muller cell

这是一篇关于muller cell的思维导图

muller cell

• diabetic influence
  • glutamate increases
    • directly
      • significant decreases in glutamate transport via GLAST beginning after just 4 weeks of diabetes in rats
      • decreased glutamine synthetase activity and a subsequent decrease in the conversion of glutamate to glutamine necessary for neurotransmitter regeneration
    • indirectly
      • decreased K+uptake
        • There is decreased K+conductanceon the plasma membrane of Müller cells isolated from rat retinas after 4 months of experimental diabetes
          • Redistribution of the Kir4.1 K+channel
            • accumulation of advanced glycation endproducts (AGEs)
  • downregulate the Kir4.1 channels, but not Kir2.1
  • Deletionof the dystrophin-Dp71 protein within Müller cells caused extensive vascular leakage and edema in the mouse retina
  • growth factor
    • bad
      • Müller cells are a potential source for growth factors and cytokines when stimulated with elevated glucose levels.
      • Müller cell derived PEDF has also been suggested to have its part in diabetes-induced retinal angiogenesis
    • good
      • the intent of such growth factor production by Müller cells in the first place might have been to protect itself and the retinal neurons from a diabetic insult
        • so we should pay more atterntion on long-term anti-VEGF treatment might hamper functional integrity of Müller cells and neurons causing unexpected additional problems in treating diabetic retinopathy
  • Cytokines
    • bad
      • Müller cells release a variety of cytokines and chemokines under hyperglycemic conditions.
        • a major source of retinal interleukin-1beta (IL-1b) production
          • IL-1b produces the active cytokines IL-1band IL-18 by cleavage of their inactive proform
        • Müller cells produce other well-known pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFa) and interleukin-6 (IL-6)
      • Increased caspase-1 activation and elevated IL-1b levels
        • We have identified that targeting this pathway by knocking down caspase-1 or the IL-1 receptor (IL-1R1) or by pharmacological intervention protects against the development of diabetic retinopathy in diabetic rats and mice
    • Prolonged IL-1bproduction by Müller cells has been shown to affect endothelial cell viability in a paracrine fashion Endothelial cells are extremely susceptible to IL-1 band rapidly progress to cell death in response to this proinflammatory cytokine
    • good
      • IL-6 is an important cytokine responsible for maintaining proper neuronal function as well as stimulating neuroprotective effects
• Function of muller cell
  • Uptake and recycling of neurotransmitters,retinoids acid compounds,and ions (such as potassium k+)
  • Control of metabolism and supply of nutrients for retina
    • It has been shown that ATP production in Müller cells drastically declines when glycolysis is inhibited. However, ATP levels remained equal in aerobic versus anaerobic conditions as long as glucose was provided, indicating that Müller cells live primarily from glycolysis rather than oxidative phosphorylation
    • the metabolism of glucose and glycogen by Müller cells is regulated by light being absorbed by the photoreceptors
      • neurovascular coupling
  • Other studies have shown that Müller cells participate in regulation of vascular tone in a process of neurovascular coupling
  • Regulation of blood flow and maintenance of the blood retinal barrier
    • It has been shown that Müller cells induce blood-barrier properties in retinal endothelial cells
      • includes the secretion of factors such as pig ment epithelium-derived factor (PEDF) and thrombospondin-1 which are anti-angiogenic and increase the tightness of the endothelial barrier
• for retinal
  • muller cell are the only cell to span the entire width of the retina and have contact to almost every cell type in the retina
  • Müller cell ablation leads to photoreceptor degeneration, vascular leak, and intraretinal neovascularization demonstrating that Müller cells are necessary for both neuronal and vascular function and viability
  • They are uniquely positioned to perform a wide variety of function necessary to maintaining the retinal homeostasis
  • Changes to their environment by hyperglycemia alters functional interaction with pericytes