The neuropeptide somatostatin (somatotropin release inhibiting factor, SRIF) has been widely investigated in the retina, where it is localized to sparse amacrine cells and, in some instances, in a subset of ganglion cells. All five different SRIF subtype receptors (designated sst1 through sst5) are expressed in the mammalian retina, and their variegated expression patterns, together with the variety of signaling mechanisms activated by the different ssts, suggest that the somatostatinergic system may exert multiple actions on retinal neurons and on retinal physiology. For instance, SRIF, mostly acting through sst2, functions as a positive factor in the retina by regulating retinal homeostasis and protecting neurons against damage. In particular, a considerable amount of experimental evidence has been gathered to show that sst2 activation may effectively limit the expression of pro-angiogenic signals, thereby counteracting the growth of new, aberrant vessels that is typically seen, for instance, in diabetic retinopathy. In addition, SRIF has been shown to protect retinal neurons from excitotoxic insults caused by excess of glutamate release. This condition is frequently associated with retinal ischemia, which is a common cause of severe retinal damage in different pathologies. Several studies have described potent protective actions of SRIF in the ischemic retina mediated by sst2 activation. Taken together, these data support the notion that therapeutic strategies based on the use and implementation of SRIF analogues may be clinically relevant in different retinal diseases such as ischemic and diabetic retinopathies. This chapter reviews the literature concerning the advances in the research of the roles played by the somatostatinergic system in animal models of retinal disease.
Effects of somatostatin in animal models of retinal disease
CASINI, GIOVANNI
2013-01-01
Abstract
The neuropeptide somatostatin (somatotropin release inhibiting factor, SRIF) has been widely investigated in the retina, where it is localized to sparse amacrine cells and, in some instances, in a subset of ganglion cells. All five different SRIF subtype receptors (designated sst1 through sst5) are expressed in the mammalian retina, and their variegated expression patterns, together with the variety of signaling mechanisms activated by the different ssts, suggest that the somatostatinergic system may exert multiple actions on retinal neurons and on retinal physiology. For instance, SRIF, mostly acting through sst2, functions as a positive factor in the retina by regulating retinal homeostasis and protecting neurons against damage. In particular, a considerable amount of experimental evidence has been gathered to show that sst2 activation may effectively limit the expression of pro-angiogenic signals, thereby counteracting the growth of new, aberrant vessels that is typically seen, for instance, in diabetic retinopathy. In addition, SRIF has been shown to protect retinal neurons from excitotoxic insults caused by excess of glutamate release. This condition is frequently associated with retinal ischemia, which is a common cause of severe retinal damage in different pathologies. Several studies have described potent protective actions of SRIF in the ischemic retina mediated by sst2 activation. Taken together, these data support the notion that therapeutic strategies based on the use and implementation of SRIF analogues may be clinically relevant in different retinal diseases such as ischemic and diabetic retinopathies. This chapter reviews the literature concerning the advances in the research of the roles played by the somatostatinergic system in animal models of retinal disease.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
