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Biochem Biophys Res Commun. 2016 Feb 26;471(1):240-6. doi: 10.1016/j.bbrc.2016.01.117. Epub 2016 Jan 21.

LncRNA-HOTAIR promotes TNF-α production in cardiomyocytes of LPS-induced sepsis mice by activating NF-κB pathway.

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Department of Neonate, Xuzhou Children's Hospital, Xuzhou 221008, Jiangsu, China.
Department of Neonate, Xuzhou Children's Hospital, Xuzhou 221008, Jiangsu, China. Electronic address:



Mounting studies have illustrated an important role of HOTAIR in cancer progress, but few studies have reported its function in cardiac disease, including cardiac-associated sepsis. This study aimed to investigate the function of HOTAIR in sepsis, involving its association with the level of tumor necrosis factor-alpha (TNF-α), an important inducer of myocardial dysfunction during LPS-induced sepsis.


Sepsis mice model was established by LPS administration, and myocardial dysfunction was evaluated with hemodynamic parameters. HOTAIR expression in isolated cardiomyocytes and TNF-α production in the circulation were detected, as well as the protein levels of phosphorylated p65. HL-1 cells were subjected to LPS treatment in vitro for functional studies, including luciferase report assays for NF-κB activity.


HOTAIR expression was significantly upregulated in cardiomyocytes from sepsis mice, in line with increased TNF-α production and p65 phosphorylation, while similar results were also observed in LPS treated HL-1 cells, which was then reversed by HOTAIR interference. Functional studies demonstrated that HOTAIR showed positive regulation on p65 phosphorylation and NF-κB activation, while HOTAIR-induced TNF-α production was repressed by NF-κB inhibitor. Further in vivo studies confirmed that HOTAIR silence can improve cardiac function of sepsis mice, and markedly decreased TNF-α production in the circulation.


HOTAIR upregulation in cardiomyocytes of LPS-induced sepsis mice promoted TNF-α production in the circulation by activating NF-κB, involving the phosphorylation of NF-κB p65 subunit. Moreover, HOTAIR silence preserved cardiac function of sepsis mice during LPS-induced sepsis.


HOTAIR; LPS-induced sepsis; NF-κB activation; TNF-α production; p65 phosphorylation

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