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Hyperammonemia-induced changes in the cerebral transcriptome and proteome.

Alina Schrimpf¹, Olivia Knappe¹, Natalia Qvartskhava¹

¹Clinic for Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Germany.

Analytical Biochemistry

|January 15, 2022

Summary

Molecular changes in the brain linked to hyperammonemia and hepatic encephalopathy (HE) were investigated. Researchers identified key genes and proteins, including CARM1, TROVE2, and LCN2, potentially contributing to brain dysfunction in HE.

Keywords:

Ammonia Astrocytes Hepatic encephalopathy Oxidative stress

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Area of Science:

Neuroscience
Molecular Biology
Biochemistry

Background:

Cerebral impairment in hyperammonemic disorders like hepatic encephalopathy (HE) has poorly understood molecular underpinnings.
Systemic hyperammonemia is a key factor contributing to brain dysfunction in HE.

Purpose of the Study:

To identify molecular alterations in the brain associated with hyperammonemia.
To investigate the role of specific genes and proteins in astrocyte function under hyperammonemic conditions.

Main Methods:

Transcriptomics and proteomics were employed on the brains of hepatic glutamine synthetase knockout (LGS-KO) mice.
Cultured astrocytes were challenged with ammonium chloride (NH4Cl) to mimic hyperammonemic conditions.
Expression levels of CARM1, TROVE2, and LCN2 were analyzed in rodent models and human patient samples.

Main Results:

Over 200 genes and 30 proteins showed altered expression in LGS-KO mouse brains in a region-specific manner.
Differentially expressed genes were enriched in pathways related to oxidative stress, cell proliferation, and heme metabolism.
CARM1, TROVE2, and LCN2 were identified as key candidates, with roles in senescence, RNA quality control, and iron homeostasis, respectively, in ammonia-exposed astrocytes.

Conclusions:

This study identified novel molecular players, including CARM1, TROVE2, and LCN2, implicated in cerebral dysfunction in HE.
Findings suggest specific roles for these molecules in astrocyte function under hyperammonemia.
Elevated LCN2 and Trove2 levels were observed in animal models and human HE patients, supporting their relevance.