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Specific role of tight junction proteins claudin-5, occludin, and ZO-1 of the blood-brain barrier in a focal cerebral ischemic insult.
J Mol Neurosci. 2011 Jun; 44(2):130-9.JM

Abstract

Blood-brain barrier (BBB) leakage plays a key role in cerebral ischemia-reperfusion injury. It is quite necessary to further explore the characteristic and mechanism of BBB leakage during stroke. We induced a focal cerebral ischemia model by transient middle cerebral artery occlusion in male rats for defining the time course of BBB permeability within 120 h following reperfusion and evaluate the specific role of tight junction (TJ) associated proteins claudin-5, occludin, and ZO-1 as well as protein kinase C delta (PKCδ) pathway in BBB leakage induced by reperfusion injury. We verified a bimodal increase in the permeability of the BBB following focal ischemia by Evans blue assay. Two peaks of BBB permeability appeared at 3 h and 72 h of reperfusion after 2 h focal ischemia, respectively. The leak at the endothelial cell was represented at the level of transmission electron microscopy. TTC staining results showed increased infarct size with time after cerebral ischemia reperfusion. The mRNA and protein expression levels of these three TJ associated proteins were significantly decreased compared with the sham-operated group within 120 h of reperfusion, corresponding to the time-dependent change of the biphasic pattern in BBB leakage. The redistribution of claudin-5, occludin, and ZO-1 in ischemia brain microvascular endothelial cells was observed at the same time points. In addition, Western blot assay revealed PKCδ level was also significantly increased in a similar biphasic pattern to above results within 120 h after cerebral ischemia-reperfusion. This study demonstrates the timing of TJ associated proteins claudin-5, occludin, and ZO-1 in light of BBB permeability associated with cerebral ischemia reperfusion, and suggests PKCδ pathway may participate in TJ barrier open and BBB leakage during reperfusion injury in a time-dependent manner.

Authors+Show Affiliations

Department of Neurobiology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning Province, People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21318404

Citation

Jiao, Haixia, et al. "Specific Role of Tight Junction Proteins Claudin-5, Occludin, and ZO-1 of the Blood-brain Barrier in a Focal Cerebral Ischemic Insult." Journal of Molecular Neuroscience : MN, vol. 44, no. 2, 2011, pp. 130-9.
Jiao H, Wang Z, Liu Y, et al. Specific role of tight junction proteins claudin-5, occludin, and ZO-1 of the blood-brain barrier in a focal cerebral ischemic insult. J Mol Neurosci. 2011;44(2):130-9.
Jiao, H., Wang, Z., Liu, Y., Wang, P., & Xue, Y. (2011). Specific role of tight junction proteins claudin-5, occludin, and ZO-1 of the blood-brain barrier in a focal cerebral ischemic insult. Journal of Molecular Neuroscience : MN, 44(2), 130-9. https://doi.org/10.1007/s12031-011-9496-4
Jiao H, et al. Specific Role of Tight Junction Proteins Claudin-5, Occludin, and ZO-1 of the Blood-brain Barrier in a Focal Cerebral Ischemic Insult. J Mol Neurosci. 2011;44(2):130-9. PubMed PMID: 21318404.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Specific role of tight junction proteins claudin-5, occludin, and ZO-1 of the blood-brain barrier in a focal cerebral ischemic insult. AU - Jiao,Haixia, AU - Wang,Zhenhua, AU - Liu,Yunhui, AU - Wang,Ping, AU - Xue,Yixue, Y1 - 2011/02/12/ PY - 2010/12/18/received PY - 2011/01/19/accepted PY - 2011/2/15/entrez PY - 2011/2/15/pubmed PY - 2011/9/1/medline SP - 130 EP - 9 JF - Journal of molecular neuroscience : MN JO - J. Mol. Neurosci. VL - 44 IS - 2 N2 - Blood-brain barrier (BBB) leakage plays a key role in cerebral ischemia-reperfusion injury. It is quite necessary to further explore the characteristic and mechanism of BBB leakage during stroke. We induced a focal cerebral ischemia model by transient middle cerebral artery occlusion in male rats for defining the time course of BBB permeability within 120 h following reperfusion and evaluate the specific role of tight junction (TJ) associated proteins claudin-5, occludin, and ZO-1 as well as protein kinase C delta (PKCδ) pathway in BBB leakage induced by reperfusion injury. We verified a bimodal increase in the permeability of the BBB following focal ischemia by Evans blue assay. Two peaks of BBB permeability appeared at 3 h and 72 h of reperfusion after 2 h focal ischemia, respectively. The leak at the endothelial cell was represented at the level of transmission electron microscopy. TTC staining results showed increased infarct size with time after cerebral ischemia reperfusion. The mRNA and protein expression levels of these three TJ associated proteins were significantly decreased compared with the sham-operated group within 120 h of reperfusion, corresponding to the time-dependent change of the biphasic pattern in BBB leakage. The redistribution of claudin-5, occludin, and ZO-1 in ischemia brain microvascular endothelial cells was observed at the same time points. In addition, Western blot assay revealed PKCδ level was also significantly increased in a similar biphasic pattern to above results within 120 h after cerebral ischemia-reperfusion. This study demonstrates the timing of TJ associated proteins claudin-5, occludin, and ZO-1 in light of BBB permeability associated with cerebral ischemia reperfusion, and suggests PKCδ pathway may participate in TJ barrier open and BBB leakage during reperfusion injury in a time-dependent manner. SN - 1559-1166 UR - https://www.unboundmedicine.com/medline/citation/21318404/Specific_role_of_tight_junction_proteins_claudin_5_occludin_and_ZO_1_of_the_blood_brain_barrier_in_a_focal_cerebral_ischemic_insult_ L2 - https://dx.doi.org/10.1007/s12031-011-9496-4 DB - PRIME DP - Unbound Medicine ER -