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   <subfield code="a">10.1007/s00011-010-0232-2</subfield>
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   <subfield code="a">Toll-like receptor 4 signaling in dysfunction of cardiac microvascular endothelial cells under hypoxia/reoxygenation</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Zheng Zhang, Weijie Li, Dongdong Sun, Li Zhao, Rongqing Zhang, Yabin Wang, Xuan Zhou, Haichang Wang, Feng Cao]</subfield>
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   <subfield code="a">Objective: This study was designed to detect the role of Toll-like receptor 4 (TLR4) signaling in the dysfunction of cardiac microvascular endothelial cells (CMECs) after hypoxia/reoxygenation (H/R). Methods: The cell viability of CMECs was measured by MTT assay. The migration of CMECs was detected by cell scratch wound assay. The expressions of TLR4, nuclear factor-kappa B (NF-κB) and eNOS were analyzed by Western blot. Secretions of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were determined by NO detection kit and ELISA. Results: Lipopolysaccharide (LPS) incubation increased the expressions of TLR4, NF-κB, IL-6 and TNF-α in CMECs (P&lt;0.05 vs. control). The CMECs after H/R injury had impaired cell viability (P&lt;0.01 vs. control) and migration ability (P&lt;0.05 vs. control). Moreover, the expressions of TLR4, NF-κB, IL-6 and TNF-α were elevated after H/R in CMECs (P&lt;0.01 vs. control), while NO and the eNOS expression were significantly decreased. In contrast, administration of the TLR4-neutralizing antibody MTS510 prior to H/R injury down-regulated the expressions of IL-6 and TNF-α and attenuated the dysfunction of CMECs. Conclusion: TLR4 and its signaling components can be activated by LPS and H/R in CMECs. Blocking the TLR4 signal pathway before H/R injury attenuates CMEC dysfunction.</subfield>
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   <subfield code="a">Toll-like receptor 4</subfield>
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   <subfield code="a">Cardiac microvascular endothelial cells</subfield>
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   <subfield code="a">Apoptosis</subfield>
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   <subfield code="a">Zhang</subfield>
   <subfield code="D">Zheng</subfield>
   <subfield code="u">Department of Cardiology, Xijing Hospital, Fourth Military Medical University, 710032, Xi'an, Shaanxi, China</subfield>
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   <subfield code="a">Li</subfield>
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   <subfield code="u">Department of Cardiology, Xijing Hospital, Fourth Military Medical University, 710032, Xi'an, Shaanxi, China</subfield>
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   <subfield code="a">Sun</subfield>
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   <subfield code="u">Department of Cardiology, Xijing Hospital, Fourth Military Medical University, 710032, Xi'an, Shaanxi, China</subfield>
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   <subfield code="a">Zhao</subfield>
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   <subfield code="u">Department of Cardiology, Xijing Hospital, Fourth Military Medical University, 710032, Xi'an, Shaanxi, China</subfield>
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   <subfield code="a">Zhang</subfield>
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   <subfield code="u">Department of Cardiology, Xijing Hospital, Fourth Military Medical University, 710032, Xi'an, Shaanxi, China</subfield>
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   <subfield code="u">Department of Cardiology, Xijing Hospital, Fourth Military Medical University, 710032, Xi'an, Shaanxi, China</subfield>
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