Effects of Histidine-Rich Glycoprotein on Cerebral Blood Vessels | Zendy

Samantha M. Steelman | Zendy; Travis W. Hein | Zendy; Amy A. Gorman | Zendy; Gregory Bix | Zendy

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Effects of Histidine-Rich Glycoprotein on Cerebral Blood Vessels

Author(s) -

Samantha M. Steelman,

Travis W. Hein,

Amy A. Gorman,

Gregory Bix

Publication year - 2013

Publication title -

journal of cerebral blood flow and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.167

H-Index - 193

eISSN - 1559-7016

pISSN - 0271-678X

DOI - 10.1038/jcbfm.2013.106

Subject(s) - subarachnoid hemorrhage , medicine , vasospasm , vasoactive , cerebral blood flow , cerebral vasospasm , autologous blood , vasodilation , blood vessel , blood–brain barrier , cardiology , anesthesia , pathology , central nervous system

Delayed cerebral vasospasm is thought to be caused by factors released from a subarachnoid blood clot. Because vasospasm occurs several days after hemorrhage, we hypothesized that clotted blood releases vasoactive factors as it ages. Targeted proteomics identified histidine-rich glycoprotein (HRG) as a potentially vasoactive factor released within the first 72 hours of clot formation. In vitro studies revealed that HRG caused moderate (~30%) dilation of cannulated cerebral arterioles and proliferation of cerebrovascular endothelial cells. We conclude that HRG released from clotted blood, while unlikely to contribute to cerebral vasospasm, might provide important vasodilatory or angiogenic stimuli after hemorrhagic stroke.

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