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Updated: Jun 19, 2026

In vivo Electroporation of Developing Mouse Retina
Published on: June 24, 2011
ATP controls cell cycle and induces proliferation in the mouse developing retina
Alfred Sholl-Franco1, Lucianne Fragel-Madeira, Arciolanda da Canceição Cauaia Macama
1Instituto de Biofísica Carlos Chagas Filho, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21949-900, Brazil. asholl@biof.ufrj.br
Adenosine triphosphate (ATP) stimulates cell proliferation in newborn mouse retinal explants by activating P2Y(1) receptors. This process involves promoting late-developing progenitors to enter the cell cycle, influencing cyclin D1 and p27(kip1) expression.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Nucleotides, including adenosine triphosphate (ATP), are implicated as mitogens in developing retinal tissues.
- Previous studies suggested a role for nucleotides in chick retinal development.
- The specific mechanisms of ATP-mediated proliferation in mammalian retinal development require further elucidation.
Purpose of the Study:
- To investigate the mitogenic effect of ATP on newborn mouse retinal explants.
- To determine the role of P2Y(1) receptors in ATP-induced retinal cell proliferation.
- To elucidate the cell cycle progression events influenced by ATP in retinal progenitors.
Main Methods:
- Cultured retinal explants from newborn C57bl/6 mice.
- Assessed cell proliferation using [(3)H]-thymidine incorporation and bromodeoxyuridine (BrdU) labeling.
- Investigated receptor distribution via immunohistochemistry and analyzed cell cycle regulators (cyclin D1, p27(kip1)) and mitotic markers (p-histone H3).
Main Results:
- P2Y(1) receptors were widely distributed in the mouse retina, co-localizing with proliferating cell nuclear antigen (PCNA)-positive cells.
- ATP and ADP, but not UTP, dose-dependently increased [(3)H]-thymidine incorporation, an effect blocked by the P2 antagonist PPADS.
- ATP treatment increased BrdU-positive cells in the neuroblastic layer and modulated cyclin D1 and p27(kip1) expression, indicating progression through the cell cycle.
Conclusions:
- ATP, acting through P2Y(1) receptors, induces proliferation of late-developing retinal progenitors in newborn mice.
- ATP facilitates cell cycle progression from G1 to S phase and subsequently to G2 phase.
- These findings highlight the role of purinergic signaling in mammalian retinal development and progenitor cell regulation.
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