Anti-PROM1 Monoclonal antibody, clone 24B5 [PerCP-eFluor® 710]

In this study, we describe a novel insight about the use of bone marrow-derived mesenchymal stem cells (BM-MSCs) for fallopian tube (FT) regeneration. Seventy rats' tubes were involved in this study and divided into 4 groups: control (15), ethanol injured (20), mesenchymal stem cell (MSC)-recipient without injury (15), and MSC recipient after injury (20). The BM-MSCs were isolated from male rats, and their incorporation into the tissues was confirmed by the detection of Sry gene in MSC-recipient rats using RT-PCR. Histological and immunohistological sections of the 4 groups were comparably evaluated. We found that direct injection of ethanol into FT caused structural impairment, which was restored largely after receiving MSCs. We have revealed for the first time that prominin 1 (Prom1, stem cell marker) was expressed in the fimbriated distal tubal end. The MSC transplantation caused (1) significant increase in the tissue level and immunoexpresstion of Prom1 (P < .001 and P = .017, respectively) and vascular endothelial growth factor (VEGF; vasculogenic marker; P < .001 and P = .004, respectively), (2) significant increase in the immunoexpresstion of proliferating cell nuclear antigen (PCNA; proliferation marker; P < .001), and (3) significant decrease in the immunoexpresstion of caspase 3 (CASP-3; apoptotic marker; P < .001) compared to the injured tissues. In conclusion, MSCs could exhibit its restorative effect on FT through their ability to (1) activate the resident stem cells in the distal tubal end, (2) mediate the expression of VEGF and PCNA, and (3) influence tissue apoptosis. This study laid the foundation for assessing the contribution of stem cells in the distal tubal end in direct repair of the tube when required to assist reproduction.

In glioblastoma high expression of the CD133 gene, also called Prominin1, is associated with poor prognosis. The PDGF-driven proneural group represents a subset of glioblastoma in which CD133 is not overexpressed. Interestingly, this particular subset shows a relatively good prognosis. As with many other tumors, gliobastoma is believed to arise and be maintained by a restricted population of stem-like cancer cells that express the CD133 transmembrane protein. The significance of CD133(+) cells for gliomagenesis is controversial because of conflicting supporting evidence. Contributing to this inconsistency is the fact that the isolation of CD133(+) cells has largely relied on the use of antibodies against ill-defined glycosylated epitopes of CD133. To overcome this problem, we used a knock-in lacZ reporter mouse, Prom1(lacZ/+), to track Prom1(+) cells in the brain. We found that Prom1 (prominin1, murine CD133 homologue) is expressed by cells that express markers characteristic of the neuronal, glial or vascular lineages. In proneural tumors derived from injection of RCAS-PDGF into the brains of tv-a;Ink4a-Arf(-/-) Prom1(lacZ/+) mice, Prom1(+) cells expressed markers for astrocytes or endothelial cells. Mice co-transplanted with proneural tumor sphere cells and Prom1(+) endothelium had a significantly increased tumor burden and more vascular proliferation (angiogenesis) than those co-transplanted with Prom1(-) endothelium. We also identified specific genes in Prom1(+) endothelium that code for endothelial signaling modulators that were not overexpressed in Prom1(-) endothelium. These factors may support proneural tumor progression and could be potential targets for anti-angiogenic therapy.