Enhanced Expression of Human Endogenous Retroviruses, TRIM28 and SETDB1 in Autism Spectrum Disorder

Human endogenous retroviruses (HERVs) are relics of ancestral infections and represent 8% of the human genome. They are no longer infectious, but their activation has been associated with several disorders, including neuropsychiatric conditions. Enhanced expression of HERV-K and HERV-H envelope gene...

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Veröffentlicht in:	International journal of molecular sciences Jg. 23; H. 11; S. 5964
Hauptverfasser:	Tovo, Pier-Angelo, Davico, Chiara, Marcotulli, Daniele, Vitiello, Benedetto, Daprà, Valentina, Calvi, Cristina, Montanari, Paola, Carpino, Andrea, Galliano, Ilaria, Bergallo, Massimiliano
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Switzerland MDPI AG 25.05.2022 MDPI
Schlagworte:	Age Autism Spectrum Disorder - genetics Autistic children Brain Child Cytokines DNA methylation Endogenous Retroviruses - genetics Endogenous Retroviruses - metabolism Epigenetics Families & family life Gene Products, env - metabolism Genes Genome, Human Genomes Histone-Lysine N-Methyltransferase - genetics Histone-Lysine N-Methyltransferase - metabolism Humans Immune system Male Multiple Sclerosis - pathology Proteins Transcription Factors - genetics Tripartite Motif-Containing Protein 28 - genetics Tripartite Motif-Containing Protein 28 - metabolism SETDB1 TRIM28 autism spectrum disorder human endogenous retroviruses children
ISSN:	1422-0067, 1661-6596, 1422-0067
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Abstract	Human endogenous retroviruses (HERVs) are relics of ancestral infections and represent 8% of the human genome. They are no longer infectious, but their activation has been associated with several disorders, including neuropsychiatric conditions. Enhanced expression of HERV-K and HERV-H envelope genes has been found in the blood of autism spectrum disorder (ASD) patients, but no information is available on syncytin 1 (SYN1), SYN2, and multiple sclerosis-associated retrovirus (MSRV), which are thought to be implicated in brain development and immune responses. HERV activation is regulated by TRIM28 and SETDB1, which are part of the epigenetic mechanisms that organize the chromatin architecture in response to external stimuli and are involved in neural cell differentiation and brain inflammation. We assessed, through a PCR realtime Taqman amplification assay, the transcription levels of pol genes of HERV-H, -K, and -W families, of env genes of SYN1, SYN2, and MSRV, as well as of TRIM28 and SETDB1 in the blood of 33 ASD children (28 males, median 3.8 years, 25–75% interquartile range 3.0–6.0 y) and healthy controls (HC). Significantly higher expressions of TRIM28 and SETDB1, as well as of all the HERV genes tested, except for HERV-W-pol, were found in ASD, as compared with HC. Positive correlations were observed between the mRNA levels of TRIM28 or SETDB1 and every HERV gene in ASD patients, but not in HC. Overexpression of TRIM28/SETDB1 and several HERVs in children with ASD and the positive correlations between their transcriptional levels suggest that these may be main players in pathogenetic mechanisms leading to ASD.
AbstractList	Human endogenous retroviruses (HERVs) are relics of ancestral infections and represent 8% of the human genome. They are no longer infectious, but their activation has been associated with several disorders, including neuropsychiatric conditions. Enhanced expression of HERV-K and HERV-H envelope genes has been found in the blood of autism spectrum disorder (ASD) patients, but no information is available on syncytin 1 (SYN1), SYN2, and multiple sclerosis-associated retrovirus (MSRV), which are thought to be implicated in brain development and immune responses. HERV activation is regulated by TRIM28 and SETDB1, which are part of the epigenetic mechanisms that organize the chromatin architecture in response to external stimuli and are involved in neural cell differentiation and brain inflammation. We assessed, through a PCR realtime Taqman amplification assay, the transcription levels of genes of HERV-H, -K, and -W families, of genes of SYN1, SYN2, and MSRV, as well as of TRIM28 and SETDB1 in the blood of 33 ASD children (28 males, median 3.8 years, 25-75% interquartile range 3.0-6.0 y) and healthy controls (HC). Significantly higher expressions of TRIM28 and SETDB1, as well as of all the HERV genes tested, except for HERV-W- , were found in ASD, as compared with HC. Positive correlations were observed between the mRNA levels of TRIM28 or SETDB1 and every HERV gene in ASD patients, but not in HC. Overexpression of TRIM28/SETDB1 and several HERVs in children with ASD and the positive correlations between their transcriptional levels suggest that these may be main players in pathogenetic mechanisms leading to ASD. Human endogenous retroviruses (HERVs) are relics of ancestral infections and represent 8% of the human genome. They are no longer infectious, but their activation has been associated with several disorders, including neuropsychiatric conditions. Enhanced expression of HERV-K and HERV-H envelope genes has been found in the blood of autism spectrum disorder (ASD) patients, but no information is available on syncytin 1 (SYN1), SYN2, and multiple sclerosis-associated retrovirus (MSRV), which are thought to be implicated in brain development and immune responses. HERV activation is regulated by TRIM28 and SETDB1, which are part of the epigenetic mechanisms that organize the chromatin architecture in response to external stimuli and are involved in neural cell differentiation and brain inflammation. We assessed, through a PCR realtime Taqman amplification assay, the transcription levels of pol genes of HERV-H, -K, and -W families, of env genes of SYN1, SYN2, and MSRV, as well as of TRIM28 and SETDB1 in the blood of 33 ASD children (28 males, median 3.8 years, 25–75% interquartile range 3.0–6.0 y) and healthy controls (HC). Significantly higher expressions of TRIM28 and SETDB1, as well as of all the HERV genes tested, except for HERV-W-pol, were found in ASD, as compared with HC. Positive correlations were observed between the mRNA levels of TRIM28 or SETDB1 and every HERV gene in ASD patients, but not in HC. Overexpression of TRIM28/SETDB1 and several HERVs in children with ASD and the positive correlations between their transcriptional levels suggest that these may be main players in pathogenetic mechanisms leading to ASD. Human endogenous retroviruses (HERVs) are relics of ancestral infections and represent 8% of the human genome. They are no longer infectious, but their activation has been associated with several disorders, including neuropsychiatric conditions. Enhanced expression of HERV-K and HERV-H envelope genes has been found in the blood of autism spectrum disorder (ASD) patients, but no information is available on syncytin 1 (SYN1), SYN2, and multiple sclerosis-associated retrovirus (MSRV), which are thought to be implicated in brain development and immune responses. HERV activation is regulated by TRIM28 and SETDB1, which are part of the epigenetic mechanisms that organize the chromatin architecture in response to external stimuli and are involved in neural cell differentiation and brain inflammation. We assessed, through a PCR realtime Taqman amplification assay, the transcription levels of pol genes of HERV-H, -K, and -W families, of env genes of SYN1, SYN2, and MSRV, as well as of TRIM28 and SETDB1 in the blood of 33 ASD children (28 males, median 3.8 years, 25-75% interquartile range 3.0-6.0 y) and healthy controls (HC). Significantly higher expressions of TRIM28 and SETDB1, as well as of all the HERV genes tested, except for HERV-W-pol, were found in ASD, as compared with HC. Positive correlations were observed between the mRNA levels of TRIM28 or SETDB1 and every HERV gene in ASD patients, but not in HC. Overexpression of TRIM28/SETDB1 and several HERVs in children with ASD and the positive correlations between their transcriptional levels suggest that these may be main players in pathogenetic mechanisms leading to ASD.Human endogenous retroviruses (HERVs) are relics of ancestral infections and represent 8% of the human genome. They are no longer infectious, but their activation has been associated with several disorders, including neuropsychiatric conditions. Enhanced expression of HERV-K and HERV-H envelope genes has been found in the blood of autism spectrum disorder (ASD) patients, but no information is available on syncytin 1 (SYN1), SYN2, and multiple sclerosis-associated retrovirus (MSRV), which are thought to be implicated in brain development and immune responses. HERV activation is regulated by TRIM28 and SETDB1, which are part of the epigenetic mechanisms that organize the chromatin architecture in response to external stimuli and are involved in neural cell differentiation and brain inflammation. We assessed, through a PCR realtime Taqman amplification assay, the transcription levels of pol genes of HERV-H, -K, and -W families, of env genes of SYN1, SYN2, and MSRV, as well as of TRIM28 and SETDB1 in the blood of 33 ASD children (28 males, median 3.8 years, 25-75% interquartile range 3.0-6.0 y) and healthy controls (HC). Significantly higher expressions of TRIM28 and SETDB1, as well as of all the HERV genes tested, except for HERV-W-pol, were found in ASD, as compared with HC. Positive correlations were observed between the mRNA levels of TRIM28 or SETDB1 and every HERV gene in ASD patients, but not in HC. Overexpression of TRIM28/SETDB1 and several HERVs in children with ASD and the positive correlations between their transcriptional levels suggest that these may be main players in pathogenetic mechanisms leading to ASD.
Author	Davico, Chiara Vitiello, Benedetto Calvi, Cristina Montanari, Paola Daprà, Valentina Galliano, Ilaria Carpino, Andrea Bergallo, Massimiliano Marcotulli, Daniele Tovo, Pier-Angelo
AuthorAffiliation	3 Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94, 10126 Turin, Italy 4 Postgraduate School of Pediatrics, University of Turin, Piazza Polonia 94, 10126 Turin, Italy; andrea.carpino@unito.it 2 Division of Child and Adolescent Neuropsychiatry, Department of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94, 10126 Turin, Italy; chiara.davico@unito.it (C.D.); daniele.marcotulli@unito.it (D.M.); benedetto.vitiello@unito.it (B.V.) 1 Department of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94, 10126 Turin, Italy; valentina.dapr@yahoo.it (V.D.); cristina.calvi@unito.it (C.C.); paola.montanari@unito.it (P.M.); ilaria.galliano@unito.it (I.G.)
AuthorAffiliation_xml	– name: 2 Division of Child and Adolescent Neuropsychiatry, Department of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94, 10126 Turin, Italy; chiara.davico@unito.it (C.D.); daniele.marcotulli@unito.it (D.M.); benedetto.vitiello@unito.it (B.V.) – name: 3 Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94, 10126 Turin, Italy – name: 4 Postgraduate School of Pediatrics, University of Turin, Piazza Polonia 94, 10126 Turin, Italy; andrea.carpino@unito.it – name: 1 Department of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94, 10126 Turin, Italy; valentina.dapr@yahoo.it (V.D.); cristina.calvi@unito.it (C.C.); paola.montanari@unito.it (P.M.); ilaria.galliano@unito.it (I.G.)
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/35682642$$D View this record in MEDLINE/PubMed
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CitedBy_id	crossref_primary_10_3390_biomedicines12081811 crossref_primary_10_1038_s41380_025_02955_9 crossref_primary_10_3390_microorganisms13010009 crossref_primary_10_1111_imm_13619 crossref_primary_10_1186_s40035_025_00471_y crossref_primary_10_3390_v15030710 crossref_primary_10_1016_j_bbi_2022_10_006 crossref_primary_10_1007_s12035_024_04133_4 crossref_primary_10_1038_s41380_023_01999_z crossref_primary_10_1038_s41598_025_91541_8
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Copyright	2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2022 by the authors. 2022
Copyright_xml	– notice: 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: 2022 by the authors. 2022
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Snippet	Human endogenous retroviruses (HERVs) are relics of ancestral infections and represent 8% of the human genome. They are no longer infectious, but their...
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SubjectTerms	Age Autism Spectrum Disorder - genetics Autistic children Brain Child Cytokines DNA methylation Endogenous Retroviruses - genetics Endogenous Retroviruses - metabolism Epigenetics Families & family life Gene Products, env - metabolism Genes Genome, Human Genomes Histone-Lysine N-Methyltransferase - genetics Histone-Lysine N-Methyltransferase - metabolism Humans Immune system Male Multiple Sclerosis - pathology Proteins Transcription Factors - genetics Tripartite Motif-Containing Protein 28 - genetics Tripartite Motif-Containing Protein 28 - metabolism
Title	Enhanced Expression of Human Endogenous Retroviruses, TRIM28 and SETDB1 in Autism Spectrum Disorder
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