Published May 2021 | Version v1
Journal article

HMGB1 expression in leukocytes as a biomarker of cellular damage induced by [99mTc]Tc-HMPAO-labelling procedure: A quality control study

  • 1. Molecular Medicine PhD Program, Department of Molecular Medicine, "Sapienza" University of Rome (Italy)
  • 2. Nuclear Medicine Unit, Department of Radiology, Oncology and Human Pathology, "Sapienza" University of Rome (Italy)
  • 3. Department of Experimental Medicine, "Sapienza" University of Rome (Italy)

Description

Highlights: • Autologous White Blood Cells scintigraphy is based on a multi-step sequence of cell separation and radiolabelling • No molecular tool is available to evaluate WBC damage secondary to cell manipulation • High Mobility Group Box 1 (HMGB1) is a alarmin protein released from the nucleus of damaged cells following injury • HMGB1 levels in WBC cytosol after radiolabelling with [99mTc]Tc-HMPAO did not differ to those from the cold cellular sample • HMGB1 monitoring may represent a specific tool for secondary damage of WBC induced by radiolabelling procedure Autologous White Blood Cells (WBC) scintigraphy is based on a multi-step sequence of cell separation and radiolabelling. Besides in vivo imaging quality control, no molecular tool is available to evaluate WBC damage secondary to cell manipulation. High Mobility Group Box 1 (HMGB1) is a protein of the alarmins family, secreted by innate immune cells and released from the nucleus of damaged cells following different types of injury. Aim of this study was to evaluate HMGB1 levels in WBC cytosolic extracts (CE) before and after [99mTc]Tc-HMPAO labelling procedure, as a biomarker of induced WBC damage.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.nucmedbio.2021.03.008

Additional details

Identifiers

DOI
10.1016/j.nucmedbio.2021.03.008;
PII
S0969805121000512;

Publishing Information

Journal Title
Nuclear Medicine and Biology
Journal Volume
96
Journal Page Range
p. 94-100
ISSN
0969-8051
CODEN
NMBIEO

Optional Information

Copyright
Copyright (c) 2021 Elsevier Inc. All rights reserved.