Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus Erythematous
Accumulating evidence supports the implication of long non-coding RNAs (lncRNAs) in autoimmune diseases, including systemic lupus erythematosus (SLE). LncRNA variants could impact the development and/or outcome of the disease with variable diagnostic/prognostic utility in the clinic. We aimed to exp...
Main Authors: | , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2022-05-01
|
Series: | Diagnostics |
Subjects: | |
Online Access: | https://www.mdpi.com/2075-4418/12/5/1197 |
_version_ | 1797500455405748224 |
---|---|
author | Nesreen M. Ismail Eman A. Toraih Amany I. Almars Essam Al Ageeli Manal S. Fawzy Shymaa Ahmed Maher |
author_facet | Nesreen M. Ismail Eman A. Toraih Amany I. Almars Essam Al Ageeli Manal S. Fawzy Shymaa Ahmed Maher |
author_sort | Nesreen M. Ismail |
collection | DOAJ |
description | Accumulating evidence supports the implication of long non-coding RNAs (lncRNAs) in autoimmune diseases, including systemic lupus erythematosus (SLE). LncRNA variants could impact the development and/or outcome of the disease with variable diagnostic/prognostic utility in the clinic. We aimed to explore the contribution of <i>HOTAIR</i> (rs10783618), <i>LINC-ROR</i> (rs1942347), and <i>MALAT1</i> (rs3200401) variants to SLE susceptibility and/or severity in 163 SLE patients and age-/sex-matched controls using real-time TaqMan allelic discrimination PCR. <i>HOTAIR</i> rs10783618*C/C was associated with a 77% increased risk of SLE (OR = 1.77, 95%CI = 1.09–2.87, <i>p</i> = 0.020) under the recessive model. Similarly, <i>MALAT1</i> rs3200401*T/T carriers were three times more likely to develop SLE (OR = 2.89, 95%CI = 1.42–5.90) under the recessive model. While the rs3200401*T/C genotype was associated with a 49–57% decreased risk of SLE under codominant (OR = 0.51, 95%CI = 0.31–0.82, <i>p</i> < 0.001) and over-dominant (OR = 0.43, 95%CI = 0.27–0.68, <i>p</i> < 0.001) models. <i>LINC-ROR</i> rs1942347*A/A patients were more likely to have a positive family history of SLE. At the same time, <i>HOTAIR</i> rs10783618*C/C was associated with a higher frequency of arthritis (<i>p</i> = 0.001) and the presence of oral ulcers (<i>p</i> = 0.002), while patients carrying rs10783618*T/T genotype were more likely to develop hair loss (<i>p</i> < 0.001), weight loss (<i>p</i> = 0.001), and neurological symptoms (<i>p</i> = 0.003). In conclusion, the studied lncRNAs, <i>HOTAIR,</i> and <i>MALAT1</i> gene polymorphisms confer susceptibility for SLE, providing a potential theoretical basis for their clinical translation in SLE disease. |
first_indexed | 2024-03-10T03:03:09Z |
format | Article |
id | doaj.art-ad516d5504774acc8fccfdc29d723e2b |
institution | Directory Open Access Journal |
issn | 2075-4418 |
language | English |
last_indexed | 2024-03-10T03:03:09Z |
publishDate | 2022-05-01 |
publisher | MDPI AG |
record_format | Article |
series | Diagnostics |
spelling | doaj.art-ad516d5504774acc8fccfdc29d723e2b2023-11-23T10:40:45ZengMDPI AGDiagnostics2075-44182022-05-01125119710.3390/diagnostics12051197Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus ErythematousNesreen M. Ismail0Eman A. Toraih1Amany I. Almars2Essam Al Ageeli3Manal S. Fawzy4Shymaa Ahmed Maher5Department of Rheumatology and Rehabilitation, Faculty of Medicine, Suez Canal University, Ismailia 41522, EgyptDivision of Endocrine and Oncologic Surgery, Department of Surgery, Tulane University School of Medicine, New Orleans, LA 70112, USADepartment of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah 21589, Saudi ArabiaDepartment of Clinical Biochemistry (Medical Genetics), Faculty of Medicine, Jazan University, Jazan 45142, Saudi ArabiaDepartment of Biochemistry, Faculty of Medicine, Northern Border University, Arar 1321, Saudi ArabiaDepartment of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Suez Canal University, Ismailia 41522, EgyptAccumulating evidence supports the implication of long non-coding RNAs (lncRNAs) in autoimmune diseases, including systemic lupus erythematosus (SLE). LncRNA variants could impact the development and/or outcome of the disease with variable diagnostic/prognostic utility in the clinic. We aimed to explore the contribution of <i>HOTAIR</i> (rs10783618), <i>LINC-ROR</i> (rs1942347), and <i>MALAT1</i> (rs3200401) variants to SLE susceptibility and/or severity in 163 SLE patients and age-/sex-matched controls using real-time TaqMan allelic discrimination PCR. <i>HOTAIR</i> rs10783618*C/C was associated with a 77% increased risk of SLE (OR = 1.77, 95%CI = 1.09–2.87, <i>p</i> = 0.020) under the recessive model. Similarly, <i>MALAT1</i> rs3200401*T/T carriers were three times more likely to develop SLE (OR = 2.89, 95%CI = 1.42–5.90) under the recessive model. While the rs3200401*T/C genotype was associated with a 49–57% decreased risk of SLE under codominant (OR = 0.51, 95%CI = 0.31–0.82, <i>p</i> < 0.001) and over-dominant (OR = 0.43, 95%CI = 0.27–0.68, <i>p</i> < 0.001) models. <i>LINC-ROR</i> rs1942347*A/A patients were more likely to have a positive family history of SLE. At the same time, <i>HOTAIR</i> rs10783618*C/C was associated with a higher frequency of arthritis (<i>p</i> = 0.001) and the presence of oral ulcers (<i>p</i> = 0.002), while patients carrying rs10783618*T/T genotype were more likely to develop hair loss (<i>p</i> < 0.001), weight loss (<i>p</i> = 0.001), and neurological symptoms (<i>p</i> = 0.003). In conclusion, the studied lncRNAs, <i>HOTAIR,</i> and <i>MALAT1</i> gene polymorphisms confer susceptibility for SLE, providing a potential theoretical basis for their clinical translation in SLE disease.https://www.mdpi.com/2075-4418/12/5/1197<i>HOTAIR</i><i>LINC-ROR</i>long non-coding RNAslupus nephritis<i>MALAT1</i>single nucleotide polymorphism |
spellingShingle | Nesreen M. Ismail Eman A. Toraih Amany I. Almars Essam Al Ageeli Manal S. Fawzy Shymaa Ahmed Maher Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus Erythematous Diagnostics <i>HOTAIR</i> <i>LINC-ROR</i> long non-coding RNAs lupus nephritis <i>MALAT1</i> single nucleotide polymorphism |
title | Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus Erythematous |
title_full | Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus Erythematous |
title_fullStr | Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus Erythematous |
title_full_unstemmed | Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus Erythematous |
title_short | Genotype Triad for <i>HOTAIR</i> rs10783618, <i>LINC-ROR</i> rs1942347, and <i>MALAT1</i> rs3200401 as Molecular Markers in Systemic Lupus Erythematous |
title_sort | genotype triad for i hotair i rs10783618 i linc ror i rs1942347 and i malat1 i rs3200401 as molecular markers in systemic lupus erythematous |
topic | <i>HOTAIR</i> <i>LINC-ROR</i> long non-coding RNAs lupus nephritis <i>MALAT1</i> single nucleotide polymorphism |
url | https://www.mdpi.com/2075-4418/12/5/1197 |
work_keys_str_mv | AT nesreenmismail genotypetriadforihotairirs10783618ilincrorirs1942347andimalat1irs3200401asmolecularmarkersinsystemiclupuserythematous AT emanatoraih genotypetriadforihotairirs10783618ilincrorirs1942347andimalat1irs3200401asmolecularmarkersinsystemiclupuserythematous AT amanyialmars genotypetriadforihotairirs10783618ilincrorirs1942347andimalat1irs3200401asmolecularmarkersinsystemiclupuserythematous AT essamalageeli genotypetriadforihotairirs10783618ilincrorirs1942347andimalat1irs3200401asmolecularmarkersinsystemiclupuserythematous AT manalsfawzy genotypetriadforihotairirs10783618ilincrorirs1942347andimalat1irs3200401asmolecularmarkersinsystemiclupuserythematous AT shymaaahmedmaher genotypetriadforihotairirs10783618ilincrorirs1942347andimalat1irs3200401asmolecularmarkersinsystemiclupuserythematous |