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  • 1. Gao, Tao
    et al.
    McKenna, Brian
    Li, Changhong
    Reichert, Maximilian
    Nguyen, James
    Singh, Tarjinder
    Yang, Chenghua
    Pannikar, Archana
    Doliba, Nicolai
    Zhang, Tingting
    Stoffers, Doris A.
    Edlund, Helena
    Umeå University, Faculty of Medicine, Umeå Centre for Molecular Medicine (UCMM).
    Matschinsky, Franz
    Stein, Roland
    Stanger, Ben Z.
    Pdx1 Maintains beta Cell Identity and Function by Repressing an alpha Cell Program2014In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 19, no 2, p. 259-271Article in journal (Refereed)
    Abstract [en]

    Pdx1 is a homeobox-containing transcription factor that plays a key role in pancreatic development and adult beta cell function. In this study, we traced the fate of adult beta cells after Pdx1 deletion. As expected, beta-cell-specific removal of Pdx1 resulted in severe hyperglycemia within days. Surprisingly, a large fraction of Pdx1-deleted cells rapidly acquired ultrastructural and physiological features of a cells, indicating that a robust cellular reprogramming had occurred. Reprogrammed cells exhibited a global transcriptional shift that included derepression of the alpha cell transcription factor MafB, resulting in a transcriptional profile that closely resembled that of alpha cells. These findings indicate that Pdx1 acts as a master regulator of beta cell fate by simultaneously activating genes essential for beta cell identity and repressing those associated with alpha cell identity. We discuss the significance of these findings in the context of the emerging notion that loss of beta cell identity contributes to the pathogenesis of type 2 diabetes.

  • 2. Rauch, Alexander
    et al.
    Seitz, Sebastian
    Baschant, Ulrike
    Schilling, Arndt F
    Illing, Anett
    Stride, Brenda
    Kirilov, Milen
    Mandic, Vice
    Takacz, Andrea
    Schmidt-Ullrich, Ruth
    Ostermay, Susanne
    Schinke, Thorsten
    Spanbroek, Rainer
    Zaiss, Mario M
    Angel, Peter E
    Lerner, Ulf H
    Umeå University, Faculty of Medicine, Department of Odontology, Oral Cell Biology.
    David, Jean-Pierre
    Reichardt, Holger M
    Amling, Michael
    Schütz, Günther
    Tuckermann, Jan P
    Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor2010In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 11, no 6, p. 517-531Article in journal (Refereed)
    Abstract [en]

    Development of osteoporosis severely complicates long-term glucocorticoid (GC) therapy. Using a Cre-transgenic mouse line, we now demonstrate that GCs are unable to repress bone formation in the absence of glucocorticoid receptor (GR) expression in osteoblasts as they become refractory to hormone-induced apoptosis, inhibition of proliferation, and differentiation. In contrast, GC treatment still reduces bone formation in mice carrying a mutation that only disrupts GR dimerization, resulting in bone loss in vivo, enhanced apoptosis, and suppressed differentiation in vitro. The inhibitory GC effects on osteoblasts can be explained by a mechanism involving suppression of cytokines, such as interleukin 11, via interaction of the monomeric GR with AP-1, but not NF-kappaB. Thus, GCs inhibit cytokines independent of GR dimerization and thereby attenuate osteoblast differentiation, which accounts, in part, for bone loss during GC therapy.

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