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Article ; Online: Proximity Extension Assay (PEA) Platform to Detect Vitreous Biomarkers of Diabetic Retinopathy.

Lamy, Ricardo / Ma'ayeh, Showgy / Chlamydas, Sarantis / Stewart, Jay M

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2678, Page(s) 135–145

Abstract: Diabetic retinopathy (DR) is one of the leading causes of blindness, affecting more than 100 million people worldwide. Currently, DR prognosis and management are based mainly on biomarkers identified by direct retinal fundus observation or by imaging ... ...

Abstract	Diabetic retinopathy (DR) is one of the leading causes of blindness, affecting more than 100 million people worldwide. Currently, DR prognosis and management are based mainly on biomarkers identified by direct retinal fundus observation or by imaging devices. The use of molecular biology to discover biomarkers of DR has great potential to impact the standard of care, and the vitreous humor can serve as an indirect source for those molecular biomarkers because it is rich in proteins secreted by the retina. Proximity extension assay (PEA) is a technology that combines antibody-based immunoassays with DNA-coupled methodology to obtain information on the abundance of multiple proteins while using minimal sample volume, with high specificity and sensitivity. Matched antibodies labelled with a complementary sequence of oligonucleotides are used to simultaneously bind a target protein in solution, and when in proximity, the complementary sequences on each antibody hybridize, serving as template for DNA polymerase-dependent extension and the generation of a unique double-stranded DNA "barcode." PEA works well with vitreous matrix and has great potential to support the identification of novel predictive and prognostic biomarkers of DR.
MeSH term(s)	Humans ; Diabetic Retinopathy/diagnosis ; Diabetic Retinopathy/metabolism ; Pisum sativum/metabolism ; Retina/metabolism ; Vitreous Body/metabolism ; Biomarkers/metabolism ; Diabetes Mellitus/metabolism
Chemical Substances	Biomarkers
Language	English
Publishing date	2023-06-16
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3255-0_9
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Article ; Online: Epigenetic mechanisms regulate sex-specific bias in disease manifestations.

Chlamydas, Sarantis / Markouli, Mariam / Strepkos, Dimitrios / Piperi, Christina

Journal of molecular medicine (Berlin, Germany)

2022 Volume 100, Issue 8, Page(s) 1111–1123

Abstract: Sex presents a vital determinant of a person's physiology, anatomy, and development. Recent clinical studies indicate that sex is also involved in the differential manifestation of various diseases, affecting both clinical outcome as well as response to ... ...

Abstract	Sex presents a vital determinant of a person's physiology, anatomy, and development. Recent clinical studies indicate that sex is also involved in the differential manifestation of various diseases, affecting both clinical outcome as well as response to therapy. Genetic and epigenetic changes are implicated in sex bias and regulate disease onset, including the inactivation of the X chromosome as well as sex chromosome aneuploidy. The differential expression of X-linked genes, along with the presence of sex-specific hormones, exhibits a significant impact on immune system function. Several studies have revealed differences between the two sexes in response to infections, including respiratory diseases and COVID-19 infection, autoimmune disorders, liver fibrosis, neuropsychiatric diseases, and cancer susceptibility, which can be explained by sex-biased immune responses. In the present review, we explore the input of genetic and epigenetic interplay in the sex bias underlying disease manifestation and discuss their effects along with sex hormones on disease development and progression, aiming to reveal potential new therapeutic targets. KEY MESSAGES: Sex is involved in the differential manifestation of various diseases. Epigenetic modifications influence X-linked gene expression, affecting immune response to infections, including COVID-19. Epigenetic mechanisms are responsible for the sex bias observed in several respiratory and autoimmune disorders, liver fibrosis, neuropsychiatric diseases, and cancer.
MeSH term(s)	Autoimmune Diseases ; COVID-19/genetics ; Epigenesis, Genetic ; Female ; Gonadal Steroid Hormones ; Humans ; Liver Cirrhosis ; Male ; Sex Characteristics ; Sexism
Chemical Substances	Gonadal Steroid Hormones
Language	English
Publishing date	2022-06-29
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-022-02227-x
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Article: Structure, Activity and Function of the MLL2 (KMT2B) Protein Lysine Methyltransferase.

Klonou, Alexia / Chlamydas, Sarantis / Piperi, Christina

Life (Basel, Switzerland)

2021 Volume 11, Issue 8

Abstract: The Mixed Lineage Leukemia 2 (MLL2) protein, also known as KMT2B, belongs to the family of mammalian histone H3 lysine 4 (H3K4) methyltransferases. It is a large protein of 2715 amino acids, widely expressed in adult human tissues and a paralog of the ... ...

Abstract	The Mixed Lineage Leukemia 2 (MLL2) protein, also known as KMT2B, belongs to the family of mammalian histone H3 lysine 4 (H3K4) methyltransferases. It is a large protein of 2715 amino acids, widely expressed in adult human tissues and a paralog of the MLL1 protein. MLL2 contains a characteristic C-terminal SET domain responsible for methyltransferase activity and forms a protein complex with WRAD (WDR5, RbBP5, ASH2L and DPY30), host cell factors 1/2 (HCF 1/2) and Menin. The MLL2 complex is responsible for H3K4 trimethylation (H3K4me3) on specific gene promoters and nearby
Language	English
Publishing date	2021-08-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life11080823
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Article ; Online: Structure, Activity and Function of the MLL2 (KMT2B) Protein Lysine Methyltransferase

Alexia Klonou / Sarantis Chlamydas / Christina Piperi

Life, Vol 11, Iss 823, p

2021 Volume 823

Abstract	The Mixed Lineage Leukemia 2 (MLL2) protein, also known as KMT2B, belongs to the family of mammalian histone H3 lysine 4 (H3K4) methyltransferases. It is a large protein of 2715 amino acids, widely expressed in adult human tissues and a paralog of the MLL1 protein. MLL2 contains a characteristic C-terminal SET domain responsible for methyltransferase activity and forms a protein complex with WRAD (WDR5, RbBP5, ASH2L and DPY30), host cell factors 1/2 (HCF 1/2) and Menin. The MLL2 complex is responsible for H3K4 trimethylation (H3K4me3) on specific gene promoters and nearby cis -regulatory sites, regulating bivalent developmental genes as well as stem cell and germinal cell differentiation gene sets. Moreover, MLL2 plays a critical role in development and germ line deletions of Mll2 have been associated with early growth retardation, neural tube defects and apoptosis that leads to embryonic death. It has also been involved in the control of voluntary movement and the pathogenesis of early stage childhood dystonia. Additionally, tumor-promoting functions of MLL2 have been detected in several cancer types, including colorectal, hepatocellular, follicular cancer and gliomas. In this review, we discuss the main structural and functional aspects of the MLL2 methyltransferase with particular emphasis on transcriptional mechanisms, gene regulation and association with diseases.
Keywords	MLL2 ; structure ; H3K4me3 ; chromatin regulation ; disease ; dystonia ; Science ; Q
Subject code	572
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Epigenetic mechanisms regulating COVID-19 infection.

Chlamydas, Sarantis / Papavassiliou, Athanasios G / Piperi, Christina

Epigenetics

2020 Volume 16, Issue 3, Page(s) 263–270

Abstract: Coronavirus disease 2019 (COVID-2019) outbreak originating in December 2019 in Wuhan, China has emerged as a global threat to human health. The highly contagious SARS-CoV-2 infection and transmission presents a diversity of human host and increased ... ...

Abstract	Coronavirus disease 2019 (COVID-2019) outbreak originating in December 2019 in Wuhan, China has emerged as a global threat to human health. The highly contagious SARS-CoV-2 infection and transmission presents a diversity of human host and increased disease risk with advancing age, highlighting the importance of in-depth understanding of its biological properties. Structural analyses have elucidated hot spots in viral binding domains, mutations, and specific proteins in the host such as the receptor angiotensin-converting enzyme 2 (ACE2) and the transmembrane protease serine 2 (TMPRSS2) to be implicated in cell entry and viral infectivity. Furthermore, epigenetic changes that regulate chromatin structure have shown a major impact in genome stabilization and maintenance of cellular homoeostasis and they have been implicated in the pathophysiology of the virus infection. Epigenetic research has revealed that global DNA methylation along with
MeSH term(s)	Angiotensin-Converting Enzyme 2/genetics ; Angiotensin-Converting Enzyme 2/metabolism ; COVID-19/genetics ; COVID-19/metabolism ; Epigenesis, Genetic ; Gene Expression Regulation, Viral ; Humans ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism ; Serine Endopeptidases/genetics ; Serine Endopeptidases/metabolism
Chemical Substances	ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Serine Endopeptidases (EC 3.4.21.-) ; TMPRSS2 protein, human (EC 3.4.21.-)
Keywords	covid19
Language	English
Publishing date	2020-07-30
Publishing country	United States
Document type	Journal Article ; Review ; Video-Audio Media
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.1080/15592294.2020.1796896
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Article ; Online: Histone lysine methyltransferase SETDB1 as a novel target for central nervous system diseases.

Markouli, Mariam / Strepkos, Dimitrios / Chlamydas, Sarantis / Piperi, Christina

Progress in neurobiology

2020 Volume 200, Page(s) 101968

Abstract: Epigenetic changes that regulate chromatin structure have a major impact in genome stabilization and maintenance of cellular homeostasis, been recently implicated in the pathophysiology of central nervous system (CNS). Aberrant expression and ... ...

Abstract	Epigenetic changes that regulate chromatin structure have a major impact in genome stabilization and maintenance of cellular homeostasis, been recently implicated in the pathophysiology of central nervous system (CNS). Aberrant expression and dysregulation of histone modification enzymes has been associated with the development of several CNS disorders, revealing these enzymes as putative targets for drug development and novel therapeutic approaches. SETDB1 is a histone lysine methyltransferase responsible for the di- and tri-methylation of histone 3 (H3) at lysine (K) 9 in euchromatic regions further promoting gene silencing through heterochromatin formation. By this way, SETDB1 has been shown to regulate gene expression and influence normal cellular homeostasis required for nervous system function while it is also implicated in the pathogenesis of CNS disorders. Among them, brain tumors, schizophrenia, Huntington's disease, autism spectrum disorders along with alcohol-induced fetal neurobehavioral deficits and Prader-Willi syndrome are representative examples, indicating the aberrant expression and function of SETDB1 as a common pathogenic factor. In this review, we focus on SETDB1-associated molecular mechanisms implicated in CNS physiology and disease while we further discuss current pharmacological approaches targeting SETDB1 enzymatic activity with beneficial effects.
MeSH term(s)	Central Nervous System Diseases/drug therapy ; Histone-Lysine N-Methyltransferase/metabolism ; Histones/metabolism ; Humans ; Lysine/metabolism ; Methylation
Chemical Substances	Histones ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; SETDB1 protein, human (EC 2.1.1.43) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2020-12-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2020.101968
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Article ; Online: Epigenetic mechanisms regulating COVID-19 infection

Chlamydas, Sarantis / Papavassiliou, Athanasios G. / Piperi, Christina

Epigenetics

2020 , Page(s) 1–8

Keywords	Cancer Research ; Molecular Biology ; covid19
Language	English
Publisher	Informa UK Limited
Publishing country	uk
Document type	Article ; Online
ISSN	1559-2294
DOI	10.1080/15592294.2020.1796896
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Epigenetic mechanisms regulating COVID-19 infection

Chlamydas, Sarantis / Papavassiliou, Athanasios G / Piperi, Christina

Epigenetics

Abstract	Coronavirus disease 2019 (COVID-2019) outbreak originating in December 2019 in Wuhan, China has emerged as a global threat to human health. The highly contagious SARS-CoV-2 infection and transmission presents a diversity of human host and increased disease risk with advancing age, highlighting the importance of in-depth understanding of its biological properties. Structural analyses have elucidated hot spots in viral binding domains, mutations, and specific proteins in the host such as the receptor angiotensin-converting enzyme 2 (ACE2) and the transmembrane protease serine 2 (TMPRSS2) to be implicated in cell entry and viral infectivity. Furthermore, epigenetic changes that regulate chromatin structure have shown a major impact in genome stabilization and maintenance of cellular homoeostasis and they have been implicated in the pathophysiology of the virus infection. Epigenetic research has revealed that global DNA methylation along with ACE2 gene methylation and post-translational histone modifications may drive differences in host tissue-, biological age- and sex-biased patterns of viral infection. Moreover, modulation of the host cells epigenetic landscape following infection represents a molecular tool used by viruses to antagonize cellular signalling as well as sensing components that regulate the induction of the host innate immune and antiviral defence programmes in order to enhance viral replication and infection efficiency. In this review, we provide an update of the main research findings at the interface of epigenetics and coronavirus infection. In particular, we highlight the epigenetic factors that interfere with viral replication and infection and may contribute to COVID-19 susceptibility, offering new ways of thinking in respect to host viral response.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #656207
Database	COVID19

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Article ; Online: Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk.

Tran, Duc / Beeler, J Scott / Liu, Jie / Wiley, Brian / Chan, Irenaeus C C / Xin, Zilan / Kramer, Michael H / Batchi-Bouyou, Armel L / Zong, Xiaoyu / Walter, Matthew J / Petrone, Giulia E M / Chlamydas, Sarantis / Ferraro, Francesca / Oh, Stephen T / Link, Daniel C / Busby, Ben / Cao, Yin / Bolton, Kelly L

Clinical cancer research : an official journal of the American Association for Cancer Research

2024

Abstract: Purpose: Clonal hematopoiesis (CH) is thought to be the origin of myeloid neoplasms (MN). Yet our understanding of the mechanisms driving CH progression to MN and clinical risk prediction of MN remains limited. The human proteome reflects complex ... ...

Abstract	Purpose: Clonal hematopoiesis (CH) is thought to be the origin of myeloid neoplasms (MN). Yet our understanding of the mechanisms driving CH progression to MN and clinical risk prediction of MN remains limited. The human proteome reflects complex interactions between genetic and epigenetic regulation of biological systems. We hypothesized that the plasma proteome might predict MN risk and inform our understanding of the mechanisms promoting MN development. Experimental design: We jointly characterized CH and plasma proteomic profiles of 46,237 individuals in the UK Biobank at baseline study entry. During 500,036 person-years of follow-up, 115 individuals developed MN. Cox proportional hazard regression was used to test for an association between plasma protein levels and MN risk. Results: We identified 115 proteins associated with MN risk of which 30% (N=34) were also associated with CH. These were enriched for known regulators of the innate and adaptive immune system. Plasma proteomics improved the prediction of MN risk (AUC=0.85, p=5×10-9) beyond clinical factors and CH (AUC=0.80). In an independent group (N=381,485), we used inherited polygenic risk scores (PRS) for plasma protein levels to validate the relevance of these proteins to MN development. PRS analyses suggest that most MN-associated proteins we identified are not directly causally linked to MN risk, but rather represent downstream markers of pathways regulating the progression of CH to MN. Conclusions: These data highlight the role of immune cell regulation in the progression of CH to MN and the promise of leveraging multi-omic characterization of CH to improve MN risk stratification.
Language	English
Publishing date	2024-03-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-23-3468
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Article ; Online: Histone Mark Profiling in Pediatric Astrocytomas Reveals Prognostic Significance of H3K9 Trimethylation and Histone Methyltransferase SUV39H1.

Klonou, Alexia / Korkolopoulou, Penelope / Gargalionis, Antonios N / Kanakoglou, Dimitrios S / Katifelis, Hector / Gazouli, Maria / Chlamydas, Sarantis / Mitsios, Andreas / Kalamatianos, Theodosis / Stranjalis, George / Themistocleous, Marios S / Papavassiliou, Kostas A / Sgouros, Spyros / Papavassiliou, Athanasios G / Piperi, Christina

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2021 Volume 18, Issue 3, Page(s) 2073–2090

Abstract: Alterations in global histone methylation regulate gene expression and participate in cancer onset and progression. The profile of histone methylation marks in pediatric astrocytomas is currently understudied with limited data on their distribution among ...

Abstract	Alterations in global histone methylation regulate gene expression and participate in cancer onset and progression. The profile of histone methylation marks in pediatric astrocytomas is currently understudied with limited data on their distribution among grades. The global expression patterns of repressive histone marks H3K9me3, H3K27me3, and H4K20me3 and active H3K4me3 and H3K36me3 along with their writers SUV39H1, SETDB1, EZH2, MLL2, and SETD2 were investigated in 46 pediatric astrocytomas and normal brain tissues. Associations between histone marks and modifying enzymes with clinicopathological characteristics and disease-specific survival were studied along with their functional impact in proliferation and migration of pediatric astrocytoma cell lines using selective inhibitors in vitro. Upregulation of histone methyltransferase gene expression and deregulation of histone code were detected in astrocytomas compared to normal brain tissues, with higher levels of SUV39H1, SETDB1, and SETD2 as well as H4K20me3 and H3K4me3 histone marks. Pilocytic astrocytomas exhibited lower MLL2 levels compared to diffusely infiltrating tumors indicating a differential pattern of epigenetic regulator expression between the two types of astrocytic neoplasms. Moreover, higher H3K9me3, H3K36me3, and SETDB1 expression was detected in grade IIΙ/IV compared to grade II astrocytomas. In univariate analysis, elevated H3K9me3 and MLL2 and diminished SUV39H1 expression adversely affected survival. Upon multivariate survival analysis, only SUV39H1 expression was revealed as an independent prognostic factor of adverse significance. Treatment of pediatric astrocytoma cell lines with SUV39H1 inhibitor reduced proliferation and cell migration. Our data implicate H3K9me3 and SUV39H1 in the pathobiology of pediatric astrocytomas, with SUV39H1 yielding prognostic information independent of other clinicopathologic variables.
MeSH term(s)	Adolescent ; Astrocytoma/diagnosis ; Astrocytoma/genetics ; Astrocytoma/metabolism ; Brain Neoplasms/diagnosis ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; Cell Line, Tumor ; Child ; Child, Preschool ; Cohort Studies ; Female ; Gene Expression Profiling/methods ; Histone Code/physiology ; Histone-Lysine N-Methyltransferase/biosynthesis ; Histone-Lysine N-Methyltransferase/genetics ; Humans ; Infant ; Male ; Methylation ; Methyltransferases/biosynthesis ; Methyltransferases/genetics ; Prognosis ; Repressor Proteins/biosynthesis ; Repressor Proteins/genetics
Chemical Substances	Repressor Proteins ; SUV39H1 protein, human (EC 2.1.1.) ; Methyltransferases (EC 2.1.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2021-07-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-021-01090-x
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