Dataset: Intestinal Structure and Microbiome in Mouse Models of Osteogenesis Imperfecta

Description

Osteogenesis imperfecta (OI) is an inherited connective tissue disorder primarily caused by genetic variants affecting collagen type I, a key structural component not only of bone but also of the intestine. While OI patients show an increased risk of gastrointestinal disorders, intestinal structural and microbiome alterations associated with collagen-I defects remain poorly understood. This dataset comprises intestinal morphological, functional, and microbiome data obtained from two OI mouse models—Col1a1Jrt/+ (COL1A1 mutation, FVB background) and oim-/- (COL1A2 mutation, C57BL/6 background)—and their wild-type littermates. Female and male mice were maintained on a regular chow diet and analyzed at 4, 8, and 12 weeks of age. The dataset includes measurements of body mass and intestinal length, quantification of intestinal collagen content, gene expression analyses of extracellular matrix components, assessment of intestinal permeability, gut microbiome composition, and microbial activity assessed by short-chain and branched-chain fatty acid concentrations. Data are provided at the level of individual animals across ages and sexes. These data reveal collagen-I–dependent, sex-specific alterations in intestinal structure and microbial metabolic activity in OI mouse models. The dataset can be reused for comparative analyses of collagen-related intestinal phenotypes across different genetic backgrounds and disease models. Detailed interpretation and analysis of these data are presented in the associated manuscript: “Exploring the impact of collagen-I genetic variants on intestinal structure and gut microbiota in mouse models of osteogenesis imperfecta” by Zhang YK, Iskandar MM, Kubow S, Komarova SV, and Tauer JT.

Steps to reproduce

Male and female Col1a1Jrt/+ (FVB background) and oim-/- (C57BL/6 background) mouse models of osteogenesis imperfecta, along with their wild-type littermates, were maintained on a standard chow diet (Teklad Global 18% Protein Rodent Diet (#2918, Envigo)) under controlled housing conditions in accordance with institutional animal care guidelines, with unlimited access to water and food. Mice were examined at 4, 8, and 12 weeks of age, with body mass recorded prior to tissue collection. After euthanasia using approved methods, the gastrointestinal tract was dissected to measure the total intestinal length (inserted photographs and length measured using ImageJ), and tissues from the duodenum, jejunum, ileum, and colon (each 5-mm segments) were collected for further analyses. Intestinal morphology was assessed through histological analysis in 5um thick sections. Ten well-oriented villus–crypt units were randomly selected, and measurements of villus height (tip to crypt mouth), villus width (midpoint), and crypt depth (crypt mouth to base) were manually recorded. Collagen content in the intestine was quantified by collagen staining (Fast Green and Sirius Red, #9046, Chondrex), and extracellular matrix–related gene expression was analyzed via qPCR. In vivo intestinal permeability was evaluated using FITC Dextran (4 kDa). Fecal samples of the cecum were collected for microbiome profiling through 16S rRNA gene sequencing (analyzed using MicrobiomeAnalyst software), and microbial metabolic activity was assessed by quantifying cecal short-chain and branched-chain fatty acids. Data were analyzed at the individual animal level, stratified by sex, genotype, and age. Detailed procedures, analytical pipelines, and statistical methods are described in the related manuscript: “Exploring the impact of collagen-I genetic variants on intestinal structure and gut microbiota in mouse models of osteogenesis imperfecta” by Zhang YK, Iskandar MM, Kubow S, Komarova SV, and Tauer JT.

Institutions

• University of Alberta

  AB, Edmonton
• Shriners Hospitals for Children Canada

  QC, Montreal
• McGill University Faculty of Dentistry

  QC, Montreal
• McGill University School of Human Nutrition

  QC, Sainte-Anne-de-Bellevue
• Johannes Kepler Universitat Medizinische Fakultat

  Oberösterreich, Linz

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