RGD Reference Report - Protein therapy using heme-oxygenase-1 fused to a polyarginine transduction domain attenuates cerebral vasospasm after experimental subarachnoid hemorrhage.

General

Protein therapy using heme-oxygenase-1 fused to a polyarginine transduction domain attenuates cerebral vasospasm after experimental subarachnoid hemorrhage.
Authors:	Ogawa, T Hanggi, D Wu, Y Michiue, H Tomizawa, K Ono, S Matsui, H Date, I Steiger, HJ
Citation:	Ogawa T, etal., J Cereb Blood Flow Metab. 2011 Nov;31(11):2231-42. doi: 10.1038/jcbfm.2011.87. Epub 2011 Jun 8.
RGD ID:	10755572
Pubmed:	PMID:21654696 (View Abstract at PubMed)
PMCID:	PMC3210347 (View Article at PubMed Central)
DOI:	DOI:10.1038/jcbfm.2011.87 (Journal Full-text)
A sequence of 11 consecutive arginine residues (11R) is one of the best protein transduction domains for introducing proteins into cell membranes. Heme-oxygenase-1 (HO-1) is involved in heme catabolism and reduces the contractile effect of hemoglobin after subarachnoid hemorrhage (SAH). Therefore, we constructed 11R-fused HO-1 protein to achieve successful transduction of the protein into the cerebral arteries and examined the therapeutic effect of the 11R-HO-1 protein for cerebral vasospasm (CV) after SAH. We injected the 11R-HO-1 protein into the cisterna magna of male rats and, several hours after the injection, performed immunofluorescence staining and western blotting analysis of the rat basilar arteries (BAs) to determine transduction efficacy. We also assessed intraarterial HO-1 activity as cGMP (cyclic guanosine 3', 5'-cyclic monophosphate) accumulation in SAH and determined whether protein transduction of 11R-HO-1 quantified the therapeutic effect in a rat double-hemorrhage model of SAH. The BAs expressed significantly more HO-1 in the group injected with 11R-HO-1 (3.56+/-0.54 (11R-HO-1) versus control (saline)), and transduction of 11R-HO-1 resulted in higher activity (>3.25-fold) in rat BAs with SAH. Moreover, the results of the rat double-hemorrhage model showed that the 11R-HO-1 protein significantly attenuated CV after SAH (317.59+/-23.48 mum (11R-HO-1) versus 270.08+/-14.66 mum (11R-fused enhanced green fluorescent protein), 252.05+/-13.95 mum (saline), P<0.01).

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
intracranial vasospasm	treatment	IMP		10755572	associated with Subarachnoid Hemorrhage	RGD
intracranial vasospasm	treatment	ISO	HMOX1 (Homo sapiens)	10755572; 10755572	associated with Subarachnoid Hemorrhage	RGD

Objects Annotated

Genes (Rattus norvegicus)

Hmox1 (heme oxygenase 1)

Genes (Mus musculus)

Hmox1 (heme oxygenase 1)

Genes (Homo sapiens)

HMOX1 (heme oxygenase 1)

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Protein therapy using heme-oxygenase-1 fused to a polyarginine transduction domain attenuates cerebral vasospasm after experimental subarachnoid hemorrhage.