Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia Symptoms
Background: Thalassemia, a prevalent genetic disorder, is characterized by a point mutation affecting the globin gene expression. One manifestation of this disorder, β-thalassemia, arises from compromised β-globin chain production. Objectives: The objective of this research was to explore the presen...
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Wolters Kluwer Medknow Publications
2024-10-01
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| Series: | Medical Journal of Babylon |
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| Online Access: | https://doi.org/10.4103/MJBL.MJBL_1337_23 |
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| author | Mohammed M. Salih Al-Khafaji Anas Y. Al-Hayawi |
| author_facet | Mohammed M. Salih Al-Khafaji Anas Y. Al-Hayawi |
| author_sort | Mohammed M. Salih Al-Khafaji |
| collection | DOAJ |
| description | Background: Thalassemia, a prevalent genetic disorder, is characterized by a point mutation affecting the globin gene expression. One manifestation of this disorder, β-thalassemia, arises from compromised β-globin chain production. Objectives: The objective of this research was to explore the presence of miR-92a expression in the bloodstream of individuals affected by severe thalassemia. Moreover, the study aimed to uncover the functional role of miR-92a and its influence on the expression of γ-globin (HGB gene) and oxidative stress within blood cells. Materials and Methods: As an initial step, the real-time quantitative polymerase chain reaction (RT-qPCR) was employed to assess gene expression levels subsequent to RNA extraction. The process involved the addition of the polyadenosine monophosphate enzyme Poly-A to facilitate the production of mature messenger RNA (mRNA) from DNA. Results: The study revealed significantly elevated miR-92a expression in blood cells. Furthermore, higher levels of gamma-globin, glutathione (GSH), and superoxide dismutase (SOD), along with a decrease in malondialdehyde (MDA) and BCL11A expression, were identified as targets of miR-92a-3p and were downregulated by this microRNA. Additionally, individual knockdown of BCL11A led to increased expression of β-globin (HBB gene), SOD, and GSH, accompanied by a reduction in MDA levels. However, the patterns observed were altered upon subsequent inhibition of miR-92a. Conclusion: The findings of this study propose that through the suppression of BCL11A, miR-92a may elevate γ-globin levels while concurrently mitigating oxidative stress in blood cells. |
| format | Article |
| id | doaj-art-f7b27973349947d3be0bd45a944329dd |
| institution | Kabale University |
| issn | 1812-156X 2312-6760 |
| language | English |
| publishDate | 2024-10-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Medical Journal of Babylon |
| spelling | doaj-art-f7b27973349947d3be0bd45a944329dd2025-01-14T11:24:47ZengWolters Kluwer Medknow PublicationsMedical Journal of Babylon1812-156X2312-67602024-10-0121Suppl 2S250S25710.4103/MJBL.MJBL_1337_23Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia SymptomsMohammed M. Salih Al-KhafajiAnas Y. Al-HayawiBackground: Thalassemia, a prevalent genetic disorder, is characterized by a point mutation affecting the globin gene expression. One manifestation of this disorder, β-thalassemia, arises from compromised β-globin chain production. Objectives: The objective of this research was to explore the presence of miR-92a expression in the bloodstream of individuals affected by severe thalassemia. Moreover, the study aimed to uncover the functional role of miR-92a and its influence on the expression of γ-globin (HGB gene) and oxidative stress within blood cells. Materials and Methods: As an initial step, the real-time quantitative polymerase chain reaction (RT-qPCR) was employed to assess gene expression levels subsequent to RNA extraction. The process involved the addition of the polyadenosine monophosphate enzyme Poly-A to facilitate the production of mature messenger RNA (mRNA) from DNA. Results: The study revealed significantly elevated miR-92a expression in blood cells. Furthermore, higher levels of gamma-globin, glutathione (GSH), and superoxide dismutase (SOD), along with a decrease in malondialdehyde (MDA) and BCL11A expression, were identified as targets of miR-92a-3p and were downregulated by this microRNA. Additionally, individual knockdown of BCL11A led to increased expression of β-globin (HBB gene), SOD, and GSH, accompanied by a reduction in MDA levels. However, the patterns observed were altered upon subsequent inhibition of miR-92a. Conclusion: The findings of this study propose that through the suppression of BCL11A, miR-92a may elevate γ-globin levels while concurrently mitigating oxidative stress in blood cells.https://doi.org/10.4103/MJBL.MJBL_1337_23bcl11agene expressionmir-92a-3psymptomsthalassemia |
| spellingShingle | Mohammed M. Salih Al-Khafaji Anas Y. Al-Hayawi Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia Symptoms Medical Journal of Babylon bcl11a gene expression mir-92a-3p symptoms thalassemia |
| title | Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia Symptoms |
| title_full | Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia Symptoms |
| title_fullStr | Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia Symptoms |
| title_full_unstemmed | Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia Symptoms |
| title_short | Deciphering the Impact of miR-92a-3p on Controlling BCL11A Gene Expression and Its Implication in Easing Thalassemia Symptoms |
| title_sort | deciphering the impact of mir 92a 3p on controlling bcl11a gene expression and its implication in easing thalassemia symptoms |
| topic | bcl11a gene expression mir-92a-3p symptoms thalassemia |
| url | https://doi.org/10.4103/MJBL.MJBL_1337_23 |
| work_keys_str_mv | AT mohammedmsalihalkhafaji decipheringtheimpactofmir92a3poncontrollingbcl11ageneexpressionanditsimplicationineasingthalassemiasymptoms AT anasyalhayawi decipheringtheimpactofmir92a3poncontrollingbcl11ageneexpressionanditsimplicationineasingthalassemiasymptoms |