Abstract
This study aimed to investigate the mechanism of human umbilical cord blood stem cell (HUCBSC) transplantation on restenosis after percutaneous transluminal angioplasty (PTA) for diabetic hindlimb vascular disease in rabbits. After successfully preparing a rabbit model of diabetic hindlimb vascular disease, 16 rabbits were randomly assigned to two groups. Of these, 8 rabbits received PTA surgery alone (PTA group), and the other 8 rabbits received PTA and HUCBSC (PTA+HUCBSC group) treatments. Five more healthy rabbits were set as healthy control (HC group). Samples were collected after 4 weeks of treatment. The expressions of regulator of calcineurin 1 (RCAN1) and calcineurin A (CnA) in the diseased artery were detected by immunofluorescence staining. The distribution of HUCBSCs was observed by pathological examination in transplanted artery, distal artery, and liver. Cytology experiments were applied to assess the levels of JAK and STAT3, and the migration and proliferation of human aortic vascular smooth muscle cells (HA-VSMC). In the rabbit model of diabetic vascular lesions in the hindlimbs, we found the stenosis of the femoral artery became more and more serious with time, and the expression level of PCNA positive cells was also gradually increased. The expression levels of RCAN1 and CnA in the PTA+HUCBSC group were significantly lower than those in PTA group. HUCBSC inhibited the migration and proliferation of HA-VSMC via JAK/STAT3 pathway. After HUCBSC local transplantation, HUCBSC had no distal tissue distribution. HUCBSC transplantation may prevent restenosis after PTA of diabetic hindlimb vascular disease through JAK/STAT3 pathway.
Highlights
Local injection of cord blood stem cells was performed in the transplantation group, which showed the intimal area and the ratio of intima area to media area in the dilated occlusion site were significantly decreased, indicating that human umbilical cord blood stem cell (HUCBSC) transplantation could effectively intervene the inflammatory response after endothelial injury and prevent restenosis [12]
The cell migration experiment showed that the number of cells that migrated in the HUCBSC group and paclitaxel group were 45.33±4.52/high power field and 66.38±5.34/hpf, respectively, which were lower than the control group 108.45±8.45/hpf (P
Effect of HUCBSC on restenosis of diabetic hind limb arteries in rabbits Compared with the percutaneous transluminal angioplasty (PTA) group, the expression of regulator of calcineurin 1 (RCAN1) and calcineurin A (CnA) in the arterial tissues of the PTA+HUCBSC group was significantly reduced, which was comparable to the normal group (Fig 3)
Summary
The incidence of diabetic lower extremity arterial disease (LEAD) has increased year by year, and the results of epidemiological investigation show that the overall prevalence. Local injection of cord blood stem cells was performed in the transplantation group, which showed the intimal area and the ratio of intima area to media area in the dilated occlusion site were significantly decreased, indicating that human umbilical cord blood stem cell (HUCBSC) transplantation could effectively intervene the inflammatory response after endothelial injury and prevent restenosis [12]. This study intends to observe whether interventional therapy combined with HUCBSC transplantation can inhibit restenosis by changing the expression levels of RCAN1 and CnA. JAK/STAT3 signaling pathway plays an important regulatory role in cell proliferation and apoptosis, and whether it is involved in the prevention of restenosis after HUCBSC transplantation has not yet been reported. The possible downstream mechanism of HUCBSC transplantation for restenosis after interventional therapy in diabetic LEAD is to be studied in depth
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