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Platelet-rich plasma (PRP) is an inexpensive and safe substitute of recombinant growth factors in Vitro and in vivo. Due to its putative effect on tissue repair, the use of autologous PRP has become largely popular. Recently, a jellified PRP derivative obtained from umbilical cord blood (CB) has been utilized in vivo to treat mucosal and cutaneous lesions. Nevertheless, whether PRP derived from CB and adult blood display different potency in promoting cell growth in Vitro has been rarely investigated. In this study, we compared cytokine profile and mesenchymal cell growth supporting the ability of platelet lysate obtained from adult and cord blood. Our in vitro results strongly back the utilization of CB platelet lysate in vivo, as an efficacious, safe and inexpensive alternative to promote damaged tissue healing when the autologous PRP is contraindicated. Moreover, the policy of manufacturing CB platelet lysate can limit the current disposal of many collected CB units not suitable for transplant due to their low nucleated cell count.

Background Human cord blood (CB) endothelial colony forming cells (ECFCs) are endowed with high vascular regenerative ability in immunodeficient mice, but their immunogenicity and susceptibility to rejection in immunocompetent models has yet to be explored. Methods We injected CB ECFCs in non-immuno-suppressed C57BL/6 J mice after having induced the hindlimb ischemia and we investigated their contribution to the recovery from the ischemic injury. Human ECFCs (hECFCs) were administered by intramuscular injection and hindlimb blood perfusion was measured by laser Doppler analysis at 7-day intervals for 28 days after treatment. Mice were sacrificed after 7 and 28 days and immunohistochemistry for specific human (CD31) and mouse (von Willebrand factor) endothelial antigens was carried out. Before euthanasia, blood samples to assess cytokines and angiogenic growth factor levels were collected. Results Mice injected with hECFCs showed a prompter and greater recovery of blood flow than controls. Several endothelial cells of human origin were detected at day7 after injection and their number declined progressively. Likewise, a progressive increase of mouse-derived vascular structures were observed, paralleled by the amplified endogenous production of various soluble mediators of angiogenesis, including Vascular Endothelial Growth Factor and Fibroblast Growth Factor. Conclusions Overall, our findings are consistent with the hypothesis that human ECFCs might expand the endogenous vascular repair potential of recipients and support their possible HLA-independent unconventional use.

Background HIV infection is an independent risk factor for cardiovascular disease. HIV-sustained impairment of endothelial progenitor cells (EPCs) could contribute to this process, so that it is important to assess whether antiviral therapy (ART) is able to revert these abnormalities. Methods We quantified in 21 naives and 34 treated patients two functionally distinct clonogenic progenitors which have been acknowledged important for vascular repair: the hematopoietic progenitor colony forming unit - endothelial cells (CFU-EC) and the true endothelial progenitor, the endothelial colony forming cells (ECFC). We correlated results obtained with conventional vascular risk factors and with HIV-related parameters. Results We found that these progenitors behaved differently in naive and treated patients. In particular, CFU-EC level was significantly low in all naive patients and slowly recovered during ART. In contrast, the ECFC level was abnormally high in naive patients while it decreased upon ART. The CFU-EC level was related to conventional cardiovascular risk factors, as reported in general population, but also to inflammatory indexes and CD4 cell count. In contrast, the ECFC number was exclusively related to viral replication activity and to CD4 cell count. Conclusions In HIV-infected people, the levels of CFU-EC and ECFC are related to classical cardiovascular risk factors but, in addition, they are also significantly influenced by the infection itself and by antiviral therapy.

Chronic HIV infection induces significant changes in the trafficking of circulating endothelial progenitor cells (EPCs). Specifically, it causes marked depletion of proangiogenic hematopoietic cells, the so-called colony-forming unit-endothelial cells (CFU-ECs). In this study we evaluated CFU-ECs in two subjects with acute HIV infection. We found that both patients already had a low CFU-EC level at the time of diagnosis. Nevertheless, after 6 months of antiretroviral therapy, the CFU-EC concentration reverted to normal values in both cases. HIV significantly depletes the CFU-EC compartment even in the early phase of infection, while 6-month therapy appears to be able to restore it.