Human stromal (mesenchymal) stem cells (hMSCs) are multipotent stem cells with ability to differentiate into mesoderm-type cells e.g. osteoblasts and adipocytes and thus they are being introduced into clinical trials for tissue regeneration. Traditionally, hMSCs have been isolated from bone marrow, but the number of cells obtained is limited. Here, we compared the MSC-like cell populations, obtained from alternative sources for MSC: adipose tissue and skin, with the standard phenotype of human bone marrow MSC (BM-MSCs). MSC from human adipose tissue (human adipose stromal cells (hATSCs)) and human skin (human adult skin stromal cells, (hASSCs) and human new-born skin stromal cells (hNSSCs)) grew readily in culture and the growth rate was highest in hNSSCs and lowest in hATSCs. Compared with phenotype of hBM-MSC, all cell populations were CD34−, CD45−, CD14−, CD31−, HLA-DR−, CD13+, CD29+, CD44+, CD73+, CD90+,and CD105+. When exposed to in vitro differentiation, hATSCs, hASSCs and hNSSCs exhibited quantitative differences in their ability to differentiate into adipocytes and to osteoblastic cells. Using a microarray-based approach we have unveiled a common MSC molecular signature composed of 33 CD markers including known MSC markers and several novel markers e.g. CD165, CD276, and CD82. However, significant differences in the molecular phenotype between these different stromal cell populations were observed suggesting ontological and functional differences. In conclusion, MSC populations obtained from different tissues exhibit significant differences in their proliferation, differentiation and molecular phenotype, which should be taken into consideration when planning their use in clinical protocols.Electronic supplementary materialThe online version of this article (doi:10.1007/s12015-012-9365-8) contains supplementary material, which is available to authorized users.

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Aflatoxin B1 (AFB1) and ochratoxin A (OTA) are important food-borne mycotoxins that have been implicated in human health. In this study, independent and combinative toxicities of AFB1 and OTA were tested in cultured monkey kidney Vero cells. The experiments reported here were conducted to evaluate the effect of these toxins on cell viability followed by the determination of cell death pathways, using the quantification of DNA fragmentation and the expression of p53 and bcl-2 protein levels. Our results showed that AFB1 and OTA caused a marked decrease of cell viability in a dose-dependent manner. Under the same conditions, these mycotoxins increased fragmented DNA levels. In addition, p53 was activated in response to DNA damage and the expression of the antiapoptotic factor bcl-2 decreased significantly. According to these data, AFB1 and OTA seemed to be involved in an apoptotic process. Moreover, combined AFB1 and OTA induced all the toxicities observed with the mycotoxins separately. Therefore, this combination was classified as an additive response of the two mycotoxins.

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Ochratoxin A (OTA) and citrinin (CTN) are two mycotoxins, quite common contaminants, that can occur jointly in a wide range of food commodities. Both mycotoxins have several toxic effects but both share a significant nephrotoxic potential since OTA and CTN were reported to be responsible for naturally occurring human and animal kidney diseases. Considering the concomitant production of OTA and CTN, it is very likely that humans and animals are always exposed to the mixture rather than to individual compounds. Therefore, the aim of the present study was to investigate, using kidney cell culture (Vero cells), whether cytotoxicity and essentially oxidative cell damage (a key determinant of renal diseases) are enhanced by combination of both mycotoxins as compared to their effect separately. To this end, we have assessed their effects individually or combined on cell proliferation using three different cell viability assays (MTT, Trypan Blue, and Neutral Red). In addition, the role of oxidative stress was investigated by measuring the malondialdehyde (MDA) level and the expression of the heat shock protein Hsp 70. Our results clearly showed that cultured renal cells respond to OTA and CTN exposure by a moderate and weak inhibition of cell proliferation and induction of oxidative stress, respectively. However, when combined, they exert a significant increase in inhibition of cell viability as well as the induction of MDA level and Hsp 70 expression. OTA and CTN combination effects are clearly of synergistic nature. The enhanced induction of oxidative stress observed with OTA and CTN simultaneously could be relevant to explain the molecular basis of the renal diseases induced by these mycotoxins.