Regular ArticleExpression of Endothelin-B Receptors by Gliain VivoIs Increased after CNS Injury in Rats, Rabbits, and Humans
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Neuroprotective Effect of Sovateltide (IRL 1620, PMZ 1620) in a Neonatal Rat Model of Hypoxic-Ischemic Encephalopathy
2022, NeuroscienceCitation Excerpt :It is widely recognized that ETB receptors are essential for the developing nervous system (Gulati, 2016). They help to regulate the differentiation, proliferation and migration of neurons, melanocytes, and glia in both the peripheral and central nervous system (Rogers et al., 1997; Druckenbrod et al., 2008). In this study, similar to a report by Cifuentes (Cifuentes et al., 2018) the upregulation of ETB receptors likely exerted neuroprotective effects.
Endothelin, astrocytes and glaucoma
2011, Experimental Eye ResearchCitation Excerpt :There have been several studies dating back to the 1990s right after the discovery of ETs indicating that ET-1 in addition to being a potent vasoregulator (i.e. both vasoconstriction and vasorelaxation) was also a potent mitogenic agent for different cell types including smooth muscle and astrocytes (MacCumber et al., 1990; Baba, 1998). Several papers have also described a putative role for ETs in exacerbation of various neuropathologies and neurotrauma via direct actions on neuronal tissues or by altering the blood–brain barrier (e.g. hypoxia, vasospasms, etc.) as well as those actions involving astrogliosis (Nie and Olsson, 1996; Rogers et al., 1997; Baba, 1998; Schinelli, 2006; Yorio et al., 2002). Specifically, ET-1 being a potent vasoconstrictor and mitogen is considered to play a key role in regulating vascular, neuronal and astroglial interactions.
Increase in endothelin B receptor expression in optic nerve astrocytes in endothelin-1 induced chronic experimental optic neuropathy
2009, Experimental Eye ResearchCitation Excerpt :While there was no RGC loss at 10−11 M ET-1 there was an increase in ETB expression. Increased ETB expression has recently been reported in optic nerves of glaucoma patients (Wang et al., 2006), in rabbit optic nerves following crush injury (Rogers et al., 2003) or transection (Rogers et al., 1997), and in rat optic nerves with elevated IOP (Prasanna et al., 2005). Upregulation of ETB gene expression was also reported recently in retinas of rats with experimentally induced glaucoma (Yang et al., 2007).
Endothelin-1 (ET-1) causes death of retinal neurons through activation of nitric oxide synthase (NOS) and production of superoxide anion
2008, Experimental Eye ResearchCitation Excerpt :For example, secretion of ET-2 from photoreceptors is increased with an up-regulation of ETB receptors in Mueller cells after photoreceptor damage, which leads to activation and proliferation of Mueller cells (Rattner and Nathans, 2005). Also, the expression of ETB receptors is up-regulated after optic nerve transection, which mediates glial proliferation in the injured optic nerve (Rogers et al., 1997, 2003). On the other hand, ET-1 inhibits axonal transport (Stokely et al., 2002; Taniguchi et al., 2006) and induces proliferation of optic nerve head astrocytes (Prasanna et al., 2002).