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A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl
Published on: November 28, 2014
Granzyme-b mediated cell death in the spinal cord-injured rat model
Ganta Vijay Chaitanya1, Mayuri Kolli, Phanithi Prakash Babu
1Department of Biotechnology and Department of Animal Sciences, School of Life Sciences, University of Hyderabad, Hyderabad, Andhra Pradesh, India.
Spinal cord injury initiates a complex series of inflammatory and immune responses including the influx of monocytes, macrophages, T-cells, NK cells and so on, into the injured area. In the present study, we found a significant increase in the levels of granzyme-b (gra-b) from the first day after the transection until the third day, with decrease in intensity thereafter. The chemokine IP-10/CXCL10 was also found to be elevated along with gra-b correlating with the infiltration of CD-8(+) cytotoxic T lymphocytes (CTLs) into the injured spinal cord. We observed an increase in the levels of the 64 kDa poly ADP ribose polymerase fragment, known to be a signature fragment produced by gra-b. Localization of gra-b in TUNEL positive neurons indicates that gra-b might play a crucial role in neuronal death and contributes to the pathophysiology of spinal cord injury.
Spinal cord injury initiates a complex series of inflammatory and immune responses including the influx of monocytes, macrophages, T-cells, NK cells and so on, into the injured area. In the present study, we found a significant increase in the levels of granzyme-b (gra-b) from the first day after the transection until the third day, with decrease in intensity thereafter. The chemokine IP-10/CXCL10 was also found to be elevated along with gra-b correlating with the infiltration of CD-8(+) cytotoxic T lymphocytes (CTLs) into the injured spinal cord. We observed an increase in the levels of the 64 kDa poly ADP ribose polymerase fragment, known to be a signature fragment produced by gra-b. Localization of gra-b in TUNEL positive neurons indicates that gra-b might play a crucial role in neuronal death and contributes to the pathophysiology of spinal cord injury.