Our previous work showed that arsenic trioxide down-regulated Cx43 and attenuated the angiogenic potential of human late endothelial progenitor cells (EPC). However, the relation between Cx43 and angiogenic activity of the EPC remained unclear. In the study, human late EPC were treated with siRNA specific to Cx43 (Cx43siRNA). The expression profiles as well as activity of the treated cells were examined. In parallel, the angiogenic potential of human EPC treated with Cx43siRNA was evaluated using murine hind limb ischemic model. The results showed that, in the EPC treated with Cx43siRNA, the activity of migration, proliferation, and angiogenic potential were attenuated, accompanied by reduction in vascular endothelial growth factor (VEGF) expression. In hind limb ischemia mice, EPC treated with Cx43siRNA lost the therapeutic angiogenic potential. VEGF supplementation partially recovered the activity impaired by Cx43 down-regulation. In conclusion, reduced Cx43 expression per se in the EPC causes decreased expression of VEGF and impaired angiogenic potential of the cells. Prevention of Cx43 reduction is a potential target to maintain the angiogenic potential of the EPC.

The incidence of symptomatic newly developed large pleural effusions first diagnosed at more than 30 days post CABG was 3.1%. Those who were diagnosed between 30 and 90 days post CABG tended to have exudative effusions, whereas those diagnosed more than 90 days post CABG often had left ventricular impairment and transudative effusions. Most of these effusions settled with conservative management and did not recur.

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Objectives: We examined the role of atrial gap junctions, NF-κB and fibrosis in the occurrence of postoperative atrial fibrillation (AF) in patients undergoing coronary artery bypass graft (CABG) surgery. Methods: Forty-five patients with sinus rhythm were randomly assigned to the beating heart (n = 22) or cardioplegic cardiac arrest (n = 23) technique for surgery. Of them, 14 patients experienced post-CABG AF. Atrial samples taken before and after CABG surgery were analyzed. Results: During surgery, Cx43 and Cx40 proteins were significantly reduced (both p < 0.05) in the arrested heart group, but only mildly decreased in the beating heart group. However, the change of either connexin was not associated with AF. In contrast, patients with AF had a higher baseline expression of NF-κB and more fibrosis compared to those without AF (both p < 0.05). Conclusions: CABG surgery with the beating heart technique attenuated the reduction of atrial Cx43 and Cx40 compared to the cardioplegic cardiac arrest technique. Atrial inflammation and fibrosis status before surgery, but not the changes of connexins during surgery, were associated with the occurrence of post-CABG AF.