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Neuroprotective actions of hydrogen sulfide (H2S) and sulfhydration in the brain

Hydrogen sulfide (H2S) has emerged as an important signaling molecule joining the ranks of the gasotransmitters, nitric oxide (NO) and carbon monoxide (CO). Analogous to NO, H2S signals via a posttranslational modification termed sulfhydration, wherein H2S mediates the conversion of –SH groups of reactive cysteine residues on target proteins to –SSH or persulfide groups. Ever since its characterization, sulfhydration has been shown to participate in a myriad of physiological processes ranging from vasorelaxation to neuroprotection. Recently we have shown that aberrant H2S metabolism and sulfhydration play key roles in the progression of neurodegeneration in Parkinson's disease (PD) and Huntington's disease (HD). In HD, mutant huntingtin disrupts the transcriptional regulatory machinery of cystathionine gamma lyase (CSE), the biosynthetic enzyme for H2S as well as its precursor cysteine. mHtt affects transcription factors responsible for expression of CSE leading to its depletion in HD. H2S also modulates the disposition of second messengers such as cGMP which results in cognitive deficits, a feature shared by several neurodegenerative disorders including PD and HD. This presentation focuses on how H2S regulates redox homeostasis via gene regulatory mechanisms, the disruption of which is a contributor to disease progression in neuronal degeneration.