Human placenta-derived mesenchymal stem cells (P-MSCs) have drawn increasing attention in the field of stem cell research due to their potential in clinical applications as well as their rich and easy to procure cell source. While studies demonstrating the potential of P-MSCs for therapeutic transplantations have been documented, a clinically compliant procedure for P-MSC expansion in vitro has yet to be established. To this end, previous studies have demonstrated that MSCs of bone marrow and cord blood origins cultured in human cord blood serum (hCBS) are comparable to those cultured in fetal bovine serum (FBS), indicating that hCBS may be an alternative to FBS for the development of in vitro cell expansion procedures free of animal components. However, stem cells from origins other than bone marrow or cord blood, particularly from human placental tissues, which have demonstrated a good potential for clinical applications, have not been characterized under similar conditions. In this study, in an attempt to define a clinically compliant protocol for P-MSC expansion in vitro, we examined the effects of human hCBS as a replacement for FBS on cell proliferation capacity, differentiation potential, MSC-specific phenotypic expression and the genetic stability of P-MSCs in cultures. P-MSCs expanded in vitro in autologous hCBS maintained the capacity of self‑renewal and expressed surface antigens characteristic of bone marrow-derived mesenchymal stem cells. Under differentiation conditions, the P-MSCs expanded in hCBS developed into adipogenic, osteogenic and neurogenic cell phenotypes. Chromosomal karyotyping and single cell gel electrophoresis analysis demonstrated that P-MSCs cultured in autologous hCBS were genetically stable. These results suggest that autologous hCBS may be used as an alternative to FBS for the in vitro expansion of P-MSCs for clinical applications.

There is increasing evidence supporting the cancer stem cell (CSC) hypothesis, which suggests that a population of tumor cells with stem cell characteristics is responsible for tumor growth, resistance, and recurrence as well as drug resistance. In colorectal cancer, the CD133 antigen defines distinct cell subpopulations that are rich in tumor-initiating cells; however, the drug resistance properties of these CD133-positive cells have not been well defined. The breast cancer resistance protein (BCRP)/ATP-binding cassette subfamily G member 2 (ABCG2) is present on the plasma membrane of many types of human cancer cells and contributes to multidrug resistance during chemotherapy. The results of the present study showed that ABCG2 is expressed in CD133-positive CSCs from human colorectal tumors. Furthermore, the downregulation of ABCG2 expression inhibited the self-renewal capacity of these cells, and significantly enhanced the efficacy of chemotherapy-induced apoptosis in LS174T colon adenocarcinoma cells and CD133-positive colorectal carcinoma cells. Together, these data show that ABCG2 expression correlates with the presence of CD133-positive cancer cells, and thus is a possible therapeutic target for colorectal cancer.

Ghrelin is a very important brain-gut peptide that modulates appetite and energy metabolism in mammals. The yak is the only large mammal that can adapt to the cold temperatures and hypoxia conditions present in the Qinghai-Tibet Plateau. However, there are no reports on ghrelin molecular characterization and expression in the hypothalamus-pituitary-digestive tract axis of the yak to date. In this study, the coding region sequence of the yak ghrelin, containing a complete ORF (351) encoding for 117 amino acids, was cloned. Immunohistochemistry analysis of the yak samples showed that ghrelin-immunoreactive cells were expressed at the arcuate nucleus (ARC), the ventromedial nucleus (VMN), the dorsomedial nucleus (DMN) of the hypothalamus and also at the anterior pituitary. Ghrelin-positive cells were also present in approximately two thirds of the submucosa of the abomasum fundic gland and mucous layer of the duodenum intestinal gland. Ghrelin's mRNA highest expression occurred in the abomasum sample, followed by the duodenum, hypothalamus and lowest at the pituitary gland. The level of ghrelin mRNA measured in yak was higher than in cattle for all the tissues that were compared. The ghrelin protein and mRNA expression profiles were similar. These data imply that the high expression of ghrelin in the hypothalamus-pituitary-digestive tract axis of yak could aid adaptation to the extreme environment better than cattle, by improving appetite and fat accumulation, regulating body temperature and reducing energy consumption via regulating energy metabolism.

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In this study, we aimed to clarify the protective effect of umbilical cord-derived mesenchymal stem cell conditioned medium (UC-MSC-CM) on neuronal oxidative injury and its potential mechanism. Neuronal oxidative damage was mimicked by H2O2 treatment of the HT22 cell line. Immunofluorescence staining was used to analyze the expression of cleaved Caspase3 and TRPM2. Cytotropic factors secreted by UC-MSCs were analyzed by enzyme-linked immunosorbent assay. Whole-cell patch clamping was used to detect TRPM2-like currents. Western blotting was utilized to analyze the protein levels of SOD, p-ERK1/2, p-JNK1/2/3 and cleaved-Caspase-9. The number of cleaved-Caspase-3-positive cells and protein expression of Caspase-9 induced by H2O2 treatment were decreased by UC-MSC-CM treatment. Furthermore, SOD protein expression was increased in the MSC-CM group compared with that in the H2O2 group. The H2O2-induced TRPM2-like currents in HT22 cells were attenuated by MSC-CM treatment. In addition, H2O2 treatment downregulated the expression of p-JNK protein in HT22 cells, and this the downward trend was reversed by incubation with MSC-CM. Thus, we showed that UC-MSC-CM protects neurons against oxidative injury, possibly by inhibiting activation of TRPM2 and the JNK signaling pathway.