Adenine Nucleotides Control Proliferation In Vivo of Rat Retinal Progenitors by P2Y 1 Receptor
Previous studies demonstrated that exogenous ATP is able to regulate proliferation of retinal progenitor cells (RPCs) in vitro possibly via P2Y receptor, a G protein-coupled receptor. Here, we evaluated the function of adenine nucleotides in vivo during retinal development of newborn rats. Intravitr...
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Published in | Molecular neurobiology Vol. 54; no. 7; p. 5142 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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United States
01.09.2017
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Abstract | Previous studies demonstrated that exogenous ATP is able to regulate proliferation of retinal progenitor cells (RPCs) in vitro possibly via P2Y
receptor, a G protein-coupled receptor. Here, we evaluated the function of adenine nucleotides in vivo during retinal development of newborn rats. Intravitreal injection of apyrase, an enzyme that hydrolyzes nucleotides, reduced cell proliferation in retinas at postnatal day 2 (P2). This decrease was reversed when retinas were treated together with ATPγ-S or ADPβ-S, two hydrolysis-resistant analogs of ATP and ADP, respectively. During early postnatal days (P0 to P5), an increase in ectonucleotidase (E-NTPDase) activity was observed in the retina, suggesting a decrease in the availability of adenine nucleotides, coinciding with the end of proliferation. Interestingly, intravitreal injection of the E-NTPDase inhibitor ARL67156 increased proliferation by around 60 % at P5 rats. Furthermore, immunolabeling against P2Y
receptor was observed overall in retina layers from P2 rats, including proliferating Ki-67-positive cells in the neuroblastic layer (NBL), suggesting that this receptor could be responsible for the action of adenine nucleotides upon proliferation of RPCs. Accordingly, intravitreal injection of MRS2179, a selective antagonist of P2Y
receptors, reduced cell proliferation by approximately 20 % in P2 rats. Moreover, treatment with MRS 2179 caused an increase in p57
and cyclin D1 expression, a reduction in cyclin E and Rb phosphorylated expression and in BrdU-positive cell number. These data suggest that the adenine nucleotides modulate the proliferation of rat RPCs via activation of P2Y
receptors regulating transition from G1 to S phase of the cell cycle. |
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AbstractList | Previous studies demonstrated that exogenous ATP is able to regulate proliferation of retinal progenitor cells (RPCs) in vitro possibly via P2Y
receptor, a G protein-coupled receptor. Here, we evaluated the function of adenine nucleotides in vivo during retinal development of newborn rats. Intravitreal injection of apyrase, an enzyme that hydrolyzes nucleotides, reduced cell proliferation in retinas at postnatal day 2 (P2). This decrease was reversed when retinas were treated together with ATPγ-S or ADPβ-S, two hydrolysis-resistant analogs of ATP and ADP, respectively. During early postnatal days (P0 to P5), an increase in ectonucleotidase (E-NTPDase) activity was observed in the retina, suggesting a decrease in the availability of adenine nucleotides, coinciding with the end of proliferation. Interestingly, intravitreal injection of the E-NTPDase inhibitor ARL67156 increased proliferation by around 60 % at P5 rats. Furthermore, immunolabeling against P2Y
receptor was observed overall in retina layers from P2 rats, including proliferating Ki-67-positive cells in the neuroblastic layer (NBL), suggesting that this receptor could be responsible for the action of adenine nucleotides upon proliferation of RPCs. Accordingly, intravitreal injection of MRS2179, a selective antagonist of P2Y
receptors, reduced cell proliferation by approximately 20 % in P2 rats. Moreover, treatment with MRS 2179 caused an increase in p57
and cyclin D1 expression, a reduction in cyclin E and Rb phosphorylated expression and in BrdU-positive cell number. These data suggest that the adenine nucleotides modulate the proliferation of rat RPCs via activation of P2Y
receptors regulating transition from G1 to S phase of the cell cycle. |
Author | Sholl-Franco, Alfred Fragel-Madeira, Lucianne de Almeida-Pereira, Luana Thorstenberg, Maria Luiza Prates Repossi, Marinna Garcia Coutinho-Silva, Robson Ventura, Ana Lucia Marques Magalhães, Camila Feitosa |
Author_xml | – sequence: 1 givenname: Luana surname: de Almeida-Pereira fullname: de Almeida-Pereira, Luana organization: Department of Neurobiology, Institute of Biology, Fluminense Federal University, Niterói, Brazil – sequence: 2 givenname: Camila Feitosa surname: Magalhães fullname: Magalhães, Camila Feitosa organization: Department of Neurobiology, Institute of Biology, Fluminense Federal University, Niterói, Brazil – sequence: 3 givenname: Marinna Garcia surname: Repossi fullname: Repossi, Marinna Garcia organization: Department of Neurobiology, Institute of Biology, Fluminense Federal University, Niterói, Brazil – sequence: 4 givenname: Maria Luiza Prates surname: Thorstenberg fullname: Thorstenberg, Maria Luiza Prates organization: Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil – sequence: 5 givenname: Alfred surname: Sholl-Franco fullname: Sholl-Franco, Alfred organization: Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil – sequence: 6 givenname: Robson surname: Coutinho-Silva fullname: Coutinho-Silva, Robson organization: Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil – sequence: 7 givenname: Ana Lucia Marques surname: Ventura fullname: Ventura, Ana Lucia Marques organization: Department of Neurobiology, Institute of Biology, Fluminense Federal University, Niterói, Brazil – sequence: 8 givenname: Lucianne orcidid: 0000-0001-6747-2828 surname: Fragel-Madeira fullname: Fragel-Madeira, Lucianne email: lfragel@id.uff.br, lfragel@id.uff.br organization: Laboratório de Desenvolvimento e Regeneração Neural, Departmento de Neurobiologia, Universidade Federal Fluminense, Cx. Postal 100180, Niterói, RJ, 24020-141, Brazil. lfragel@id.uff.br |
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Keywords | P2Y1 receptor Purines Development Retina Proliferation |
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Snippet | Previous studies demonstrated that exogenous ATP is able to regulate proliferation of retinal progenitor cells (RPCs) in vitro possibly via P2Y
receptor, a G... |
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SubjectTerms | Adenosine Diphosphate - analogs & derivatives Adenosine Diphosphate - pharmacology Adenosine Triphosphatases - metabolism Adenosine Triphosphate - metabolism Animals Bromodeoxyuridine - metabolism Cell Cycle - drug effects Cell Division - drug effects Cell Proliferation - drug effects Rats Receptors, Purinergic P2Y1 - metabolism Retina - drug effects Retina - metabolism Stem Cells - cytology Stem Cells - drug effects |
Title | Adenine Nucleotides Control Proliferation In Vivo of Rat Retinal Progenitors by P2Y 1 Receptor |
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