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BAM15 attenuates transportation-induced apoptosis in iPS-differentiated retinal tissue

Study · human · Stem cell research & therapy · 2019 · DOI 10.1186/s13287-019-1151-y · PMID 30795805

Plain-language summary

Paraphrased from the published abstract below — not a verdict on whether anything works.

In this study of human-induced pluripotent stem (hiPS)-cell-differentiated retinal tissue, the authors examined whether the mitochondrial uncoupler BAM15 affects apoptosis during 5-day transport of retinal tissue grown for 30 days and 60 days, transported with or without BAM15 in the laboratory or by real express. Transportation increased expression of the apoptosis marker cleaved caspase3 and of p53, NFkappaB, and TNF-a, and this increase was reduced when BAM15 was included. Neurons showed disrupted, tortuous axons (by NEFL staining) after transport, and adding BAM15 was associated with preserved neuronal structure and increased cell viability, without altering the location of retinal cell subtypes, as measured by CCK8 assay and immunofluorescence.

Abstract

BAM15 is a novel mitochondrial protonophore uncoupler capable of protecting mammals from acute renal ischemic-reperfusion injury and cold-induced microtubule damage. The purpose of our study was to investigate the effect of BAM15 on apoptosis during 5-day transportation of human-induced pluripotent stem (hiPS)-differentiated retinal tissue. Retinal tissues of 30 days and 60 days were transported with or without BAM15 for 5 days in the laboratory or by real express. Immunofluorescence staining of apoptosis marker cleaved caspase3, proliferation marker Ki67, and neural axon marker NEFL was performed. And expression of apoptotic-related factors p53, NFkappaB, and TNF-a was detected by real-time PCR. Also, location of ganglion cells, photoreceptor cells, amacrine cells, and precursors of neuronal cell types in retinal tissue was stained by immunofluorescence after transportation. Furthermore, cell viability was assessed by CCK8 assay. Results showed transportation remarkably intensified expression of apoptotic factor cleaved caspase3, p53, NFkappaB, and TNF-a, which could be reduced by supplement of BAM15. In addition, neurons were severely injured after transportation, with axons manifesting disrupted and tortuous by staining NEFL. And the addition of BAM15 in transportation was able to protect neuronal structure and increase cell viability without affecting subtypes cells location of retinal tissue. BAM15 might be used as a protective reagent on apoptosis during transporting retinal tissues, holding great potential in research and clinical applications.

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