Immunocytochemistry of mouse and human retina with antisera to insulin and S-100 protein

Abstract

Immunocytochemistry using peroxidase antiperoxidase (PAP) techniques showed insulin-like immunoreactivity in the human retina, and in the mouse retina and optic nerve. The immunoreaction product was seen in the inner nuclear, ganglion cell, outer and inner plexiform layers of the retinas, and in glial cell bodies of the optic nerve. A similar staining pattern using antiserum to S-100 protein, a marker for glial elements, was also seen in these tissues. This demonstrates that insulin or insulin-like immunoreactivity appears to be limited to glial cells of the retina and optic nerve. Our study suggests that the presence of insulin or a similar peptide in retina and optic nerve may be important for their normal function and metabolism.

Insulin inhibits voltage-dependent calcium influx into rod photoreceptors

“…Although it appears that insulin is unable to cross the blood-retinal barrier [19], the retina is capable of synthesizing insulin [20]; in situ hybridization and RT-PCR show that Müller cells contain mRNA for the prepro form of insulin [21,22]; and insulin and insulinlike immunoreactivity have been demonstrated throughout the retina, particularly in Müller cells [23]. Insulin levels in blood and various tissues are reported to range from 0.3 to 3.0 nM [24].…”

Beta-2-Adrenergic Receptor Regulates Insulin Signaling to Reduce Cell Death in Müller Cells

“…40 In these studies, using insulin antibodies in rodent retinal glial cells, Das found that these cells could produce insulin and that insulin receptors were present in glial cells, likely Müller cells. 40 From these initial studies, recent results have further suggested that receptors for insulin are present in the eye, specifically the retina. [41][42][43][44] Further studies by found the presence of the precursor of insulin, preproinsulin, in mRNA from an intact rat retina.…”

“…37,39 Following insulin stimulation, phosphorylation of Akt on Ser 473 will occur downstream of the IRS complexes to inhibit apoptosis. Das et al (1984) suggested the possibility of insulin being produced in other tissues beyond the beta cells of the pancreas. 40 In these studies, using insulin antibodies in rodent retinal glial cells, Das found that these cells could produce insulin and that insulin receptors were present in glial cells, likely Müller cells.…”

“…Das et al (1984) suggested the possibility of insulin being produced in other tissues beyond the beta cells of the pancreas. 40 In these studies, using insulin antibodies in rodent retinal glial cells, Das found that these cells could produce insulin and that insulin receptors were present in glial cells, likely Müller cells. 40 From these initial studies, recent results have further suggested that receptors for insulin are present in the eye, specifically the retina.…”

“…29 Since -adrenergic receptors can decrease TNF-and TNF-negatively regulates insulin receptor signaling to induce apoptosis, our studies sought to determine the mechanisms by which -adrenergic receptors modulate insulin receptor signaling and apoptosis in retinal Müller cells. Previous investigations have concentrated on insulin signaling in the retina, 37,39,40,45,52,94,95 with less work focusing on the role of -adrenergic receptor regulation of insulin signaling in the retina. Our recent work with IRS-1 (Chapter 2) suggests that -adrenergic receptors on retinal Müller cells may play a role in insulin signaling, as it relates to diabetic retinopathy.…”