Protein kinase A inhibition of macrophage maturation is accompanied by an increase in DNA methylation of the colonyâ stimulating factor 1 receptor gene

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134212/1/imm12641.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134212/2/imm12641_am.pd

Regulation of alveolar macrophage p40phox: hierarchy of activating kinases and their inhibition by PGE2

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141717/1/jlb0219.pd

A placebo-controlled trial of folic acid and betaine in identical twins with Angelman syndrome.

BackgroundAngelman syndrome (AS) is a neurodevelopmental disorder that is caused by maternal genetic deficiency of a gene that encodes E6-AP ubiquitin-protein ligase (gene symbol UBE3A) mapping to chromosome 15q11-q13. AS leads to stiff and jerky gait, excess laughter, seizures, and severe intellectual disability. In some parts of the brain, the paternally inherited UBE3A gene is subject to genomic imprinting by the action of the UBE3A-antisense transcript (UBE3A-ATS) on the paternally inherited allele. Consequently, only the maternally inherited UBE3A gene is expressed in mature neurons. AS occurs due to deletions of the maternal 15q11 - 13 region, paternal uniparental disomy (UPD), imprinting center defects, mutations in the maternal UBE3A gene, or other unknown genetic malfunctions that result in a silenced maternal UBE3A gene in the specific imprinted regions of the brain.ResultsA potential treatment strategy for AS is to increase methylation of UBE3A-ATS to promote expression of the paternal UBE3A gene and thus ameliorate the clinical phenotypes of AS. We treated two sets of male identical twins with class I deletions with a 1 year treatment trial of either betaine and folic acid versus placebo. We found no statistically significant changes in the clinical parameters tested at the end of the 1 year trial, nor did we find any significant adverse events.ConclusionsThis study tested the hypothesis that by increasing the methylation of the UBE3A-antisense transcript in Angelman syndrome to promote expression of the silenced paternal UBE3A gene we may ameliorate the clinical phenotypes of AS. We treated two sets of identical twins with placebo versus betaine and folic acid. Although this study represented a novel approach to treating Angelman syndrome, the differences in the developmental testing results was not significant. This paper also discusses the value of monozygotic twin studies in minimizing confounding variables and its utility in conducting small treatment studies.Trial registrationNCT00348933 . Registered 6 July 2006

Simultaneously Targeting Myofibroblast Contractility and Extracellular Matrix Crossâ Linking as a Therapeutic Concept in Airway Fibrosis

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/136664/1/ajt14103-sup-0002-FigureS2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/136664/2/ajt14103-sup-0003-FigureS3.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/136664/3/ajt14103.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/136664/4/ajt14103_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/136664/5/ajt14103-sup-0001-FigureS1.pd

NADPH oxidase deficiency results in reduced alveolar macrophage 5â lipoxygenase expression and decreased leukotriene synthesis

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141933/1/jlb1585.pd

Prostaglandin E2 increases fibroblast geneâ specific and global DNA methylation via increased DNA methyltransferase expression

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154365/1/fsb2026009012.pd

Differential regulation by leukotrienes and calcium of Fcγ receptorâ induced phagocytosis and Syk activation in dendritic cells versus macrophages

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141597/1/jlb1234.pd