» Articles » PMID: 24236295

Immunization with a Neural-derived Peptide Protects the Spinal Cord from Apoptosis After Traumatic Injury

Abstract

Apoptosis is one of the most destructive mechanisms that develop after spinal cord (SC) injury. Immunization with neural-derived peptides (INDPs) such as A91 has shown to reduce the deleterious proinflammatory response and the amount of harmful compounds produced after SC injury. With the notion that the aforementioned elements are apoptotic inducers, we hypothesized that INDPs would reduce apoptosis after SC injury. In order to test this assumption, adult rats were subjected to SC contusion and immunized either with A91 or phosphate buffered saline (PBS; control group). Seven days after injury, animals were euthanized to evaluate the number of apoptotic cells at the injury site. Apoptosis was evaluated using DAPI and TUNEL techniques; caspase-3 activity was also evaluated. To further elucidate the mechanisms through which A91 exerts this antiapoptotic effects we quantified tumor necrosis factor-alpha (TNF-α). To also demonstrate that the decrease in apoptotic cells correlated with a functional improvement, locomotor recovery was evaluated. Immunization with A91 significantly reduced the number of apoptotic cells and decreased caspase-3 activity and TNF-α concentration. Immunization with A91 also improved the functional recovery of injured rats. The present study shows the beneficial effect of INDPs on preventing apoptosis and provides more evidence on the neuroprotective mechanisms exerted by this strategy.

Citing Articles

Use of Cells, Supplements, and Peptides as Therapeutic Strategies for Modulating Inflammation after Spinal Cord Injury: An Update.

Garcia E, Buzoianu-Anguiano V, Silva-Garcia R, Esparza-Salazar F, Arriero-Cabanero A, Escandon A Int J Mol Sci. 2023; 24(18).

PMID: 37762251 PMC: 10531377. DOI: 10.3390/ijms241813946.


Title: Immunotherapy; a ground-breaking remedy for spinal cord injury with stumbling blocks: An overview.

Saeed Y Front Pharmacol. 2023; 14:1110008.

PMID: 36778022 PMC: 9909832. DOI: 10.3389/fphar.2023.1110008.


Supplementation With Vitamin E, Zinc, Selenium, and Copper Re-Establishes T-Cell Function and Improves Motor Recovery in a Rat Model of Spinal Cord Injury.

Garcia E, Hernandez-Ayvar F, Rodriguez-Barrera R, Flores-Romero A, Borlongan C, Ibarra A Cell Transplant. 2022; 31:9636897221109884.

PMID: 35808825 PMC: 9272473. DOI: 10.1177/09636897221109884.


Immunomodulation induced by central nervous system-related peptides as a therapeutic strategy for neurodegenerative disorders.

Palumbo M, Moroni A, Quiroga S, Castro M, Burgueno A, Genaro A Pharmacol Res Perspect. 2021; 9(5):e00795.

PMID: 34609083 PMC: 8491457. DOI: 10.1002/prp2.795.


Active and Passive Immunization with Myelin Basic Protein as a Method for Early Treatment of Traumatic Spinal Cord Injury; a Meta-Analysis.

Yousefifard M, Madani Neishaboori A, Alavi S, Toloui A, Gubari M, Zareie Shab Khaneh A Arch Acad Emerg Med. 2021; 9(1):e57.

PMID: 34580655 PMC: 8464018. DOI: 10.22037/aaem.v9i1.1316.


References
1.
Martin L, Adams N, Pan Y, Price A, Wong M . The mitochondrial permeability transition pore regulates nitric oxide-mediated apoptosis of neurons induced by target deprivation. J Neurosci. 2011; 31(1):359-70. PMC: 3078575. DOI: 10.1523/JNEUROSCI.2225-10.2011. View

2.
Solomon A, Hirschberg D, Lavie V, Schwartz M . Transplantation of activated macrophages overcomes central nervous system regrowth failure. FASEB J. 1996; 10(11):1296-302. DOI: 10.1096/fasebj.10.11.8836043. View

3.
Laemmli U . Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature. 1970; 227(5259):680-5. DOI: 10.1038/227680a0. View

4.
Fujita K, Tatsumi K, Kondoh E, Chigusa Y, Mogami H, Fujii T . Differential expression and the anti-apoptotic effect of human placental neurotrophins and their receptors. Placenta. 2011; 32(10):737-44. DOI: 10.1016/j.placenta.2011.07.001. View

5.
Lee J, Choi S, Oh T, Yune T . 17β-Estradiol inhibits apoptotic cell death of oligodendrocytes by inhibiting RhoA-JNK3 activation after spinal cord injury. Endocrinology. 2012; 153(8):3815-27. DOI: 10.1210/en.2012-1068. View