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Assessing Neuronal and Astrocyte Derived Exosomes From Individuals With Mild Traumatic Brain Injury for Markers of Neurodegeneration and Cytotoxic Activity

Winston, Charisse N., Romero, Haylie K., Ellisman, Maya, Nauss, Sophie, Julovich, David A., Conger, Tori, Hall, James R., Campana, Wendy, O’Bryant, Sid E., Nievergelt, Caroline M., Baker, Dewleen G., Risbrough, Victoria B., Rissman, Robert A.·2019·Frontiers in Neuroscience
DOI 10.3389/fnins.2019.01005PMC PMC6797846
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FIGURE 1 Fluorescent activated cell sorting (FACS) enrichment of plasma NDEs from service members with and without mTBI during deployment. Schematic cartoon of FACS enrichment via the formation of a bead-antibody-exosome (BAE) – FITC complex (A). Representative FACS plot for non-exosome, negative control (red) and BAE – FITC complexes exosomes (green) isolated from control subject, 12207 (age: 22) and mTBI subject, 11541 (age: 21) and enriched against anti-human CD171 biotin (L1CAM) or anti-GLAST antibody (B). Total number of FITC+ events were not significantly different between the two populations (C; 114719 ± 3712 FITC+ events vs. 116121 ± 4969 FITC+ events). Plasma NDE and ADE concentrations of exosome marker, CD81 were not statistically different between the two populations as measured by standard ELISA (D).
FIGURE 1 Fluorescent activated cell sorting (FACS) enrichment of plasma NDEs from service members with and without mTBI during deployment. Schematic cartoon of FACS enrichment via the formation of a bead-antibody-exosome (BAE) – FITC complex (A). Representative FACS plot for non-exosome, negative control (red) and BAE – FITC complexes exosomes (green) isolated from control subject, 12207 (age: 22) and mTBI subject, 11541 (age: 21) and enriched against anti-human CD171 biotin (L1CAM) or anti-GLAST antibody (B). Total number of FITC+ events were not significantly different between the two populations (C; 114719 ± 3712 FITC+ events vs. 116121 ± 4969 FITC+ events). Plasma NDE and ADE concentrations of exosome marker, CD81 were not statistically different between the two populations as measured by standard ELISA (D).CC BY · PubMed Central
FIGURE 2 Human plasma NDE and ADE levels Aβ1–42 and NRGN differentiate young mTBI individuals from individuals with no TBI history. Plasma NDE and ADE (A) concentrations of Aβ42 were significantly higher, whereas plasma NDE and ADE (B) concentrations of NRGN were significantly lower in young individuals with mTBI (n = 17) compared to age-matched controls (n = 20). Plasma NDE and ADE concentrations of P-T181-tau (C), and P-S396-tau (D) were not significantly different between the two groups. Non-parametric t-test, ∗P < 0.05 vs. control.
FIGURE 2 Human plasma NDE and ADE levels Aβ1–42 and NRGN differentiate young mTBI individuals from individuals with no TBI history. Plasma NDE and ADE (A) concentrations of Aβ42 were significantly higher, whereas plasma NDE and ADE (B) concentrations of NRGN were significantly lower in young individuals with mTBI (n = 17) compared to age-matched controls (n = 20). Plasma NDE and ADE concentrations of P-T181-tau (C), and P-S396-tau (D) were not significantly different between the two groups. Non-parametric t-test, ∗P < 0.05 vs. control.CC BY · PubMed Central
FIGURE 3 Plasma NDE levels of Aβ40, total tau, and NFL are not significantly different between individuals with and without mTBI. Plasma NDE levels of Aβ40 (A), NFL (B), and total tau (C), were not significantly different between the two populations while plasma ADE Aβ40 (A), NFL (B), and total tau (C) were not detectable by the Simoa Assay.
FIGURE 3 Plasma NDE levels of Aβ40, total tau, and NFL are not significantly different between individuals with and without mTBI. Plasma NDE levels of Aβ40 (A), NFL (B), and total tau (C), were not significantly different between the two populations while plasma ADE Aβ40 (A), NFL (B), and total tau (C) were not detectable by the Simoa Assay.CC BY · PubMed Central
FIGURE 4 Plasma NDE cargo from individuals with mTBI compromise membrane integrity and are toxic to neuron-like cells in vitro. Differentiated PC12 cells and SH-SY5Y cells were incubated with 100 ng/ml of NDE and ADE for 48 h. Representative photomicrographs indicate exosome-induced cytotoxicity. Signs of cytotoxicity include dendritic blebbing (indicated by arrows), suppressed neurite outgrowth and cell death in NGF + PC12 cells (A). Compared to controls (100% viability), there was a threefold increase in exosome-induced cytotoxicity (LDH release) in wells that were treated with NDEs derived from service members with mTBI (B), ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability. SH-SY5Y cells were treated with NDE and ADE preparations from control and mTBI service members and AD patients. A similar level of cytotoxicity was observed in cultured SH-SY5Y. A threefold increase in exosome-induced cytotoxicity (LDH release) was observed in wells that were treated with NDEs derived from mTBI samples and a fourfold increase exosome-induced cytotoxicity in wells that were treated with NDEs derived from AD samples as compared to NDEs derived from control samples (C). Non-parametric t-test; ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability.
FIGURE 4 Plasma NDE cargo from individuals with mTBI compromise membrane integrity and are toxic to neuron-like cells in vitro. Differentiated PC12 cells and SH-SY5Y cells were incubated with 100 ng/ml of NDE and ADE for 48 h. Representative photomicrographs indicate exosome-induced cytotoxicity. Signs of cytotoxicity include dendritic blebbing (indicated by arrows), suppressed neurite outgrowth and cell death in NGF + PC12 cells (A). Compared to controls (100% viability), there was a threefold increase in exosome-induced cytotoxicity (LDH release) in wells that were treated with NDEs derived from service members with mTBI (B), ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability. SH-SY5Y cells were treated with NDE and ADE preparations from control and mTBI service members and AD patients. A similar level of cytotoxicity was observed in cultured SH-SY5Y. A threefold increase in exosome-induced cytotoxicity (LDH release) was observed in wells that were treated with NDEs derived from mTBI samples and a fourfold increase exosome-induced cytotoxicity in wells that were treated with NDEs derived from AD samples as compared to NDEs derived from control samples (C). Non-parametric t-test; ∗P < 0.05 vs. control, dashed horizontal line represents 100% viability.CC BY · PubMed Central

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Metadata

Authors
Winston, C. N., Romero, H. K., Ellisman, M., Nauss, S., Julovich, D. A., Conger, T., Hall, J. R., Campana, W., O’Bryant, S. E., Nievergelt, C. M., Baker, D. G., Risbrough, V. B., & Rissman, R. A.
Venue
Frontiers in Neuroscience
Publisher
Frontiers Media SA
Published
2019-10-02
Volume
13
ISSN
1662-453X
DOI
10.3389/fnins.2019.01005
PMC
PMC6797846
Cited by
105
References
8
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Institute on Aging (AG057459, AG057469, AG051848, AG18440, AG005131)
  • Veterans Affairs San Diego Healthcare System (BX004312, BX003040)

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