A potential role for somatostatin signaling in regulating retinal neurogenesis

Abstract Neuropeptides have been reported to regulate progenitor proliferation and neurogenesis in the central nervous system. However, these studies have typically been conducted using pharmacological agents in ex vivo preparations, and in vivo evidence for their developmental function is generally...

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Autores principales:	Kurt Weir, Dong Won Kim, Seth Blackshaw
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/fe4c36a171e147f6ac0b66cc5e55d5e9
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spelling	oai:doaj.org-article:fe4c36a171e147f6ac0b66cc5e55d5e92021-12-02T15:49:50ZA potential role for somatostatin signaling in regulating retinal neurogenesis10.1038/s41598-021-90554-32045-2322https://doaj.org/article/fe4c36a171e147f6ac0b66cc5e55d5e92021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-90554-3https://doaj.org/toc/2045-2322Abstract Neuropeptides have been reported to regulate progenitor proliferation and neurogenesis in the central nervous system. However, these studies have typically been conducted using pharmacological agents in ex vivo preparations, and in vivo evidence for their developmental function is generally lacking. Recent scRNA-Seq studies have identified multiple neuropeptides and their receptors as being selectively expressed in neurogenic progenitors of the embryonic mouse and human retina. This includes Sstr2, whose ligand somatostatin is transiently expressed by immature retinal ganglion cells. By analyzing retinal explants treated with selective ligands that target these receptors, we found that Sstr2-dependent somatostatin signaling induces a modest, dose-dependent inhibition of photoreceptor generation, while correspondingly increasing the relative fraction of primary progenitor cells. These effects were confirmed by scRNA-Seq analysis of retinal explants but abolished in Sstr2-deficient retinas. Although no changes in the relative fraction of primary progenitors or photoreceptor precursors were observed in Sstr2-deficient retinas in vivo, scRNA-Seq analysis demonstrated accelerated differentiation of neurogenic progenitors. We conclude that, while Sstr2 signaling may act to negatively regulate retinal neurogenesis in combination with other retinal ganglion cell-derived secreted factors such as Shh, it is dispensable for normal retinal development.Kurt WeirDong Won KimSeth BlackshawNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Kurt Weir Dong Won Kim Seth Blackshaw A potential role for somatostatin signaling in regulating retinal neurogenesis
description	Abstract Neuropeptides have been reported to regulate progenitor proliferation and neurogenesis in the central nervous system. However, these studies have typically been conducted using pharmacological agents in ex vivo preparations, and in vivo evidence for their developmental function is generally lacking. Recent scRNA-Seq studies have identified multiple neuropeptides and their receptors as being selectively expressed in neurogenic progenitors of the embryonic mouse and human retina. This includes Sstr2, whose ligand somatostatin is transiently expressed by immature retinal ganglion cells. By analyzing retinal explants treated with selective ligands that target these receptors, we found that Sstr2-dependent somatostatin signaling induces a modest, dose-dependent inhibition of photoreceptor generation, while correspondingly increasing the relative fraction of primary progenitor cells. These effects were confirmed by scRNA-Seq analysis of retinal explants but abolished in Sstr2-deficient retinas. Although no changes in the relative fraction of primary progenitors or photoreceptor precursors were observed in Sstr2-deficient retinas in vivo, scRNA-Seq analysis demonstrated accelerated differentiation of neurogenic progenitors. We conclude that, while Sstr2 signaling may act to negatively regulate retinal neurogenesis in combination with other retinal ganglion cell-derived secreted factors such as Shh, it is dispensable for normal retinal development.
format	article
author	Kurt Weir Dong Won Kim Seth Blackshaw
author_facet	Kurt Weir Dong Won Kim Seth Blackshaw
author_sort	Kurt Weir
title	A potential role for somatostatin signaling in regulating retinal neurogenesis
title_short	A potential role for somatostatin signaling in regulating retinal neurogenesis
title_full	A potential role for somatostatin signaling in regulating retinal neurogenesis
title_fullStr	A potential role for somatostatin signaling in regulating retinal neurogenesis
title_full_unstemmed	A potential role for somatostatin signaling in regulating retinal neurogenesis
title_sort	potential role for somatostatin signaling in regulating retinal neurogenesis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/fe4c36a171e147f6ac0b66cc5e55d5e9
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_version_	1718385729157988352

A potential role for somatostatin signaling in regulating retinal neurogenesis

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