Expression of the multifunctional Y-box protein, YB-1, in myofibroblasts of the infarcted rat heart

• Published in: Biochemical and biophysical research communications Vol. 334; no. 1; pp. 239 - 244
• Main Authors: Kamalov, German, Varma, Balwantkumar R., Lu, Li, Sun, Yao, Weber, Karl T., Guntaka, Ramareddy V.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 19.08.2005
• Subjects: 60 APPLIED LIFE SCIENCES; Animals; APOPTOSIS; CCAAT-Enhancer-Binding Proteins - metabolism; CELL PROLIFERATION; Cells, Cultured; DOUBLE LABELLING; Fibroblasts - metabolism; GENE REGULATION; Heart Ventricles - metabolism; Infarction; Male; MYOCARDIAL INFARCTION; Myocardial Infarction - metabolism; MYOCARDIUM; Myofibroblast; NFI Transcription Factors; POTASSIUM IODIDES; Proliferation; PROTEINS; RATS; Rats, Sprague-Dawley; Remodeling; Tissue Distribution; Transcription Factors - metabolism; Y-Box-Binding Protein 1; YB-1; Infarction; Proliferation; YB-1; Remodeling; Myofibroblast
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2005.06.082

Intracellular signaling mechanisms regulating the turnover of α-SMA-positive myofibroblasts (myoFbs) at the site of myocardial infarction (MI) are poorly understood. Y-Box (YB)-1, a multifunctional protein, may be involved in regulation of proliferation, migration and apoptosis of myoFbs. Our objective was to study the expression of YB-1 in the infarcted rat heart and its localization in myoFbs. On days 3–28 following MI, we monitored YB-1 expression and its colocalization with α-SMA, and proliferation markers PCNA and Ki-67 in infarcted tissue by Western blot, immunohistochemistry, and immunofluorescent double-labeling. YB-1 is barely detectable in normal myocardium. At the infarct site, however, YB-1 is markedly elevated from day 3 post-MI concomitant with the induction of cell proliferation. MyoFbs are the major source of YB-1 and retain it up to day 28 post-MI. We suggest early expression of YB-1 promotes proliferation and migration of myoFbs, whereas prolonged expression may be responsible for scar formation.