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Article

Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II

  • Authors:
    • Jiasen Cui
    • Shunjiu Zhuang
    • Shaohong Qi
    • Li Li
    • Junwen Zhou
    • Wan Zhang
    • Yun Zhao
    • Ning Qi
    • Yangjun Yin
    • Lu Huang
  • View Affiliations / Copyright

    Affiliations: Department of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai 200040, P.R. China
  • Pages: 6255-6261
    |
    Published online on: August 22, 2017
       https://doi.org/10.3892/mmr.2017.7328
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Abstract

Angiotensin II (Ang II) has been reported as key in inducing endothelial cell injury, and endothelial cells may produce nitric oxide (NO) to protect themselves. However, the underlying mechanism remains elusive. Human umbilical vein endothelial cells (HUVECs) were divided into five treatment groups as follows: Normal control, Ang II, Ang II + sodium hydrosulfide [NaHS; hydrogen sulfide (H2S) donor], Ang II + Akt inhibitors + NaHS, and Ang II + endothelial nitric oxide synthases (eNOS) inhibitors + NaHS. Subsequently, cell viability, apoptosis, migration, proliferation and adhesion ability were determined. In addition, tubular structure formation was observed, and the NO and phosphorylation levels of Akt and eNOS were evaluated. Compared with the normal control group, Ang II treatment reduced the viability of HUVECs and increased the level of cell apoptosis (P<0.05). Furthermore, Ang II treatment inhibited the phosphorylation level of eNOS and Akt, as well as the generation of NO (P<0.05). H2S reversed the above‑mentioned effects significantly and increased cell proliferation, adhesion ability and promoted tubular structure formation (P<0.05); however, H2S did not reverse the impact of eNOS and Akt phosphorylation levels after being processed with Akt and eNOS inhibitors, which indicates that H2S is capable of protecting HUVECs via the eNOS/Akt signaling pathway (P<0.05). Thus, H2S stimulates the production of NO and protects HUVECs via inducing the Akt/eNOS signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Cui J, Zhuang S, Qi S, Li L, Zhou J, Zhang W, Zhao Y, Qi N, Yin Y, Huang L, Huang L, et al: Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II. Mol Med Rep 16: 6255-6261, 2017.
APA
Cui, J., Zhuang, S., Qi, S., Li, L., Zhou, J., Zhang, W. ... Huang, L. (2017). Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II. Molecular Medicine Reports, 16, 6255-6261. https://doi.org/10.3892/mmr.2017.7328
MLA
Cui, J., Zhuang, S., Qi, S., Li, L., Zhou, J., Zhang, W., Zhao, Y., Qi, N., Yin, Y., Huang, L."Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II". Molecular Medicine Reports 16.5 (2017): 6255-6261.
Chicago
Cui, J., Zhuang, S., Qi, S., Li, L., Zhou, J., Zhang, W., Zhao, Y., Qi, N., Yin, Y., Huang, L."Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II". Molecular Medicine Reports 16, no. 5 (2017): 6255-6261. https://doi.org/10.3892/mmr.2017.7328
Copy and paste a formatted citation
x
Spandidos Publications style
Cui J, Zhuang S, Qi S, Li L, Zhou J, Zhang W, Zhao Y, Qi N, Yin Y, Huang L, Huang L, et al: Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II. Mol Med Rep 16: 6255-6261, 2017.
APA
Cui, J., Zhuang, S., Qi, S., Li, L., Zhou, J., Zhang, W. ... Huang, L. (2017). Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II. Molecular Medicine Reports, 16, 6255-6261. https://doi.org/10.3892/mmr.2017.7328
MLA
Cui, J., Zhuang, S., Qi, S., Li, L., Zhou, J., Zhang, W., Zhao, Y., Qi, N., Yin, Y., Huang, L."Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II". Molecular Medicine Reports 16.5 (2017): 6255-6261.
Chicago
Cui, J., Zhuang, S., Qi, S., Li, L., Zhou, J., Zhang, W., Zhao, Y., Qi, N., Yin, Y., Huang, L."Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II". Molecular Medicine Reports 16, no. 5 (2017): 6255-6261. https://doi.org/10.3892/mmr.2017.7328
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