AB1498P Sigma-AldrichAnti-Stem Cell Factor Antibody

Background  Acral lesions of vitiligo are usually resistant to conventional lines of treatment as well as surgical interventions. Objective  To clarify causes underlying resistance of acral lesions to pigmentation in vitiligo by studying some of the factors associated with mechanisms of repigmentation following photochemotherapy. Methods  The study included twenty patients with active vitiligo. Skin biopsies were taken from lesional and perilesional skin of areas expected to respond (trunk and proximal limb) and skin of acral areas, before and after PUVA therapy. Sections were stained with H and E, Melan-A, MHCII, CD1a, SCF and c-kit protein. Results  Before treatment acral areas showed significantly lower hair follicle density, melanocyte density, Langerhans cell (LC) density, epidermal MHCII expression, lesional SCF expression and perilesional c-kit expression. Following treatment with PUVA in both non-responsive acral and repigmenting non-acral lesions identical immunohistochemical changes in the form of significant decrease in LC density, epidermal MHC-II and SCF expression were observed. Conclusion  The surprisingly similar histochemical changes in response to PUVA in acral and non-acral lesions did not manifest with clinical repigmentation except in non-acral ones. Factors such as inherent lower melanocyte density, lower melanocyte stem cell reservoirs and/or lower baseline epidermal stem cell factor may be considered as possible play makers in this respect.

Oval cells are the putative liver stem cells that proliferate during hepatocarcinogenesis and chemically-induced severe liver injury. Antigens traditionally associated with haematopoietic cells, such as c-Kit, have been reported to be expressed by oval cells. Previous studies suggested that stem cell factor (SCF) and c-Kit were critical to oval cell development. However, the role of SCF/c-Kit signals in oval cell proliferation still remains unclear. Recently, we reported the establishment of oval cell-derived liver epithelial progenitor cells (LEPCs). In this work, we showed LEPCs co-expressed c-Kit and its ligand SCF. The involvement of SCF/c-Kit signals in LEPCs proliferation was investigated either by exposing LEPCs to c-Kit inhibitors (STI571 and AG1296), SCF, anti-SCF neutralized antibody or by using small interfering RNA to knock-down c-Kit expression. Our data demonstrate that blocking SCF/c-Kit signal did not inhibit the proliferation of LEPCs, which suggest SCF/c-Kit is not necessary for the proliferation of oval cells, at least for the cultured oval cell counterpart LEPCs.

Neural stem/progenitor cell (NSPC) migration toward sites of damaged central nervous system (CNS) tissue may represent an adaptive response for the purpose of limiting and/or repairing damage. Little is known of the mechanisms responsible for this migratory response. We constructed a cDNA library of injured mouse forebrain using subtractive suppression hybridization (SSH) to identify genes that were selectively upregulated in the injured hemisphere. We demonstrate that stem cell factor (SCF) mRNA and protein are highly induced in neurons within the zone of injured brain. Additionally, the SCF receptor c-kit is expressed on NSPCs in vitro and in vivo. Finally, we demonstrate that recombinant SCF induces potent NSPC migration in vitro and in vivo through the activation of c-kit on NSPCs. These data suggest that the SCF/c-kit pathway is involved in the migration of NSPCs to sites of brain injury and that SCF may prove useful for inducing progenitor cell recruitment to specific areas of the CNS for cell-based therapeutic strategies.