Project description:The Effect of Aromatase Knockout on Gene Expression in the Mouse Lacrimal and Meibomoan Gland. Keywords: Aromatase Knockout vs Wild Type Control Lacrimal and meibomian glands were harvested from homozygous male and female aromatase knockout mice and age matched wild type controls. Tissues were pooled into 3 biological replicates and were hybridized to separate microarrays. Each cRNA prep was hybridized to a GE Healthcare/Amersham Biosciences CodeLink UniSet Mouse 20K I Bioarray and a Affymetrix GeneChip Mouse Expression Array 430A.
Project description:The Effect of Aromatase Knockout on Gene Expression in the Mouse Lacrimal and Meibomoan Gland. Keywords: Aromatase Knockout vs Wild Type Control
Project description:NOD mice spontaneously develop lacrimal gland inflammation. NOD mice that lack TLR7 or that lack IFNAR1 are protected from developing lacrimal gland inflammation. RNA sequencing studies were performed to compare gene expression profiles in lacrimal glands from wild-type (WT) vs Tlr7 knockout or Ifnar1 knockout nonobese diabetic (NOD) mice to determine disease-relevant gene and pathway profiles upregulated in WT lacrimal glands in either a TLR7- or IFNAR1-dependent manner.
Project description:Tears are essential for the maintenance of the terrestrial animal ocular surface and the lacrimal gland is the source of the aqueous layer of the tear film. Despite the importance of the lacrimal gland in ocular health, molecular aspects of its development remain poorly understood. We have identified a noncoding RNA (miR-205) as an essential gene for lacrimal gland development. Knockout mice lacking miR-205 fail to develop lacrimal glands, establishing this noncoding RNA as a key regulator of lacrimal bud initiation. RNA-seq analysis uncovered several up-regulated miR-205 targets, including Inppl1, a negative regulator of Akt signaling. Data indicate that Akt signaling is required within lacrimal gland epithelia and is activated by Fgf10. Furthermore, combinatorial epistatic deletion of Fgf10 and miR-205 in mice exacerbates the lacrimal gland phenotype. We develop a molecular rheostat model where miR-205 modulates signaling pathways downstream of Fgf10 to regulate glandular development. These data show that a single microRNA is a key regulator for lacrimal gland initiation in mice and highlights the important role of microRNAs during organogenesis.
Project description:We used RNAsequencing to reveal the differential gene expression in Ectodysplasin knock-out lacrimal gland compared to wild-type. We show that the mutant adult lacrimal gland differentially express specific genes, demonstrating a modifed maturation process when the Ectodysplasin gene is mutated.
Project description:The purpose of this study was to determine the pathogenic changes that occur in myoepithelial cells (MECs) from lacrimal glands of a mouse model of Sjogren’s syndrome. MECs were cultured from lacrimal glands of C57BL/6J (wild type, WT), and thrombospondin 1 knockout null (TSP1 -/- ) mice. We used microarray to analyzed the differential expression of genes in cultured MECs of TSP1-/- and wild type (WT) mice.
