title: MicroRNA miR-7 is preferentially expressed in endocrine cells of the developing and adult human pancreas.
abstract: 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.
authors.affiliation: Cell Transplant Center, Diabetes Research Institute University of Miami Leonard M. Miller School of Medicine, 1450 NW 10th Avenue, Miami, FL 33136, USA.
authors.forename: Mayrin
authors.initials: M
authors.lastname: Correa-Medina
authors.forename: Valia
authors.initials: V
authors.lastname: Bravo-Egana
authors.forename: Samuel
authors.initials: S
authors.lastname: Rosero
authors.forename: Camillo
authors.initials: C
authors.lastname: Ricordi
authors.forename: Helena
authors.initials: H
authors.lastname: Edlund
authors.forename: Juan
authors.initials: J
authors.lastname: Diez
authors.forename: Ricardo L
authors.initials: RL
authors.lastname: Pastori
mesh_terms: D000328:Adult; D051792:Basic Helix-Loop-Helix Proteins / Q000235:genetics / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000166:cytology / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental; D005865:Gestational Age; D005934:Glucagon / Q000235:genetics / Q000378:metabolism; D006801:Humans; D017403:In Situ Hybridization; D007328:Insulin / Q000235:genetics / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D018613:Microscopy, Confocal; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D010179:Pancreas / Q000166:cytology / Q000196:embryology / Q000378:metabolism*; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013004:Somatostatin / Q000235:genetics / Q000378:metabolism
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D005934:Glucagon; D007328:Insulin; D035683:MicroRNAs; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D013004:Somatostatin; C498695:NEUROG3 protein, human