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2A and 2B). We also observed that the level of Rac-1, a small GTPase that is required for cell adhesion and spreading [23], was significantly decreased in H2O2-treated MSCs compared to control MSCs (Fig. 2E). These results indicate that ROS hinders MSC adhesion through downregulating integrin-dependent adhesion molecules. Since FAK and Src-dependent integrin signaling events culminate in reorganization of the actin cytoskeleton, which is a prerequisite for changes in cell shape, adhesion, and gene expression, we investigated the distribution and localization of focal adhesion proteins in H2O2-treated MSCs. We first observed that the cells treated with H2O2 were round and brilliant and did not show any cytoskeletal organization, whereas the control and H2O2-treated cells in the presence of NAC displayed a tightly http://www.selleckchem.com/ adhesive and widened morphology with membrane ruffles, which began to extend filopodia 3-mercaptopyruvate sulfurtransferase around 3 hours after adhesion (Fig. 3). Furthermore, double-immunostaining showed that integrin ��1 and p-FAK were colocalized at the site of filopodia growth in both the control and H2O2-treated MSCs in the presence of NAC. This colocalization suggests that integrin molecules are involved in focal adhesion formation and cytoskeletal organization in MSCs (Fig. 3A). In addition, we did not observe any specific staining for focal adhesion proteins such as paxillin, vinculin, or talin in the H2O2-treated MSCs, whereas both the control and H2O2-treated cells in the presence of NAC produced numerous peripherally distributed proteins at the site of the prominent membrane ruffles (Fig. 3B). Our results clearly indicate that ROS impairs MSC adhesion through the disruption of integrin-related focal adhesion, which can be rescued by treatment with antioxidants such as NAC. To investigate whether scavenging ROS facilitated the adhesion of implanted MSCs, we transplanted MSCs labeled with DAPI with/without NAC into the border region between the infarcted HDAC activation and normal areas of the heart after coronary ligation. After three days, the hearts were removed and the fate of the MSCs was investigated using confocal microscopy. A higher number of MSCs coupled with NAC were retained in the border region than in the control MSCs (MSCs-NAC vs. MSCs: 722 �� 55 vs. 263 �� 48, respectively, p < .001) (Fig. 4A). In addition, time course experiments indicated enhanced survival of MSCs in the presence of NAC compared to MSCs in the absence of NAC (data not shown). One week after coronary ligation, the size of the left ventricular infarct was evaluated in both the transplanted and control groups using TTC staining. The infarct size was significantly lower in the MSC coupled with NAC-transplanted group than in the na?ve MSC-transplanted group (MSCs vs. MSCs�CNAC: 15.8 �� 1.03 vs. 6.0 �� 0.88, respectively, p < .05) (Fig. 4B).