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“The spleen of human adults uniquely possesses P5091 order a reservoir of multilineage adult stem cells that express the developmental transcription factor Hox11. In contrast to hematopoietic stem cells, Hox11+ stem cells hold potentially broader therapeutic applications because they are less lineage restricted. Hox11/Tlx1 is part of a homeodomain gene family essential for organogenesis of the spleen and for contributions to development of hindbrain, cochlea, pancreas, salivary glands, among other organs and tissues. While Hox11/Tlx1 displays widespread patterns
of expression during embryogenesis, its expression was thought to cease after birth. Recent findings in human post-mortem tissue have shattered this dogma, finding that Hox11/Tlx1 stem cells are uniquely and abundantly expressed throughout adulthood in the human spleen. While their
role in humans is not yet understood, Hox11/Tlx1 stem cells from the spleen of normal mice have been harvested to assist in both the treatment and cure at least two autoimmune diseases: type 1 diabetes, Sjogren’s syndrome, and possibly their comorbid hearing loss. The splenic stem cells are infused, with an immune therapy, into diseased NOD mice, where they can home to the diseased organ, differentiate into the appropriate cell type, and assume normal functioning with the endogenous regeneration of the SYN-117 manufacturer animal due to disease removal. GSK2126458 cost This review covers Hox11/Tlx1+ stem cells’ success in an animal model and their potential for treating autoimmune diseases in organs that mirror their extensive expression patterns during embryogenesis.”
“Background: Alpha-sarcoglycan (alpha-SG) deficiency (limb-girdle muscular dystrophy [LGMD] type 2D) is the most common form of sarcoglycan-LGMD. No treatment is currently available. Prior studies suggest that overexpression of alpha-SG via adeno-associated virus (AAV)-mediated gene transfer results in poorly sustained gene expression related to transgene toxicity. These
findings potentially preclude gene therapy as a treatment approach for LGMD2D.\n\nMethods: The human alpha-SG gene (h alpha-SG) was directly transferred to the tibialis anterior muscle of 4- to 5-week-old alpha-SG KO mice using AAV, type 1. The gene was placed under control of either the ubiquitously expressed cytomegalovirus (CMV) promoter or muscle specific promoters that included desmin, muscle creatine kinase (MCK), and its further modification, truncated MCK (tMCK). Low ( 3 x 10(9) vg) and high (3 x 10(10) vg) doses of AAV1. h alpha-SG were administered.\n\nResults: Sustained gene expression was observed irrespective of promoters at 6 and 12 weeks post gene transfer. Quantitation of alpha-SG gene expression by fiber counts yielded similar levels of myofiber transduction for both MCK promoters (60 to 70%), while 34% of fibers were transduced with the DES promoter.
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