Tumor Necrosis Factor Alpha Deficiency Improves Endothelial Function and Cardiovascular Injury in Deoxycorticosterone AcetateSalt-Hypertensive Mice
Joint Authors
Zhou, Ming-Sheng
Cai, Ruiping
Hao, Yun
Liu, Yue-Yang
Huang, Lei
Yao, Yang
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-02-28
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
It has been shown that the inflammatory cytokine tumor necrosis factor α (TNFα) plays a role in the development of hypertension and end-stage renal diseases.
We hypothesize that TNFα contributes to endothelial dysfunction and cardiac and vascular injury in deoxycorticosterone acetate (DOCA)/salt-hypertensive mice.
The wild-type or TNFα-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).
TNFα 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 TNFα, interleukin 1β (IL1β), monocyte chemotactic protein 1 (MCP1), and monocyte/macrophage marker F4/80 were significantly increased in the aorta of DOCA-hypertensive mice; TNFα 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 β and fibronectin.
TNFα 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; TNFα deficiency prevented a decrease in eNOS expression and an increase in miR155 expression in DOCA mice.
These results support the idea that TNFα significantly contributes to vascular inflammation, vascular dysfunction, and injury in hypertension.
American Psychological Association (APA)
Cai, Ruiping& Hao, Yun& Liu, Yue-Yang& Huang, Lei& Yao, Yang& Zhou, Ming-Sheng. 2020. Tumor Necrosis Factor Alpha Deficiency Improves Endothelial Function and Cardiovascular Injury in Deoxycorticosterone AcetateSalt-Hypertensive Mice. BioMed Research International،Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1133544
Modern Language Association (MLA)
Cai, Ruiping…[et al.]. Tumor Necrosis Factor Alpha Deficiency Improves Endothelial Function and Cardiovascular Injury in Deoxycorticosterone AcetateSalt-Hypertensive Mice. BioMed Research International No. 2020 (2020), pp.1-10.
https://search.emarefa.net/detail/BIM-1133544
American Medical Association (AMA)
Cai, Ruiping& Hao, Yun& Liu, Yue-Yang& Huang, Lei& Yao, Yang& Zhou, Ming-Sheng. Tumor Necrosis Factor Alpha Deficiency Improves Endothelial Function and Cardiovascular Injury in Deoxycorticosterone AcetateSalt-Hypertensive Mice. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1133544
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1133544