Objectives To investigate the expression state of cellular retinol-binding protein-1 (CRBP-1) in myocardial infarction (MI) tissue of rat model. Since CRBP-1 is transiently expressed in tissue repairing process,so ventricular remodeling after MI is also a kind of tissue repair,in which we may find the expression of CRBP-1. Methods MI model was produced in male Wistar rats by left coronary ligation. Rats were sacrificed to obtain the heart at 3rd,6th,and 15th day after operation. Heart was cut into four cross sections,fixed and embedded in paraffin. Sections were cut and stained with hematoxylin and eosin (HE),Masson’s trichrome (MT),rabbit anti-CRBP-1 antibody and mouse anti-α-smooth muscle (SM) actin antibody. CRBP-1 and α-SM actin were also detected using Western blotting. Results Forty-five Wistar rats developed MI with infarct size ranging from 45.6% to 56.2% (mean 48.6± 3.3%). Heart sections of MI with HE and MT staining showed a remarkable myocyte necrosis,collagen disposition and ventricular remodeling. CRBP-1 expression was detected at both of the endocardial and epicardial region of infarction,where fibroblasts infiltrated with myocyte necrosis at 3rd day and 6th day after operation. At 15th day,α-SM actin positive fibroblasts in the infarcted region expressed CRBP-1. Conclusions We demonstrate that CRBP-1 is transiently and rapidly expressed by fibroblast in rat model of MI. Our results therefore indicating a potential relationship between CRBP-1 and ventricular remodeling process after MI. Objectives To investigate the expression state of cellular retinol-binding protein-1 (CRBP-1) in myocardial infarction (MI) tissue of rat model. Since CRBP-1 is transiently expressed in tissue repairing process, so ventricular remodeling after MI is also a kind of tissue repair, in which we we find the expression of CRBP-1. Methods MI model was produced in male Wistar rats by left coronary ligation. Rats were sacrificed to obtain the heart at 3rd, 6th, and 15th day after operation. Heart was cut into four cross sections, fixed and embedded in paraffin. Sections were cut and stained with hematoxylin and eosin (HE), Masson’s trichrome (MT), rabbit anti-CRBP- Results Forty-five Wistar rats developed MI with infarct size ranging from 45.6% to 56.2% (mean 48.6 ± 3.3%). Heart sections of MI with HE and MT staining showed a remarkable myocyte necrosis, collagen disposition and ventricular remodeling. CRBP-1 expression was detected at both of the endocardial and epicardial region of infarction, where fibroblasts infiltrated with myocyte necrosis at 3rd and 6th day after operation. At 15th day, α-SM actin positive fibroblasts in the infarcted region expressed CRBP-1. Conclusions We demonstrate that CRBP-1 is transiently and rapidly expressed by fibroblast in rat model of MI. Our results therefore indicate indicating a potential relationship between CRBP-1 and ventricular remodeling process after MI.