Corpus ID: 79996645

The Contribution Of Toll-Like Receptors In The Pathogenesis Of Diabetic Retinopathy In Human Microvascular Retinal Endothelial Cells In Vitro

  title={The Contribution Of Toll-Like Receptors In The Pathogenesis Of Diabetic Retinopathy In Human Microvascular Retinal Endothelial Cells In Vitro},
  author={F. Bakhsh},
الدراسة الحالية تركز على مستقبلات مناعية معينة تدعى مستقبلات الشبيهة بمستقبلات تول (TLRs)؛ يمكن لهذه المستقبلات تحديد أنماط جزيئية محددة في مسببات الأمراض، وبالتالي القضاء عليها. في هذه الدراسة نقوم بتحديد العلاقة المرضية بين هذه المستقبلات ومرض اعتلال شبكية السكري (DR). هذا المرض من مضاعفات مرض السكري، تؤثر على الأوعية الدموية الصغيرة في شبكية العين ويمكن أن تؤدي إلى العمى. لقد أردنا في هذا البحث التحقق من مساهمة المستقبلات الشبيهة بمستقبلات تول4 (TLR4… Expand


Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces atherosclerosis and alters plaque phenotype in mice deficient in apolipoprotein E.
  • K. Michelsen, M. Wong, +6 authors M. Arditi
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 2004
An important role for TLR4 and MyD88 signaling in atherosclerosis in a hypercholesterolemic mouse model is suggested, providing a pathophysiologic link between innate immunity, inflammation, and atherogenesis. Expand
Cutting Edge: A Novel Toll/IL-1 Receptor Domain-Containing Adapter That Preferentially Activates the IFN-β Promoter in the Toll-Like Receptor Signaling1
Findings suggest that TRIF is involved in the TLR signaling, particularly in the MyD88-independent pathway. Expand
Toll-Like Receptor 4 Deficiency Decreases Atherosclerosis But Does Not Protect Against Inflammation in Obese Low-Density Lipoprotein Receptor–Deficient Mice
Whether TLR4 deficiency has a protective role in inflammation, insulin resistance, and atherosclerosis induced by a diabetogenic diet is investigated and alternative pathways may be responsible for adipose tissue macrophage infiltration and insulin resistance that occurs in obesity. Expand
Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product.
It is demonstrated that TLR4 is the gene product that regulates LPS response, and a single point mutation of the amino acid that is highly conserved among the IL-1/Toll receptor family is found. Expand
Hyperglycemia Induces Toll-Like Receptor-2 and -4 Expression and Activity in Human Microvascular Retinal Endothelial Cells: Implications for Diabetic Retinopathy
The novel data suggest that hyperglycemia induces TLR-2 andTLR-4 activation and downstream signaling mediating increased inflammation possibly via reactive oxygen species (ROS) and could contribute to DR. Expand
Toll-like Receptor-2 Is Essential for the Development of Palmitate-induced Insulin Resistance in Myotubes*
  • J. Senn
  • Biology, Medicine
  • Journal of Biological Chemistry
  • 2006
RNA interference-mediated inhibition of TLR2 and MyD88 expression in C2C12 muscle cells resulted in a near complete inhibition of palmitate-induced insulin resistance and interleukin (IL)-6 production. Expand
Endogenous ligands of Toll‐like receptors
It is essential that efforts should be directed to conclusively determine whether the reported putative endogenous ligands of TLRs are a result of the endogenous molecules or of contaminant(s), before exploring further the implication and therapeutic potential of these putative TLR ligands. Expand
Increased toll-like receptor (TLR) 2 and TLR4 expression in monocytes from patients with type 1 diabetes: further evidence of a proinflammatory state.
It is made the novel observation that TLR2 and TLR4 expression and signaling are increased in T1DM and contribute to the proinflammatory state. Expand
Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction
A protein is described, Mal (MyD88-adapter-like), which joins MyD88 as a cytoplasmic TIR-domain-containing protein in the human genome, which is therefore an adapter in TLR-4 signal transduction. Expand
A novel small molecule TLR4 antagonist (IAXO-102) negatively regulates non-hematopoietic toll like receptor 4 signalling and inhibits aortic aneurysms development.
The ability of IAXO-102 to negatively regulate TLR4 signalling and to inhibit experimental abdominal aortic aneurysm (AAA) development is demonstrated, suggesting the potential therapeutic use of thisTLR4 antagonist for pharmacological intervention of AAA. Expand