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J Tissue Eng Regen Med. 2017 Nov;11(11):3236-3240. doi: 10.1002/term.2222. Epub 2016 Dec 12.

The protective effect of human platelet lysate in models of neurodegenerative disease: involvement of the Akt and MEK pathways.

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Department of Medical Pharmacology/INSERM U1171, Lille Faculty of Medicine, Lille University Medical Center and Lille Nord de France University, Lille, France.
Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Department of Movement Disorders and Neurology, Lille University Medical Center and Lille Nord de France University, Lille, France.
Graduate Institute of Biomedical Materials and Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, Taipei, Taiwan.
Université du Littoral Cote d'Opale, Calais, France.


Neurodegenerative diseases have huge economic and societal impacts, and place an immense emotional burden on patients and caregivers. Given that platelets have an essential physiological role in wound healing and tissue repair, human platelet lysates (HPLs) are being developed as a novel, effective biotherapy for neurodegenerative diseases. HPLs constitute abundant, readily accessible sources of physiological mixtures of many growth factors (GFs), with demonstrable effects on neuron survival and thus the development, maintenance, function and plasticity of the vertebrate nervous system. Here, we found that HPLs had marked neuroprotective abilities in cell-based models of Parkinson's disease and amyotrophic lateral sclerosis (the LUHMES and NSC-34 cell lines, respectively). The HPLs protected against specific cell death pathways (apoptosis and ferroptosis) and specific oxidative stress inducers [1-methyl-4-phenylpyridinium (MPP+) and menadione], and always afforded more protection than commonly used recombinant GFs (rGFs). The mechanism of protection of HPLs involved specific signalling pathways: whereas the Akt pathway was activated by HPLs under all conditions, the MEK pathway appeared to be more specifically involved in protection against MPP+ toxicity in LUHMES and, in a lesser extent, in staurosporine toxicity in NSC-34. Our present results suggest that HPLs-based therapies could be used to prevent neuronal loss in neurodegenerative diseases while overcoming the limitations currently associated with use of rGFs.


Akt; LUHMES; MEK; NSC-34; human platelet lysates; neuroprotection

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