2. Academic Validation
  3. High Glucose Stimulates Expression of MFHAS1 to Mitigate Inflammation via Akt/HO-1 Pathway in Human Umbilical Vein Endothelial Cells

High Glucose Stimulates Expression of MFHAS1 to Mitigate Inflammation via Akt/HO-1 Pathway in Human Umbilical Vein Endothelial Cells

  • Inflammation. 2018 Mar;41(2):400-408. doi: 10.1007/s10753-017-0696-0.
Hui-Hui Wang 1,  Peng-Fei Sun 1,  Wan-Kun Chen 1,  Jing Zhong 1,  Qi-Qing Shi 2,  Mei-Lin Weng 1,  Duan Ma 3,  Chang-Hong Miao 4
Affiliations

Affiliations

  • 1 Department of Anesthesiology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
  • 2 Children's Hospital of Fudan University, Shanghai, 201102, China.
  • 3 Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Collaborative Innovation Center of Genetics and Development, Institute of Biomedical Sciences, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China. duanma@fudan.edu.cn.
  • 4 Department of Anesthesiology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. miaochh@aliyun.com.
PMID: 29168081 DOI: 10.1007/s10753-017-0696-0
Abstract

Hyperglycemia is a highly dangerous factor to various diseases, even resulting in death of people. Inflammation plays a key role in this process. The aim of this study was to explore the role of malignant fibrous histiocytoma amplified sequence 1 (MFHAS1) in high-glucose induced inflammation. Our research showed that high glucose stimulated the expression of MFHAS1, and overexpression of MFHAS1 can attenuate high-glucose induced inflammation in endothelial cells by decreasing the secretion of cytokines interleukin-1β (IL-1β), interleukin-1α (IL-1α), adhesion molecule intercellular adhesion molecule-1 (ICAM), interleukin-6 (IL-6), interleukin-8 (IL-8), and chemokine ligand 1 (CXCL-1). Furthermore, we found that MFHAS1 promoted the phosphorylation of Akt and the expression of heme oxygenase-1 (HO-1). Our results indicated that MFHAS1 deadened high-glucose induced inflammation by activating Akt/HO-1 pathway, suggesting that MFHAS1 may act as a new therapeutic target of diabetes mellitus.

Keywords

AKT; HO-1; MFHAS1; high glucose; inflammation.

Figures