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. 2018 Mar;14(1):26-30.
doi: 10.1007/s12024-017-9942-x. Epub 2018 Jan 18.

Bystin (BYSL) as a possible marker of severe hypoxic-ischemic changes in neuropathological examination of forensic cases

Mieszko Olczak  1 , Dominik Chutorański  2 , Magdalena Kwiatkowska  3 , Dorota Samojłowicz  3 , Sylwia Tarka  3   2 , Teresa Wierzba-Bobrowicz  2
Affiliations

Bystin (BYSL) as a possible marker of severe hypoxic-ischemic changes in neuropathological examination of forensic cases

Mieszko Olczak et al. Forensic Sci Med Pathol. 2018 Mar.

Abstract

Bystin (BYSL) is a 306-amino acid protein encoded in humans by the BYSL gene located on the 6p21.1 chromosome. It is conserved across a wide range of eukaryotes. BYSL was reported to be a sensitive marker for the reactive astrocytes induced by ischemia/reperfusion and chemical hypoxia in vitro and is considered to be one of the common characteristics of astrogliosis. In our study we examined whether BYSL could be used as a marker for hypoxic-ischemic changes in forensic cases. Groups suspected of acute hypoxic-ischemic changes presented strong BYSL expression in the cytoplasm of neocortical neurons especially in layers 3-5, that seemed to be short-lasting. In the hypoxic-ischemic-reperfusion group we did not find BYSL expression. BYSL expression in the cytoplasm of cortical neurons was minimal in the control group (cardiac arrest). BYSL seems to be a promising early marker of severe hypoxic-ischemic changes in neuropathological examination of forensic cases and certainly requires further studies.

Keywords: Brain ischemia; Bystin; Hypoxia-ischemia; Marker.

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Conflict of interest statement

Conflict of interest

All authors declare that they have no conflict of interest.

Ethical approval

For this type of study formal consent is not required.

Financial disclosure statement

None.

Clinical trial registry name

None.

Figures

Fig. 1
Fig. 1
Frontal lobes, magnification × 200. H&E and anti-BYSL staining in the 3rd neuronal layer of the neocortex. GFAP marks white matter. a – control group (sudden death), slightly pronounced brain edema; b - control group, normal view of astroglia; c – control group (sudden death), white matter, minimal BYSL expression in neuron cytoplasm; d – HI group - brain edema, ischemic neurons and perineuronal satellitosis; e – HI group, astroglia proliferation and clasmatodendrosis; f – HI group, white matter, statistically significant (comparing to control group) increased BYSL expression in cytoplasm of ischemic neurons; g – HIR group with brain edema, ischemic neurons and severe perineuronal satellitosis; h – HIR group, slightly more pronounced astroglia proliferation and clasmatodendrosis; i – HIR group with no BYSL expression. Inserts b, e, h shows astrocytes in higher magnification
Fig. 2
Fig. 2
Case of brain ischemic stroke with duration of over 48 h; magnification ×200. H&E - macrophages infiltration; CD68 - macrophages/phagolytic microglia infiltration (arrows) in the vicinity of blood vessel; GFAP - astrocytes (arrows) in the area of brain ischemic stroke, poor GFAP expression; BYSL - no BYSL expression in the area of brain ischemic stroke
See this image and copyright information in PMC

References

    1. Xie Y, Zacharias E, Hoff P, Tegtmeier F. Ion channel involvement in anoxic depolarization induced by cardiac arrest in rat brain. J Cereb Blood Flow Metab. 1995;15:587–594. doi: 10.1038/jcbfm.1995.72. - DOI - PubMed
    1. Katsura K, Rodriguez de Turco EB, Folbergrová J, Bazan NG, Siesjö BK. Coupling among energy failure, loss of ion homeostasis, and phospholipase A2 and C activation during ischemia. J Neurochem. 1993;61:1677–1684. doi: 10.1111/j.1471-4159.1993.tb09803.x. - DOI - PubMed
    1. Goll DE, Thompson VF, Li H, Wei W, Cong J. The calpain system. Physiol Rev. 2003;83:731–801. doi: 10.1152/physrev.00029.2002. - DOI - PubMed
    1. Smith ML, von Hanwehr R, Siesjö BK. Changes in extra- and intracellular pH in the brain during and following ischemia in hyperglycemic and in moderately hypoglycemic rats. J Cereb Blood Flow Metab. 1986;6:574–583. doi: 10.1038/jcbfm.1986.104. - DOI - PubMed
    1. Endoh M, Maiese K, Wagner J. Expression of the inducible form of nitric oxide synthase by reactive astrocytes after transient global ischemia. Brain Res. 1994;651:92–100. doi: 10.1016/0006-8993(94)90683-1. - DOI - PubMed

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