DCOM- 20201221
LR  - 20210625
IS  - 2314-6141 (Electronic)
IS  - 2314-6133 (Print)
VI  - 2020
DP  - 2020
TI  - Tumor Necrosis Factor Alpha Deficiency Improves Endothelial Function and 
      Cardiovascular Injury in Deoxycorticosterone Acetate/Salt-Hypertensive Mice.
PG  - 3921074
LID - 10.1155/2020/3921074 [doi]
LID - 3921074
AB  - It has been shown that the inflammatory cytokine tumor necrosis factor alpha (TNFalpha) 
      plays a role in the development of hypertension and end-stage renal diseases. We 
      hypothesize that TNFalpha contributes to endothelial dysfunction and cardiac and 
      vascular injury in deoxycorticosterone acetate (DOCA)/salt-hypertensive mice. The 
      wild-type or TNFalpha-deficient mice were uninephrectomized and implanted with DOCA 
      pellet treatment for 5 weeks; the mice were given either tap water or 1% NaCl 
      drinking water. DOCA mice developed hypertension (systolic blood pressure (SBP): 
      167 +/- 5 vs. 110 +/- 4 mmHg in control group, p < 0.05), cardiac and vascular 
      hypertrophy, and the impairment of endothelium-dependent relaxation to 
      acetylcholine (EDR). TNFalpha deficiency improved EDR and lowered cardiac and 
      vascular hypertrophy with a mild reduction in SBP (152 +/- 4 vs. 167 +/- 5 mmHg in 
      DOCA group, p < 0.05) in DOCA mice. The mRNA expressions of the inflammatory 
      cytokines, including TNFalpha, interleukin 1beta (IL1beta), monocyte chemotactic protein 1 
      (MCP1), and monocyte/macrophage marker F4/80 were significantly increased in the 
      aorta of DOCA-hypertensive mice; TNFalpha deficiency reduced these inflammatory gene 
      expressions. DOCA-hypertensive mice also exhibited an increase in the vascular 
      oxidative fluorescence intensities, the protein expressions of gp91phox and 
      p22phox, and the fibrotic factors transforming growth factor beta and fibronectin. 
      TNFalpha deficiency reduced oxidative stress and fibrotic protein expressions. The 
      DOCA mice also showed a decrease in the protein expression of eNOS associated 
      with increased miR155 expression; TNFalpha deficiency prevented a decrease in eNOS 
      expression and an increase in miR155 expression in DOCA mice. These results 
      support the idea that TNFalpha significantly contributes to vascular inflammation, 
      vascular dysfunction, and injury in hypertension.
CI  - Copyright (c) 2020 Ruiping Cai et al.
FAU - Cai, Ruiping
AU  - Cai R
AD  - Department of Physiology, Shenyang Medical College, Shenyang 110034, China.
FAU - Hao, Yun
AU  - Hao Y
AD  - Department of Physiology, Jinzhou Medical University, Jinzhou 121001, China.
FAU - Liu, Yue-Yang
AU  - Liu YY
AD  - Department of Physiology, Shenyang Medical College, Shenyang 110034, China.
FAU - Huang, Lei
AU  - Huang L
AD  - Department of Physiology, Shenyang Medical College, Shenyang 110034, China.
FAU - Yao, Yang
AU  - Yao Y
AD  - Department of Physiology, Shenyang Medical College, Shenyang 110034, China.
FAU - Zhou, Ming-Sheng
AU  - Zhou MS
AUID- ORCID: 0000-0001-9075-345X
AD  - Department of Physiology, Shenyang Medical College, Shenyang 110034, China.
AD  - The Open Project of Key Laboratory of Prevention and Treatment of Cardiovascular 
      and Cerebrovascular Diseases, Ministry of Education, Gannan Medical University, 
      Ganzhou 341000, China.
LA  - eng
PT  - Journal Article
DEP - 20200228
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (Acetates)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytochrome b Group)
RN  - 0 (Interleukin-1beta)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn155 microRNA, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Salts)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 40GP35YQ49 (Desoxycorticosterone)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos3 protein, mouse)
RN  - EC 1.6.3.- (Cybb protein, mouse)
RN  - EC 1.6.3.- (NADPH Oxidase 2)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 1.6.3.1 (Cyba protein, mouse)
SB  - IM
MH  - Acetates
MH  - Animals
MH  - Aorta/drug effects/metabolism
MH  - Blood Pressure/drug effects
MH  - Cardiovascular Diseases/*physiopathology
MH  - Chemokine CCL2/metabolism
MH  - Cytochrome b Group/metabolism
MH  - Desoxycorticosterone/*adverse effects
MH  - Endothelium, Vascular/*metabolism/pathology
MH  - Gene Expression
MH  - Heart/drug effects
MH  - Hypertension/*chemically induced/*metabolism/pathology/physiopathology
MH  - Inflammation
MH  - Interleukin-1beta/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - MicroRNAs/metabolism
MH  - NADPH Oxidase 2/metabolism
MH  - NADPH Oxidases/metabolism
MH  - Nitric Oxide Synthase Type III/genetics/metabolism
MH  - Oxidative Stress
MH  - RNA, Messenger/metabolism
MH  - Salts/*adverse effects
MH  - Sodium Chloride/metabolism
MH  - Tumor Necrosis Factor-alpha/*deficiency/*genetics/metabolism
PMC - PMC7064859
COIS- All authors declare no conflict of interest.
EDAT- 2020/03/20 06:00
MHDA- 2020/12/22 06:00
PMCR- 2020/02/28
CRDT- 2020/03/20 06:00
PHST- 2019/08/01 00:00 [received]
PHST- 2019/10/03 00:00 [revised]
PHST- 2019/10/14 00:00 [accepted]
PHST- 2020/03/20 06:00 [entrez]
PHST- 2020/03/20 06:00 [pubmed]
PHST- 2020/12/22 06:00 [medline]
PHST- 2020/02/28 00:00 [pmc-release]
AID - 10.1155/2020/3921074 [doi]
PST - epublish
SO  - Biomed Res Int. 2020 Feb 28;2020:3921074. doi: 10.1155/2020/3921074. eCollection 
      2020.