IndraLab

"Recently, bioinformatics predicted that QKI could bind to CACNA1C mRNA, the α1C subunit of L-type calcium channel [ xref ], indicating a potential role for QKI in AF."

"Meanwhile, QKI overexpression in atrial myocytes restored the LPS-stimulated macrophage-induced electrical remodeling through enhanced binding of QKI to CACNA1C mRNA, which upregulated the expression of CACNA1C as well as I Ca-L . In contrast, QKI knockout inhibited CACNA1C expression."

"RNA immunoprecipitation (RIP) assay showed that QKI bound to CACNA1C mRNA, which was inhibited by tachypacing."

"RNA immunoprecipitation (RIP) assay showed that QKI bound to CACNA1C mRNA, which was inhibited by tachypacing (Fig.  xref c, d)."

"The main findings of the present study are : (1) increased pro inflammatory macrophages were found in the atria of AF patients, and HL-1 cell tachypacing induced pro inflammatory macrophage polarization; (2) pro inflammatory macrophage polarization played a major role in atrial electrical remodeling as evidenced by the increased incidence of AF in chronic LPS treatment in mice and canines, which was inhibited by the depletion of LPS stimulated macrophages; (3) the effect of LPS stimulated macrophages on electrical remodeling was mediated by IL-1beta secretion, which inhibited QKI expression in atrial myocytes; (4) QKI bound to CACNA1C mRNA and regulated the level of I Ca-L; and (5) the transcription factor Satb1 mediated QKI expression."

"The main findings of the present study are: (1) increased pro-inflammatory macrophages were found in the atria of AF patients, and HL-1 cell tachypacing induced pro-inflammatory macrophage polarization; (2) pro-inflammatory macrophage polarization played a major role in atrial electrical remodeling as evidenced by the increased incidence of AF in chronic LPS treatment in mice and canines, which was inhibited by the depletion of LPS-stimulated macrophages; (3) the effect of LPS-stimulated macrophages on electrical remodeling was mediated by IL-1β secretion, which inhibited QKI expression in atrial myocytes; (4) QKI bound to CACNA1C mRNA and regulated the level of I Ca-L ; and (5) the transcription factor Satb1 mediated QKI expression."

"Bioinformatics predicted that QKI could bind to CACNA1C mRNA, which was confirmed by RIP in our study."

"Meanwhile, QKI overexpression in atrial myocytes restored the LPS stimulated macrophage induced electrical remodeling through enhanced binding of QKI to CACNA1C mRNA, which upregulated the expression of CACNA1C as well as I Ca-L."