Growth Hormone Neuroprotective Effects After an Optic Nerve Crush in the Male Rat

Growth hormone (GH) has neuroprotective effects that have not been evaluated in the mammalian visual system. This study tested the hypothesis that GH administration can promote retinal neuroprotection in an optic nerve crush (ONC) model in male rats. The ON was compressed for 10 seconds, and bovine...

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Veröffentlicht in:Investigative ophthalmology & visual science 2024-11, Vol.65 (13), p.17
Hauptverfasser: Epardo, David, Balderas-Márquez, Jerusa E, Rodríguez-Arzate, Cynthia A, Thébault, Stéphanie C, Carranza, Martha, Luna, Maricela, Ávila-Mendoza, José, Calderón-Vallejo, Denisse, Quintanar, J Luis, Arámburo, Carlos, Martínez-Moreno, Carlos G
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container_issue 13
container_start_page 17
container_title Investigative ophthalmology & visual science
container_volume 65
creator Epardo, David
Balderas-Márquez, Jerusa E
Rodríguez-Arzate, Cynthia A
Thébault, Stéphanie C
Carranza, Martha
Luna, Maricela
Ávila-Mendoza, José
Calderón-Vallejo, Denisse
Quintanar, J Luis
Arámburo, Carlos
Martínez-Moreno, Carlos G
description Growth hormone (GH) has neuroprotective effects that have not been evaluated in the mammalian visual system. This study tested the hypothesis that GH administration can promote retinal neuroprotection in an optic nerve crush (ONC) model in male rats. The ON was compressed for 10 seconds, and bovine GH was injected concomitantly to injury for 14 days (0.5 µg/g every 12 hours). At 24 hours and 14 days after ONC, we evaluated the effects of GH upon several markers by quantitative PCR (qPCR), Western blot, and immunohistochemistry; the ON integrity was assessed using CTB Alexa 488 anterograde tracer, and retinal function was tested by full-field electroretinogram. GH partially prevented the ONC-induced death of retinal ganglion cells (RGCs), as well as the increase in gliosis marker GFAP at 14 days. Most of the ONC-induced changes in mRNA retinal levels of several neurotrophic, survival, synaptogenic, gliosis, and excitotoxicity markers were prevented by GH, both at 24 hours and 14 days, and treatment also stimulated the expression of antiapoptotic proteins Bcl-2 and Bcl-xL at 24 hours. Additionally, GH partially maintained the ON integrity and active anterograde transport, as well as retinal function by avoiding the reduced amplitude and slowing of the A- and B-waves and oscillatory potentials associated with the ONC at 14 days. GH has neuroprotective effects in the ONC model in male rats, it promoted RGC survival, gliosis reduction, and axonal transport increase, likely through the regulation of genes involved in neuroprotection, survival, and synaptogenesis. Furthermore, GH prevented functional impairment, indicating its potential as a therapeutic option for retinal neurodegenerative diseases.
doi_str_mv 10.1167/iovs.65.13.17
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This study tested the hypothesis that GH administration can promote retinal neuroprotection in an optic nerve crush (ONC) model in male rats. The ON was compressed for 10 seconds, and bovine GH was injected concomitantly to injury for 14 days (0.5 µg/g every 12 hours). At 24 hours and 14 days after ONC, we evaluated the effects of GH upon several markers by quantitative PCR (qPCR), Western blot, and immunohistochemistry; the ON integrity was assessed using CTB Alexa 488 anterograde tracer, and retinal function was tested by full-field electroretinogram. GH partially prevented the ONC-induced death of retinal ganglion cells (RGCs), as well as the increase in gliosis marker GFAP at 14 days. Most of the ONC-induced changes in mRNA retinal levels of several neurotrophic, survival, synaptogenic, gliosis, and excitotoxicity markers were prevented by GH, both at 24 hours and 14 days, and treatment also stimulated the expression of antiapoptotic proteins Bcl-2 and Bcl-xL at 24 hours. Additionally, GH partially maintained the ON integrity and active anterograde transport, as well as retinal function by avoiding the reduced amplitude and slowing of the A- and B-waves and oscillatory potentials associated with the ONC at 14 days. GH has neuroprotective effects in the ONC model in male rats, it promoted RGC survival, gliosis reduction, and axonal transport increase, likely through the regulation of genes involved in neuroprotection, survival, and synaptogenesis. 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Furthermore, GH prevented functional impairment, indicating its potential as a therapeutic option for retinal neurodegenerative diseases.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Disease Models, Animal</subject><subject>Electroretinography</subject><subject>Growth Hormone - pharmacology</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Nerve Crush</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Optic Nerve Injuries - drug therapy</subject><subject>Optic Nerve Injuries - metabolism</subject><subject>Optic Nerve Injuries - pathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Retinal Cell Biology</subject><subject>Retinal Ganglion Cells - drug effects</subject><subject>Retinal Ganglion Cells - metabolism</subject><subject>Retinal Ganglion Cells - pathology</subject><issn>1552-5783</issn><issn>0146-0404</issn><issn>1552-5783</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1PAjEUbIxGED16NT162bWfu9uTIQTBRCUaPTe1vJU1yxbbLsZ_7xKQ4OnNy0zmTd4gdElJSmmW31RuHdJMppSnND9CfSolS2Re8OMD3ENnIXwSwihl5BT1uJJEEFH00fPEu--4wFPnl64B_AStdyvvIthYrQGPy7JDAQ_LCB6bBs9WsbKdzHfkyLdhgasGxwXgR1MDfjHxHJ2Upg5wsZsD9HY3fh1Nk4fZ5H40fEgs4zImRolSsrlgsgClTJFbQZSiyqrSypwrw2zGoFt50aUm1jBFMiFzUwhgqsj4AN1ufVft-xLmFproTa1Xvloa_6OdqfR_pqkW-sOtNaVSKMXyzuF65-DdVwsh6mUVLNS1acC1QXPKRKaI4rKTJlup9S4ED-X-DiV604Pe9KAzqSnXdGN9dRhur_57PP8F5RKD0w</recordid><startdate>20241106</startdate><enddate>20241106</enddate><creator>Epardo, David</creator><creator>Balderas-Márquez, Jerusa E</creator><creator>Rodríguez-Arzate, Cynthia A</creator><creator>Thébault, Stéphanie C</creator><creator>Carranza, Martha</creator><creator>Luna, Maricela</creator><creator>Ávila-Mendoza, José</creator><creator>Calderón-Vallejo, Denisse</creator><creator>Quintanar, J Luis</creator><creator>Arámburo, Carlos</creator><creator>Martínez-Moreno, Carlos G</creator><general>The Association for Research in Vision and Ophthalmology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20241106</creationdate><title>Growth Hormone Neuroprotective Effects After an Optic Nerve Crush in the Male Rat</title><author>Epardo, David ; 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visual science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Epardo, David</au><au>Balderas-Márquez, Jerusa E</au><au>Rodríguez-Arzate, Cynthia A</au><au>Thébault, Stéphanie C</au><au>Carranza, Martha</au><au>Luna, Maricela</au><au>Ávila-Mendoza, José</au><au>Calderón-Vallejo, Denisse</au><au>Quintanar, J Luis</au><au>Arámburo, Carlos</au><au>Martínez-Moreno, Carlos G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Growth Hormone Neuroprotective Effects After an Optic Nerve Crush in the Male Rat</atitle><jtitle>Investigative ophthalmology &amp; visual science</jtitle><addtitle>Invest Ophthalmol Vis Sci</addtitle><date>2024-11-06</date><risdate>2024</risdate><volume>65</volume><issue>13</issue><spage>17</spage><pages>17-</pages><issn>1552-5783</issn><issn>0146-0404</issn><eissn>1552-5783</eissn><abstract>Growth hormone (GH) has neuroprotective effects that have not been evaluated in the mammalian visual system. This study tested the hypothesis that GH administration can promote retinal neuroprotection in an optic nerve crush (ONC) model in male rats. The ON was compressed for 10 seconds, and bovine GH was injected concomitantly to injury for 14 days (0.5 µg/g every 12 hours). At 24 hours and 14 days after ONC, we evaluated the effects of GH upon several markers by quantitative PCR (qPCR), Western blot, and immunohistochemistry; the ON integrity was assessed using CTB Alexa 488 anterograde tracer, and retinal function was tested by full-field electroretinogram. GH partially prevented the ONC-induced death of retinal ganglion cells (RGCs), as well as the increase in gliosis marker GFAP at 14 days. Most of the ONC-induced changes in mRNA retinal levels of several neurotrophic, survival, synaptogenic, gliosis, and excitotoxicity markers were prevented by GH, both at 24 hours and 14 days, and treatment also stimulated the expression of antiapoptotic proteins Bcl-2 and Bcl-xL at 24 hours. Additionally, GH partially maintained the ON integrity and active anterograde transport, as well as retinal function by avoiding the reduced amplitude and slowing of the A- and B-waves and oscillatory potentials associated with the ONC at 14 days. GH has neuroprotective effects in the ONC model in male rats, it promoted RGC survival, gliosis reduction, and axonal transport increase, likely through the regulation of genes involved in neuroprotection, survival, and synaptogenesis. Furthermore, GH prevented functional impairment, indicating its potential as a therapeutic option for retinal neurodegenerative diseases.</abstract><cop>United States</cop><pub>The Association for Research in Vision and Ophthalmology</pub><pmid>39504048</pmid><doi>10.1167/iovs.65.13.17</doi><oa>free_for_read</oa></addata></record>
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subjects Animals
Blotting, Western
Disease Models, Animal
Electroretinography
Growth Hormone - pharmacology
Immunohistochemistry
Male
Nerve Crush
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Optic Nerve Injuries - drug therapy
Optic Nerve Injuries - metabolism
Optic Nerve Injuries - pathology
Rats
Rats, Sprague-Dawley
Real-Time Polymerase Chain Reaction
Retinal Cell Biology
Retinal Ganglion Cells - drug effects
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - pathology
title Growth Hormone Neuroprotective Effects After an Optic Nerve Crush in the Male Rat
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