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Starkey Lewis, P.

Publications and source records attributed to Starkey Lewis, P..

3 recordsLinked to original sources

Non-invasive quantification of hepatic necrosis from circulating alanine aminotransferase kinetics in acetaminophen-treated mice in vivo

Histological necrosis is the reference measure of hepatotoxicity but can only be obtained at terminal cull. A time course requires independent cohorts at every timepoint. Circulating alanine aminotransferase (ALT) can be sampled repeatedly in the same animal, and is released in liver injury. We asked whether serial ALT kinetics can be used to estimate histological necrosis in vivo. Forty-five fasted twelve-week-old male C57BL/6J mice received a single intraperitoneal dose of 350 mg/kg acetaminophen (paracetamol). Plasma ALT and microRNA-122 (miR-122) were measured serially from baseline to 48h as cumulative area-under-the-curve (AUC) to cull, against centrilobular necrosis on haematoxylin and eosin sections as reference (range 0 to 59%, mean 32%). A generalised additive model of necrosis on cumulative ALT AUC and time since dosing predicted necrosis with a leave-one-animal-out cross-validated mean absolute error of 7.7% necrotic area (95% CI 5.6 to 10.0; n=49). A panel of traditional regression and machine-learning models all gave equal or larger error, and adding an additional biomarker or regeneration information did not improve prediction. Serial ALT kinetics therefore provide a calibrated, longitudinal measure of hepatic necrosis in vivo and give a more stable estimate of within-group variance for study planning, while supporting reductions in animal use, because one serially-sampled cohort can replace separate cohorts at each timepoint.

pharmacology and toxicology↗

Serum CSF1 levels are elevated in patients following partial hepatectomy and acetaminophen induced acute liver failure: Reanalysis of previous data

A previous study analysed serum CSF1 concentration in patients who had undergone partial hepatectomy and patients with acute liver failure (ALF) induced by acetaminophen. A correlation between low CSF1 and poor prognosis was reported in ALF. In May 2018, an allegation of research misconduct was made against the second author of the published study, D.J.Antoine, who carried out the CSF1 analysis. The current study describes the independent reanalysis of circulating CSF1 concentration in sera from the same patient cohorts. Patient serum CSF1 levels increased following partial hepatectomy. By contrast to the published report, serum CSF1 concentration was greatest in ALF patients who died compared to survivors. The results confirm the relationship between liver injury and circulating serum CSF1.

immunology↗

Transfer of hepatocellular microRNA regulates cytochrome P450 2E1 in renal tubular cells

Extracellular microRNAs have been demonstrated to have the ability to enter kidney tubular cells and modify gene expression. We have used a Dicer-hepatocyte-specific microRNA conditional knock-out (Dicer-CKO) mouse to investigate functional microRNA transfer from liver to kidney under physiological conditions and in the context of drug toxicity. Dicer-CKO mice demonstrated a time-dependent decrease in the hepatocyte-derived microRNA, miR-122, in the kidney in the absence of other microRNA changes. During hepatotoxicity, miR-122 increased in kidney tubular cells; this was abolished in Dicer-CKO mice. Depletion of hepatocyte microRNAs increased expression and activity of the miR-122 target - cytochrome (CYP) P450 2E1 - in the kidney. Serum extracellular vesicles (ECVs) from mice with hepatotoxicity increased proximal tubular cell miR-122 and prevented cisplatin proximal tubular cell toxicity. miR-122 also increased in urinary ECVs during hepatotoxicity in humans. Transfer of microRNA was not restricted to liver injury - we detected miR-499 release with murine cardiac injury, and this correlated with an increase in the kidney. In summary, a physiological transfer of microRNA to the kidney exists, which is increased by liver injury. Regulation of renal drug response due to signalling by microRNA of hepatic origin represents a new paradigm for understanding and preventing nephrotoxicity.

pharmacology and toxicology↗