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Olthoff, K.

Publications and source records attributed to Olthoff, K..

2 recordsLinked to original sources

Ultrasensitive detection of neuronal DNA using genome-wide non-CG methylation patterns

Methylation-based liquid biopsies can identify the tissue origins of circulating cell-free DNA (cfDNA). A major constraint on the sensitivity of these assays is the limited number of cell-type-specific CpG markers. Here we exploit the high abundance of non-CpG (CpH) methylation in neurons to enable ultrasensitive detection of neuronal DNA. We show that neurons carry 100-fold higher CpH methylation than other tissues, in which apparent CpH methylation largely reflects experimental artifacts. Using a computational criterion to identify cfDNA molecules carrying clusters of methylated CpA sites, we detect neuronal DNA at proportions as low as 20 parts per million. Analysis of 231 samples from 163 individuals revealed minimal neuronal cfDNA in the plasma of healthy subjects; elevated levels in patients with measles or acute neurological conditions; strikingly high levels in brain-dead donors, indicating extensive ongoing neuronal death; and the highest levels in the cerebrospinal fluid of patients in a neurological intensive care unit. These findings establish genome-wide, fragment-level analysis of non-CpG methylation as an ultrasensitive approach for blood-based monitoring of brain injury and disease.

genomics↗

NASH patient liver derived organoids exhibit patient specific NASH phenotypes and drug responses.

To determine if patient liver derived organoids can in principle be a useful experimental model for non alcoholic staetohepatitis (NASH), we derived to our knowledge for the first time bipotent ductal organoids from endstage NASH patient livers, and for comparison from normal donor livers. We found that all tested NASH liver derived organoids exhibited a profound failure to dedifferentiate from the hepatic state back to the biliary state, consistent with the known poor regenerative capacity of NASH livers. Indeed, RNAseq on all tested NASH organoid populations confirmed down regulation of multiple cell cycle pathways. NASH liver derived hepatically differentiated organoids can slowly expand as monolayers, significantly simplifying microscopic quantitation: The monolayers show variable, but overall significantly increased lipid droplet accumulation in response to free fatty acids. Transcriptome analysis of NASH organoids reveals strong upregulation of a wide variety of pro inflammatory pathways in a NASH patient specific manner. Surprisingly, NASH liver derived organoids are highly diverse not only regarding their cytochrome cytochrome p450 metabolism and inflammatory response, but also react differentially to known antisteatotic, anti inflammatory and antifibrotic drugs, raising the possibility of using NASH patient liver biopsy derived organoids for personalized drug screening and therapy.\n\nOne Sentence SummaryNASH patient liver derived organoids replicate NASH liver phenotypes in a patient specific manner and exhibit profound differences in their response to drugs that are currently used in NASH clinical trials.

cell biology↗