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  • 1. Correa-Medina, Mayrin
    et al.
    Bravo-Egana, Valia
    Rosero, Samuel
    Ricordi, Camillo
    Diez, Juan
    Edlund, Helena
    Umeå universitet, Medicinska fakulteten, Umeå centrum för molekylär medicin (UCMM).
    Pastori, Ricardo L
    MicroRNA miR-7 is preferentially expressed in endocrine cells of the developing and adult human pancreas.2009Ingår i: Gene Expression Patterns, ISSN 1567-133X, E-ISSN 1872-7298, Vol. 9, nr 4, s. 193-9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    MicroRNAs (miRNA) are small non-coding RNAs that inhibit gene expression through binding to complementary messenger RNA sequences. miRNAs have been predicted to target genes important for pancreas development, proper endocrine cell function and metabolism. We previously described that miRNA-7 (miR-7) was the most abundant and differentially expressed islet miRNA, with 200-fold higher expression in mature human islets than in acinar tissue. Here we have analyzed the temporal and spatial expression of miR-7 in human fetal pancreas from 8 to 22 weeks of gestational age (wga). Human fetal (8-22wga) and adult pancreases were processed for immunohistochemistry, in situ hybridization, and quantitative RT-PCR of miRNA and mRNA. miR-7 was expressed in the human developing pancreas from around 9wga and reached its maximum expression levels between 14 and 18wga, coinciding with the exponential increase of the pancreatic endocrine hormones. Throughout development miR-7 expression was preferentially localized to endocrine cells and its expression persisted in the adult pancreas. The present study provides a detailed analysis of the spatiotemporal expression of miR-7 in developing human pancreas. The specific localization of miR-7 expression to fetal and adult endocrine cells indicates a potential role for miR-7 in endocrine cell differentiation and/or function. Future functional studies of a potential role for miR-7 function in islet cell differentiation and physiology are likely to identify novel targets for the treatment of diabetes and will lead to the development of improved protocols for generating insulin-producing cells for cell replacement therapy.

  • 2.
    Kolterud, Åsa
    et al.
    Umeå universitet, Medicinska fakulteten, Umeå centrum för molekylär medicin (UCMM).
    Wandzioch, Ewa
    Umeå universitet, Medicinska fakulteten, Umeå centrum för molekylär medicin (UCMM).
    Carlsson, Leif
    Umeå universitet, Medicinska fakulteten, Umeå centrum för molekylär medicin (UCMM).
    Lhx2 is expressed in the septum transversum mesenchyme that becomes an integral part of the liver and the formation of these cells is independent of functional Lhx22004Ingår i: Gene Expression Patterns, ISSN 1567-133X, E-ISSN 1872-7298, Vol. 4, nr 5, s. 521-528Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Liver development is based on reciprocal interactions between ventral foregut endoderm and adjacent mesenchymal tissues. Targeted disruption of the LIM-homeobox gene Lhx2 has revealed that it is important for the expansion of the liver during embryonic development, whereas it appears not to be involved in the induction of hepatic fate. It is not known whether Lhx2 is expressed in the endodermal or mesenchymal portion of the liver, or if the cells normally expressing Lhx2 are absent or present in the liver of Lhx2(-/-) embryos. To address this we have analyzed gene expression from the Lhx2 locus during hepatic development in wild type and Lhx2(-/-) mice. Lhx2 is expressed in cells of the septum transversum mesenchyme adjacent to the liver bud from embryonic day 9. The hepatic cords subsequently migrate into and intermingle with the Lhx2+ cells of the septum transversum mesenchyme. Lhx2 expression is thereafter maintained in a subpopulation of mesenchymal cells in the liver until adult life. In adult liver the Lhx2+ mesenchymal cells co-express desmin, a marker associated with stellate cells. At embryonic day 10.5, cells expressing the mutant Lhx2 allel are present in Lhx2(-/-) livers, and expression of Hlx, hepatocyte growth factor, Hex and Prox1, genes known to be important in liver development, is independent of functional Lhx2 expression. Thus, Lhx2 is specifically expressed in the liver-associated septum transversum mesenchyme that subsequently becomes an integral part of the liver and the formation of these mesenchymal cells does not require functional Lhx2.

  • 3.
    Sjödal, My
    et al.
    Umeå universitet, Medicinsk fakultet, Umeå centrum för molekylär medicin (UCMM).
    Gunhaga, Lena
    Umeå universitet, Medicinsk fakultet, Umeå centrum för molekylär medicin (UCMM).
    Expression patterns of Shh, Ptc2, Raldh3, Pitx2, Isl1, Lim3 and Pax6 in the developing chick hypophyseal placode and Rathke's pouch.2008Ingår i: Gene Expression Patterns, ISSN 1567-133X, E-ISSN 1872-7298, Vol. 8, nr 7-8, s. 481-5Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The adenohypophysis is derived from a structure called the Rathke's pouch, which is an invagination of the hypophyseal placode. Hedgehog (Hh) and retinoic acid (RA) signals as well as several transcription factors have been suggested to play a role in the development of the adenohypophysis. We have therefore examined the expression pattern of Sonic hedgehog (Shh), the hedgehog receptor Patched2 (Ptc2), the retinoic acid producing enzyme Retinaldehyde dehydrogenase3 (Raldh3) and four transcription factors, Pitx2, Isl1, Lim3 and Pax6 in chick embryos from head fold stage to embryonic day (E) 4.5. We show that already at the head fold stage, Ptc2 is expressed in prospective hypophyseal placodal cells and that Shh is expressed in the underlying mesoderm. Moreover, Shh continues to be expressed in tissues surrounding the prospective adenohypophysis, and Ptc2 is expressed in prospective hypophyseal cells. Lim3 and Pax6 are expressed from stage 10 in the prospective hypophyseal placode, whereas Pitx2 starts to be expressed before stage 10. Pitx2 is together with Pax6 expressed in the entire domain of the Rathke's pouch. Raldh3 is detected at the 20 somite stage and is together with Lim3 expressed in the anterior part of the Rathke's pouch. Isl1 is expressed in the most posterior part of the hypophyseal ectoderm in a complementary pattern to Raldh3 and Lim3.

  • 4.
    Skottheim Honn, John
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Johansson, Linn
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Rasmuson Lestander, Asa
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Regulation of twin of eyeless during Drosophila development2016Ingår i: Gene Expression Patterns, ISSN 1567-133X, E-ISSN 1872-7298, Vol. 20, nr 2, s. 120-129Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The Pax-6 protein is vital for eye development in all seeing animals, from sea urchins to humans. Either of the Pax6 genes in Drosophila (twin of eyeless and eyeless) can induce a gene cascade leading to formation of entire eyes when expressed ectopically. The twin of eyeless (toy) gene in Drosophila is expressed in the anterior region of the early fly embryo. At later stages it is expressed in the brain, ventral nerve cord and (eventually) the visual primordium that gives rise to the eye-antennal imaginal discs of the larvae. These discs subsequently form the major part of the adult head, including compound eyes. We have searched for genes that are required for normal toy expression in the early embryo to elucidate initiating events of eye organogenesis. Candidate genes identified by mutation analyses were subjected to further knock-out and miss-expression tests to investigate their interactions with toy. Our results indicate that the head-specific gap gene empty spiracles can act as a repressor of Toy, while ocelliless (oc) and spalt major (salm) appear to act as positive regulators of toy gene expression. (C) 2016 Elsevier B.V. All rights reserved.

  • 5.
    Vernersson, Emma
    et al.
    Umeå universitet, Medicinsk fakultet, Medicinsk biovetenskap, Patologi. Patologi.
    Khoo, Nelson K S
    Henriksson, Maria
    Umeå universitet, Medicinsk fakultet, Medicinsk biovetenskap, Patologi. Patologi.
    Roos, Göran
    Umeå universitet, Medicinsk fakultet, Medicinsk biovetenskap, Patologi. Patologi.
    Palmer, Ruth
    Umeå universitet, Medicinsk fakultet, Umeå centrum för molekylär patogenes (UCMP) (Medicinska fakulteten).
    Hallberg, Bengt
    Umeå universitet, Medicinsk fakultet, Medicinsk biovetenskap, Patologi. Patologi.
    Characterization of the expression of the ALK receptor tyrosine kinase in mice.2006Ingår i: Gene Expression Patterns, ISSN 1567-133X, E-ISSN 1872-7298, Vol. 6, nr 5, s. 448-461Artikel i tidskrift (Refereegranskat)
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