Buttgereit Jens, Qadri Fatimunnisa, Monti Jan, Langenickel Thomas H, Dietz Rainer, Braunewell Karl-Heinz, Bader Michael
Max-Delbrück-Center for Molecular Medicine (MDC), Campus Berlin-Buch, Berlin, Germany.
Regul Pept. 2010 Apr 9;161(1-3):51-7. doi: 10.1016/j.regpep.2009.12.019. Epub 2010 Jan 14.
Accumulating evidence indicates that Visinin-like protein-1 (VILIP-1), a member of the family of neuronal calcium sensor proteins (NCS), modulates a variety of processes in extra-neuronal tissues. In this study, we describe VILIP-1 expression in the human heart, rat cardiomyocytes, and H9c2 cells, and demonstrate that VILIP-1 regulates the cell surface localization of natriuretic peptide receptor B (NPR-B). In preparations from failing hearts, we observed VILIP-1 downregulation and reduced NPR-B signalling. In conclusion, VILIP-1 deficiency may be responsible for the reduced efficiency of the natriuretic peptide system in cardiac hypertrophy and heart failure and may therefore serve as pharmacological target.
越来越多的证据表明，神经元钙传感器蛋白（NCS）家族成员之一的类视锥蛋白样蛋白-1（VILIP-1）可调节神经外组织中的多种过程。在本研究中，我们描述了VILIP-1在人心脏、大鼠心肌细胞和H9c2细胞中的表达，并证明VILIP-1调节利钠肽受体B（NPR-B）的细胞表面定位。在衰竭心脏的标本中，我们观察到VILIP-1下调和NPR-B信号传导减少。总之，VILIP-1缺乏可能是导致心脏肥大和心力衰竭中利钠肽系统效率降低的原因，因此可能成为药理学靶点。
