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Role of hydrogen sulfide in early blood-brain barrier disruption following transient focal cerebral ischemia.
PLoS One. 2015; 10(2):e0117982.Plos

Abstract

We determined the role of endogenous hydrogen sulfide (H2S) in cerebral vasodilation/hyperemia and early BBB disruption following ischemic stroke. A cranial window was prepared over the left frontal, parietal and temporal cortex in mice. Transient focal cerebral Ischemia was induced by directly ligating the middle cerebral artery (MCA) for two hours. Regional vascular response and cerebral blood flow (CBF) during ischemia and reperfusion were measured in real time. Early BBB disruption was assessed by Evans Blue (EB) and sodium fluorescein (Na-F) extravasation at 3 hours of reperfusion. Topical treatment with DL-propargylglycine (PAG, an inhibitor for cystathionine γ-lyase (CSE)) and aspartate (ASP, inhibitor for cysteine aminotransferase/3-mercaptopyruvate sulfurtransferase (CAT/3-MST)), but not O-(Carboxymethyl)hydroxylamine hemihydrochloride (CHH, an inhibitor for cystathionine β-synthase (CBS)), abolished postischemic cerebral vasodilation/hyperemia and prevented EB and Na-F extravasation. CSE knockout (CSE-/-) reduced postischemic cerebral vasodilation/hyperemia but only inhibited Na-F extravasation. An upregulated CBS was found in cerebral cortex of CSE-/- mice. Topical treatment with CHH didn't further alter postischemic cerebral vasodilation/hyperemia, but prevented EB extravasation in CSE-/- mice. In addition, L-cysteine-induced hydrogen sulfide (H2S) production similarly increased in ischemic side cerebral cortex of control and CSE-/- mice. Our findings suggest that endogenous production of H2S by CSE and CAT/3-MST during reperfusion may be involved in postischemic cerebral vasodilation/hyperemia and play an important role in early BBB disruption following transient focal cerebral ischemia.

Authors+Show Affiliations

Department of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.Department of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.Department of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.Department of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.Department of Pathology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.Department of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.Department of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.Department of Cellular Biology & Anatomy, Louisiana State University Health Sciences Center-Shreveport, Shreveport, Louisiana, United States of America.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25695633

Citation

Jiang, Zheng, et al. "Role of Hydrogen Sulfide in Early Blood-brain Barrier Disruption Following Transient Focal Cerebral Ischemia." PloS One, vol. 10, no. 2, 2015, pp. e0117982.
Jiang Z, Li C, Manuel ML, et al. Role of hydrogen sulfide in early blood-brain barrier disruption following transient focal cerebral ischemia. PLoS One. 2015;10(2):e0117982.
Jiang, Z., Li, C., Manuel, M. L., Yuan, S., Kevil, C. G., McCarter, K. D., Lu, W., & Sun, H. (2015). Role of hydrogen sulfide in early blood-brain barrier disruption following transient focal cerebral ischemia. PloS One, 10(2), e0117982. https://doi.org/10.1371/journal.pone.0117982
Jiang Z, et al. Role of Hydrogen Sulfide in Early Blood-brain Barrier Disruption Following Transient Focal Cerebral Ischemia. PLoS One. 2015;10(2):e0117982. PubMed PMID: 25695633.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of hydrogen sulfide in early blood-brain barrier disruption following transient focal cerebral ischemia. AU - Jiang,Zheng, AU - Li,Chun, AU - Manuel,Morganne L, AU - Yuan,Shuai, AU - Kevil,Christopher G, AU - McCarter,Kimberly D, AU - Lu,Wei, AU - Sun,Hong, Y1 - 2015/02/19/ PY - 2014/05/02/received PY - 2015/01/06/accepted PY - 2015/2/20/entrez PY - 2015/2/20/pubmed PY - 2016/1/1/medline SP - e0117982 EP - e0117982 JF - PloS one JO - PLoS One VL - 10 IS - 2 N2 - We determined the role of endogenous hydrogen sulfide (H2S) in cerebral vasodilation/hyperemia and early BBB disruption following ischemic stroke. A cranial window was prepared over the left frontal, parietal and temporal cortex in mice. Transient focal cerebral Ischemia was induced by directly ligating the middle cerebral artery (MCA) for two hours. Regional vascular response and cerebral blood flow (CBF) during ischemia and reperfusion were measured in real time. Early BBB disruption was assessed by Evans Blue (EB) and sodium fluorescein (Na-F) extravasation at 3 hours of reperfusion. Topical treatment with DL-propargylglycine (PAG, an inhibitor for cystathionine γ-lyase (CSE)) and aspartate (ASP, inhibitor for cysteine aminotransferase/3-mercaptopyruvate sulfurtransferase (CAT/3-MST)), but not O-(Carboxymethyl)hydroxylamine hemihydrochloride (CHH, an inhibitor for cystathionine β-synthase (CBS)), abolished postischemic cerebral vasodilation/hyperemia and prevented EB and Na-F extravasation. CSE knockout (CSE-/-) reduced postischemic cerebral vasodilation/hyperemia but only inhibited Na-F extravasation. An upregulated CBS was found in cerebral cortex of CSE-/- mice. Topical treatment with CHH didn't further alter postischemic cerebral vasodilation/hyperemia, but prevented EB extravasation in CSE-/- mice. In addition, L-cysteine-induced hydrogen sulfide (H2S) production similarly increased in ischemic side cerebral cortex of control and CSE-/- mice. Our findings suggest that endogenous production of H2S by CSE and CAT/3-MST during reperfusion may be involved in postischemic cerebral vasodilation/hyperemia and play an important role in early BBB disruption following transient focal cerebral ischemia. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/25695633/Role_of_hydrogen_sulfide_in_early_blood_brain_barrier_disruption_following_transient_focal_cerebral_ischemia_ L2 - https://dx.plos.org/10.1371/journal.pone.0117982 DB - PRIME DP - Unbound Medicine ER -