Triiodo-L-thyronine (T3) downregulates Npr1 gene (coding for natriuretic peptide receptor-A) transcription in H9c2 cells: involvement of β-AR-ROS signaling
Introduction Natriuretic peptide receptor-A (NPR-A) signaling system is considered as an intrinsic productive mechanism of the heart that opposes abnormal cardiac remodeling and hypertrophic growth. NPR-A is coded by Npr1 gene, and its expression is downregulated in the hypertrophied heart. Aim We s...
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| Veröffentlicht in: | Endocrine 2024-09, Vol.85 (3), p.1075-1090 |
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| description | Introduction
Natriuretic peptide receptor-A (NPR-A) signaling system is considered as an intrinsic productive mechanism of the heart that opposes abnormal cardiac remodeling and hypertrophic growth. NPR-A is coded by
Npr1
gene, and its expression is downregulated in the hypertrophied heart.
Aim
We sought to examine the levels of
Npr1
gene transcription in triiodo-L-thyronine (T3) treated hypertrophied cardiomyocyte (H9c2) cells, in vitro, and also the involvement of β-adrenergic receptor (β-AR) - Reactive oxygen species (ROS) signaling system in the down-regulation of
Npr1
transcription also studied.
Main methods
Anti-hypertrophic
Npr1
gene transcription was monitored in control and T3-treated (dose and time dependent) H9c2 cells, using a real time PCR method. Further, cell size, intracellular cGMP, ROS, hypertrophy markers (
ANP, BNP, α-sk, α-MHC
and
β-MHC
), β-AR, and protein kinase cGMP-dependent 1 (
PKG-I
) genes expression were also determined. The intracellular cGMP and ROS levels were determined by ELISA and DCF dye method, respectively. In addition, to neutralize T3 mediated ROS generation, H9c2 cells were treated with T3 in the presence and absence of antioxidants [curcumin (CU) or N-acetyl-L-cysteine (NAC)].
Results
A dose dependent (10 pM, 100 pM, 1 nM and 10 nM) and time dependent (12 h, 24 h and 48 h) down-regulation of
Npr1
gene transcription (20, 39, 60, and 74% respectively; 18, 55, and 85%, respectively) were observed in T3-treated H9c2 cells as compared with control cells. Immunofluorescence analysis also revealed that a marked down regulation of NPR- A protein in T3-treated cells as compared with control cells. Further, a parallel downregulation of cGMP and PKG-I (2.4 fold) were noticed in the T3-treated cells. In contrast, a time dependent increased expression of β-AR (60, 72, and 80% respectively) and ROS (26, 48, and 74%, respectively) levels were noticed in T3-treated H9c2 cells as compared with control cells. Interestingly, antioxidants, CU or NAC co-treated T3 cells displayed a significant reduction in ROS (69 and 81%, respectively) generation and to increased
Npr1
gene transcription (81 and 88%, respectively) as compared with T3 alone treated cells.
Conclusion
Our result suggest that down regulation of
Npr1
gene transcription is critically involved in T3- induced hypertrophic growth in H9c2 cells, and identifies the cross-talk between T3-β-AR-ROS and NPR-A signaling. |
| doi_str_mv | 10.1007/s12020-024-03849-6 |
| format | Article |
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Natriuretic peptide receptor-A (NPR-A) signaling system is considered as an intrinsic productive mechanism of the heart that opposes abnormal cardiac remodeling and hypertrophic growth. NPR-A is coded by
Npr1
gene, and its expression is downregulated in the hypertrophied heart.
Aim
We sought to examine the levels of
Npr1
gene transcription in triiodo-L-thyronine (T3) treated hypertrophied cardiomyocyte (H9c2) cells, in vitro, and also the involvement of β-adrenergic receptor (β-AR) - Reactive oxygen species (ROS) signaling system in the down-regulation of
Npr1
transcription also studied.
Main methods
Anti-hypertrophic
Npr1
gene transcription was monitored in control and T3-treated (dose and time dependent) H9c2 cells, using a real time PCR method. Further, cell size, intracellular cGMP, ROS, hypertrophy markers (
ANP, BNP, α-sk, α-MHC
and
β-MHC
), β-AR, and protein kinase cGMP-dependent 1 (
PKG-I
) genes expression were also determined. The intracellular cGMP and ROS levels were determined by ELISA and DCF dye method, respectively. In addition, to neutralize T3 mediated ROS generation, H9c2 cells were treated with T3 in the presence and absence of antioxidants [curcumin (CU) or N-acetyl-L-cysteine (NAC)].
Results
A dose dependent (10 pM, 100 pM, 1 nM and 10 nM) and time dependent (12 h, 24 h and 48 h) down-regulation of
Npr1
gene transcription (20, 39, 60, and 74% respectively; 18, 55, and 85%, respectively) were observed in T3-treated H9c2 cells as compared with control cells. Immunofluorescence analysis also revealed that a marked down regulation of NPR- A protein in T3-treated cells as compared with control cells. Further, a parallel downregulation of cGMP and PKG-I (2.4 fold) were noticed in the T3-treated cells. In contrast, a time dependent increased expression of β-AR (60, 72, and 80% respectively) and ROS (26, 48, and 74%, respectively) levels were noticed in T3-treated H9c2 cells as compared with control cells. Interestingly, antioxidants, CU or NAC co-treated T3 cells displayed a significant reduction in ROS (69 and 81%, respectively) generation and to increased
Npr1
gene transcription (81 and 88%, respectively) as compared with T3 alone treated cells.
Conclusion
Our result suggest that down regulation of
Npr1
gene transcription is critically involved in T3- induced hypertrophic growth in H9c2 cells, and identifies the cross-talk between T3-β-AR-ROS and NPR-A signaling.</description><identifier>ISSN: 1559-0100</identifier><identifier>ISSN: 1355-008X</identifier><identifier>EISSN: 1559-0100</identifier><identifier>DOI: 10.1007/s12020-024-03849-6</identifier><identifier>PMID: 38713329</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acetylcysteine ; Adrenergic receptors ; Animals ; Antioxidants ; Brief Report ; Cardiomyocytes ; Cell Line ; Cell size ; Curcumin ; Cyclic GMP ; Cyclic GMP - metabolism ; Diabetes ; Down-regulation ; Down-Regulation - drug effects ; Endocrinology ; Enzyme-linked immunosorbent assay ; Gene regulation ; Humanities and Social Sciences ; Hypertrophy ; Immunofluorescence ; Internal Medicine ; Intracellular ; Kinases ; Major histocompatibility complex ; Medicine ; Medicine & Public Health ; multidisciplinary ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; NPR1 gene ; Peptides ; Protein folding ; Protein kinase C ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Receptors, Atrial Natriuretic Factor - genetics ; Receptors, Atrial Natriuretic Factor - metabolism ; Science ; Signal Transduction - drug effects ; Transcription ; Transcription, Genetic - drug effects ; Triiodothyronine - pharmacology</subject><ispartof>Endocrine, 2024-09, Vol.85 (3), p.1075-1090</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c326t-e85550159354e43ab3a1cfce15c432270b3cbda846a595d17d68bb6e23d7bd343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12020-024-03849-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12020-024-03849-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38713329$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nagaraj, Gopinath</creatorcontrib><creatorcontrib>Vellaichamy, Elangovan</creatorcontrib><title>Triiodo-L-thyronine (T3) downregulates Npr1 gene (coding for natriuretic peptide receptor-A) transcription in H9c2 cells: involvement of β-AR-ROS signaling</title><title>Endocrine</title><addtitle>Endocrine</addtitle><addtitle>Endocrine</addtitle><description>Introduction
Natriuretic peptide receptor-A (NPR-A) signaling system is considered as an intrinsic productive mechanism of the heart that opposes abnormal cardiac remodeling and hypertrophic growth. NPR-A is coded by
Npr1
gene, and its expression is downregulated in the hypertrophied heart.
Aim
We sought to examine the levels of
Npr1
gene transcription in triiodo-L-thyronine (T3) treated hypertrophied cardiomyocyte (H9c2) cells, in vitro, and also the involvement of β-adrenergic receptor (β-AR) - Reactive oxygen species (ROS) signaling system in the down-regulation of
Npr1
transcription also studied.
Main methods
Anti-hypertrophic
Npr1
gene transcription was monitored in control and T3-treated (dose and time dependent) H9c2 cells, using a real time PCR method. Further, cell size, intracellular cGMP, ROS, hypertrophy markers (
ANP, BNP, α-sk, α-MHC
and
β-MHC
), β-AR, and protein kinase cGMP-dependent 1 (
PKG-I
) genes expression were also determined. The intracellular cGMP and ROS levels were determined by ELISA and DCF dye method, respectively. In addition, to neutralize T3 mediated ROS generation, H9c2 cells were treated with T3 in the presence and absence of antioxidants [curcumin (CU) or N-acetyl-L-cysteine (NAC)].
Results
A dose dependent (10 pM, 100 pM, 1 nM and 10 nM) and time dependent (12 h, 24 h and 48 h) down-regulation of
Npr1
gene transcription (20, 39, 60, and 74% respectively; 18, 55, and 85%, respectively) were observed in T3-treated H9c2 cells as compared with control cells. Immunofluorescence analysis also revealed that a marked down regulation of NPR- A protein in T3-treated cells as compared with control cells. Further, a parallel downregulation of cGMP and PKG-I (2.4 fold) were noticed in the T3-treated cells. In contrast, a time dependent increased expression of β-AR (60, 72, and 80% respectively) and ROS (26, 48, and 74%, respectively) levels were noticed in T3-treated H9c2 cells as compared with control cells. Interestingly, antioxidants, CU or NAC co-treated T3 cells displayed a significant reduction in ROS (69 and 81%, respectively) generation and to increased
Npr1
gene transcription (81 and 88%, respectively) as compared with T3 alone treated cells.
Conclusion
Our result suggest that down regulation of
Npr1
gene transcription is critically involved in T3- induced hypertrophic growth in H9c2 cells, and identifies the cross-talk between T3-β-AR-ROS and NPR-A signaling.</description><subject>Acetylcysteine</subject><subject>Adrenergic receptors</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Brief Report</subject><subject>Cardiomyocytes</subject><subject>Cell Line</subject><subject>Cell size</subject><subject>Curcumin</subject><subject>Cyclic GMP</subject><subject>Cyclic GMP - metabolism</subject><subject>Diabetes</subject><subject>Down-regulation</subject><subject>Down-Regulation - drug effects</subject><subject>Endocrinology</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gene regulation</subject><subject>Humanities and Social Sciences</subject><subject>Hypertrophy</subject><subject>Immunofluorescence</subject><subject>Internal Medicine</subject><subject>Intracellular</subject><subject>Kinases</subject><subject>Major histocompatibility complex</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>multidisciplinary</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>NPR1 gene</subject><subject>Peptides</subject><subject>Protein folding</subject><subject>Protein kinase C</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, Atrial Natriuretic Factor - genetics</subject><subject>Receptors, Atrial Natriuretic Factor - metabolism</subject><subject>Science</subject><subject>Signal Transduction - drug effects</subject><subject>Transcription</subject><subject>Transcription, Genetic - drug effects</subject><subject>Triiodothyronine - pharmacology</subject><issn>1559-0100</issn><issn>1355-008X</issn><issn>1559-0100</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1TAQhS0EoqXwAiyQJTbtwuCfOInZXVVAka6oVC5ry7EnwVWuHeykqO_CU_AgPBMOt_yIBSuPdb45M5qD0FNGXzBKm5eZccopobwiVLSVIvU9dMykVIQW_f5f9RF6lPM1pZzzunmIjkTbMCG4OkZfd8n76CLZkvnTbYrBB8CnO3GGXfwSEgzLaGbI-P2UGB5gFW10Pgy4jwkHMye_JJi9xRNMs3eAE9hSxUQ2Z3hOJmSbfFFiwD7gC2U5tjCO-VX53sTxBvYQZhx7_P0b2VyRq8sPOPshmLHMeIwe9GbM8OTuPUEf37zenV-Q7eXbd-ebLbGC1zOBVkpJmVRCVlAJ0wnDbG-BSVsJzhvaCds501a1kUo61ri67boauHBN50QlTtDpwXdK8fMCedZ7n9ctTYC4ZC2oZEqocrCCPv8HvY5LKuuulGK8EZLVheIHyqaYc4JeT8nvTbrVjOo1O33ITpfs9M_s9Nr07M566fbgfrf8CqsA4gDkIoUB0p_Z_7H9AfaRpQ0</recordid><startdate>20240901</startdate><enddate>20240901</enddate><creator>Nagaraj, Gopinath</creator><creator>Vellaichamy, Elangovan</creator><general>Springer US</general><general>Springer Nature B.V</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></search><sort><creationdate>20240901</creationdate><title>Triiodo-L-thyronine (T3) downregulates Npr1 gene (coding for natriuretic peptide receptor-A) transcription in H9c2 cells: involvement of β-AR-ROS signaling</title><author>Nagaraj, Gopinath ; Vellaichamy, Elangovan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-e85550159354e43ab3a1cfce15c432270b3cbda846a595d17d68bb6e23d7bd343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acetylcysteine</topic><topic>Adrenergic receptors</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Brief Report</topic><topic>Cardiomyocytes</topic><topic>Cell Line</topic><topic>Cell size</topic><topic>Curcumin</topic><topic>Cyclic GMP</topic><topic>Cyclic GMP - metabolism</topic><topic>Diabetes</topic><topic>Down-regulation</topic><topic>Down-Regulation - drug effects</topic><topic>Endocrinology</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gene regulation</topic><topic>Humanities and Social Sciences</topic><topic>Hypertrophy</topic><topic>Immunofluorescence</topic><topic>Internal Medicine</topic><topic>Intracellular</topic><topic>Kinases</topic><topic>Major histocompatibility complex</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>multidisciplinary</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>NPR1 gene</topic><topic>Peptides</topic><topic>Protein folding</topic><topic>Protein kinase C</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Receptors, Atrial Natriuretic Factor - genetics</topic><topic>Receptors, Atrial Natriuretic Factor - metabolism</topic><topic>Science</topic><topic>Signal Transduction - drug effects</topic><topic>Transcription</topic><topic>Transcription, Genetic - drug effects</topic><topic>Triiodothyronine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nagaraj, Gopinath</creatorcontrib><creatorcontrib>Vellaichamy, Elangovan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nagaraj, Gopinath</au><au>Vellaichamy, Elangovan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Triiodo-L-thyronine (T3) downregulates Npr1 gene (coding for natriuretic peptide receptor-A) transcription in H9c2 cells: involvement of β-AR-ROS signaling</atitle><jtitle>Endocrine</jtitle><stitle>Endocrine</stitle><addtitle>Endocrine</addtitle><date>2024-09-01</date><risdate>2024</risdate><volume>85</volume><issue>3</issue><spage>1075</spage><epage>1090</epage><pages>1075-1090</pages><issn>1559-0100</issn><issn>1355-008X</issn><eissn>1559-0100</eissn><abstract>Introduction
Natriuretic peptide receptor-A (NPR-A) signaling system is considered as an intrinsic productive mechanism of the heart that opposes abnormal cardiac remodeling and hypertrophic growth. NPR-A is coded by
Npr1
gene, and its expression is downregulated in the hypertrophied heart.
Aim
We sought to examine the levels of
Npr1
gene transcription in triiodo-L-thyronine (T3) treated hypertrophied cardiomyocyte (H9c2) cells, in vitro, and also the involvement of β-adrenergic receptor (β-AR) - Reactive oxygen species (ROS) signaling system in the down-regulation of
Npr1
transcription also studied.
Main methods
Anti-hypertrophic
Npr1
gene transcription was monitored in control and T3-treated (dose and time dependent) H9c2 cells, using a real time PCR method. Further, cell size, intracellular cGMP, ROS, hypertrophy markers (
ANP, BNP, α-sk, α-MHC
and
β-MHC
), β-AR, and protein kinase cGMP-dependent 1 (
PKG-I
) genes expression were also determined. The intracellular cGMP and ROS levels were determined by ELISA and DCF dye method, respectively. In addition, to neutralize T3 mediated ROS generation, H9c2 cells were treated with T3 in the presence and absence of antioxidants [curcumin (CU) or N-acetyl-L-cysteine (NAC)].
Results
A dose dependent (10 pM, 100 pM, 1 nM and 10 nM) and time dependent (12 h, 24 h and 48 h) down-regulation of
Npr1
gene transcription (20, 39, 60, and 74% respectively; 18, 55, and 85%, respectively) were observed in T3-treated H9c2 cells as compared with control cells. Immunofluorescence analysis also revealed that a marked down regulation of NPR- A protein in T3-treated cells as compared with control cells. Further, a parallel downregulation of cGMP and PKG-I (2.4 fold) were noticed in the T3-treated cells. In contrast, a time dependent increased expression of β-AR (60, 72, and 80% respectively) and ROS (26, 48, and 74%, respectively) levels were noticed in T3-treated H9c2 cells as compared with control cells. Interestingly, antioxidants, CU or NAC co-treated T3 cells displayed a significant reduction in ROS (69 and 81%, respectively) generation and to increased
Npr1
gene transcription (81 and 88%, respectively) as compared with T3 alone treated cells.
Conclusion
Our result suggest that down regulation of
Npr1
gene transcription is critically involved in T3- induced hypertrophic growth in H9c2 cells, and identifies the cross-talk between T3-β-AR-ROS and NPR-A signaling.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>38713329</pmid><doi>10.1007/s12020-024-03849-6</doi><tpages>16</tpages></addata></record> |
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| subjects | Acetylcysteine Adrenergic receptors Animals Antioxidants Brief Report Cardiomyocytes Cell Line Cell size Curcumin Cyclic GMP Cyclic GMP - metabolism Diabetes Down-regulation Down-Regulation - drug effects Endocrinology Enzyme-linked immunosorbent assay Gene regulation Humanities and Social Sciences Hypertrophy Immunofluorescence Internal Medicine Intracellular Kinases Major histocompatibility complex Medicine Medicine & Public Health multidisciplinary Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism NPR1 gene Peptides Protein folding Protein kinase C Rats Reactive oxygen species Reactive Oxygen Species - metabolism Receptors, Atrial Natriuretic Factor - genetics Receptors, Atrial Natriuretic Factor - metabolism Science Signal Transduction - drug effects Transcription Transcription, Genetic - drug effects Triiodothyronine - pharmacology |
| title | Triiodo-L-thyronine (T3) downregulates Npr1 gene (coding for natriuretic peptide receptor-A) transcription in H9c2 cells: involvement of β-AR-ROS signaling |
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