Abstract
The efficacy of treatments for diabetes mellitus-induced erectile dysfunction (DMED) is quite poor, and stem cell therapy is emerging as a useful method. In this study, we used endothelial progenitor cells (EPCs) overexpressing human telomerase reverse transcriptase (hTERT) for the treatment of DMED. Rat EPCs were transfected with hTERT (EPCs-hTERT). EPCs-hTERT secreted more growth factors and demonstrated enhanced proliferation and resistance to oxidative stress. Twenty-four male DMED rats were subjected to four treatments: DMED (DMED group), EPCs (EPCs group), EPCs transduced with control lentivirus (EPC-control group) and EPCs-hTERT (EPCs-hTERT group). A group of healthy rats were used as the normal control group. The erectile function in the EPCs-hTERT group was markedly increased compared with the EPCs and EPCs-control groups. The EPCs-hTERT group exhibited more growth factors, smooth muscle content and retained stem cells in penile tissues. The degree of apoptosis and collagen/smooth muscle ratio in penile tissues of the EPCs-hTERT group was considerably reduced. Endothelial nitric oxide synthase (eNOS) expression increased significantly in the EPCs-hTERT group. Taken together, these data showed that the enhanced paracrine effect, resistance to oxidative stress and proliferation of EPCs-hTERT may contribute to the improvements of erectile function in DMED rats.
Highlights
Diabetes mellitus (DM) is a chronic disease that is associated with one of the most significant urological complications, erectile dysfunction (ED)
Flag was expressed in the cytoplasm of endothelial progenitor cells (EPCs)-control and EPCshTERT (Figure 2E). These results indicate that human telomerase reverse transcriptase (hTERT) was expressed in the cytoplasm of EPCs-hTERT, whereas rat TERT (rTERT) was expressed in the nucleus. rTERT expression was not altered after hTERT overexpression
Our study found that EPCs secreted vascular endothelial growth factor (VEGF), insulin-like growth factor-1 (IGF-1) and basic fibroblast growth factor (bFGF), which may contribute to the decreased corporal apoptosis and fibrosis and increased nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling pathway
Summary
Diabetes mellitus (DM) is a chronic disease that is associated with one of the most significant urological complications, erectile dysfunction (ED). The pathogenesis of diabetes mellitus-induced erectile dysfunction (DMED) is complex, and it is associated with the formation of advanced glycation end products, endothelial dysfunction, hypogonadism, peripheral neurological changes and decreased nitric oxide production [2, 3]. Stem cell therapy is one of the promising strategies with a demonstrated benefit in the treatment of DMED. Several studies reported that stem cells improved erectile function after intracavernous application [5, 6]. Stem cells secrete a variety of growth factors that exert protective www.impactjournals.com/oncotarget effects in vivo, including vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), glial cell-derived neurotrophic factor (GDNF), and stromal derived factor-1 (SDF-1) [9]
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