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High concentration glucose induces inflammation in TECs via TLR4.
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posted on 2014-05-19, 03:23 authored by Jin Ma, Steven J. Chadban, Cathy Y. Zhao, Xiaochen Chen, Tony Kwan, Usha Panchapakesan, Carol A. Pollock, Huiling WuPrimary cultures of TECs, harvested from WT and TLR4−/− mice, were cultured in media containing physiological concentration glucose (5.5 mM glucose+24.5 mM mannitol) as an osmotic control or high-concentration glucose (5.5 mM glucose+24.5 mM glucose) for 12 hours. High glucose induced upregulation of TLR4 (A), its ligands (B) and downstream molecules(C) in WT TECs compared to osmotic controls. Upregulation of downstream molecules induced by high-glucose was not seen in TLR4−/− TECs (C). Data are presented as means ± SEM; * p<0.05; ** p<0.01; *** p<0.001.
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cell biologySignal transductioncell signalingMembrane receptor signalingImmune receptor signalingImmunological signalingMolecular cell biologyMetabolic disordersDiabetes mellitusType 1 diabetestype 2 diabetesNephrologyChronic kidney diseaseModel organismsAnimal modelsMouse modelsglucoseinflammationtecs
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