Hydrocortisone 21-hemisuccinate did not prevent exogenous GAPDH-induced apoptosis in human neuroblastoma cells

Abstract

These data are related to our paper “GAPDH-targeted therapy – a new approach for secondary damage after traumatic brain injury on rats” (Lazarev et al., In press), in which we explore the role of exogenous GAPDH in traumatic brain injury-induced neuron death, and the therapeutic application of small molecules that bind to the enzyme. The current article demonstrates the induction of apoptosis by exogenous GAPDH and the effectiveness of the hydrocortisone derivative for suppressing the pathogenic action of the enzyme.

Glyceraldehyde-3-phosphate Dehydrogenase Is a Multifaceted Therapeutic Target

“…Apoptosis can also be caused by extracellular GAPDH aggregates formed due to massive cell death typical of traumatic brain injury. Recently, we showed a significant toxic effect of exogenous GAPDH aggregates on surrounding cells [28,73]. In this way, the formation of GAPDH aggregates facilitates further misfolding of the GAPDH, leading to the impairment of the enzyme molecule structure and ultimately a conversion to high molecular weight aggregates, which are usually cytotoxic and may trigger apoptosis [4,74].…”