Maha Alhelf, Laila Rashed, Sahar Ahmed, Mohamed Mady, Marwa Abdelgwad
{"title":"微RNA-24能否通过靶向YKL-40影响系统性红斑狼疮患者心血管疾病的发生?","authors":"Maha Alhelf, Laila Rashed, Sahar Ahmed, Mohamed Mady, Marwa Abdelgwad","doi":"10.52547/rbmb.11.3.511","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammatory nature. One of the leading causes of death in SLE patients is cardiovascular (CVS) morbidity. MiRNA-24 is highly expressed in vascular endothelial cells (VECs). This dysregulated expression pattern is associated with dysfunction or even damage of VECs and leads to the occurrence of cardiovascular diseases. YKL- 40 is an inflammatory glycoprotein involved in the pathogenesis of endothelial dysfunction and thereby atherosclerosis. In this work, we aimed at illustrating the possible role of miR-24 and its target YKL-40 in the pathogenesis of the CVS morbidity associated with SLE.</p><p><strong>Methods: </strong>This work was conducted on 40 SLE patients and 40 healthy controls. Quantitative real-time PCR (qPCR) was done to estimate the expression level of miRNA-24 in serum. In addition, we measured the serum level of YKL-40 using ELISA.</p><p><strong>Results: </strong>miR-24-fold change was found to be down-regulated, whereas serum YKL- 40 was up-regulated among SLE patients with observed significant and negative correlation between the two parameters.</p><p><strong>Conclusion: </strong>Our study provided an insight about the role of miR-24 and its target serum YKL-40 protein in the development of SLE-related inflammation and atherosclerosis.</p>","PeriodicalId":45319,"journal":{"name":"Reports of Biochemistry and Molecular Biology","volume":null,"pages":null},"PeriodicalIF":1.6000,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9883035/pdf/rbmb-11-511.pdf","citationCount":"0","resultStr":"{\"title\":\"Can Micro RNA-24 Affect the Cardiovascular Morbidity in Systemic Lupus Erythematosus by Targeting YKL-40?\",\"authors\":\"Maha Alhelf, Laila Rashed, Sahar Ahmed, Mohamed Mady, Marwa Abdelgwad\",\"doi\":\"10.52547/rbmb.11.3.511\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammatory nature. One of the leading causes of death in SLE patients is cardiovascular (CVS) morbidity. MiRNA-24 is highly expressed in vascular endothelial cells (VECs). This dysregulated expression pattern is associated with dysfunction or even damage of VECs and leads to the occurrence of cardiovascular diseases. YKL- 40 is an inflammatory glycoprotein involved in the pathogenesis of endothelial dysfunction and thereby atherosclerosis. In this work, we aimed at illustrating the possible role of miR-24 and its target YKL-40 in the pathogenesis of the CVS morbidity associated with SLE.</p><p><strong>Methods: </strong>This work was conducted on 40 SLE patients and 40 healthy controls. Quantitative real-time PCR (qPCR) was done to estimate the expression level of miRNA-24 in serum. In addition, we measured the serum level of YKL-40 using ELISA.</p><p><strong>Results: </strong>miR-24-fold change was found to be down-regulated, whereas serum YKL- 40 was up-regulated among SLE patients with observed significant and negative correlation between the two parameters.</p><p><strong>Conclusion: </strong>Our study provided an insight about the role of miR-24 and its target serum YKL-40 protein in the development of SLE-related inflammation and atherosclerosis.</p>\",\"PeriodicalId\":45319,\"journal\":{\"name\":\"Reports of Biochemistry and Molecular Biology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2022-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9883035/pdf/rbmb-11-511.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Reports of Biochemistry and Molecular Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.52547/rbmb.11.3.511\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Reports of Biochemistry and Molecular Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.52547/rbmb.11.3.511","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Can Micro RNA-24 Affect the Cardiovascular Morbidity in Systemic Lupus Erythematosus by Targeting YKL-40?
Background: Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammatory nature. One of the leading causes of death in SLE patients is cardiovascular (CVS) morbidity. MiRNA-24 is highly expressed in vascular endothelial cells (VECs). This dysregulated expression pattern is associated with dysfunction or even damage of VECs and leads to the occurrence of cardiovascular diseases. YKL- 40 is an inflammatory glycoprotein involved in the pathogenesis of endothelial dysfunction and thereby atherosclerosis. In this work, we aimed at illustrating the possible role of miR-24 and its target YKL-40 in the pathogenesis of the CVS morbidity associated with SLE.
Methods: This work was conducted on 40 SLE patients and 40 healthy controls. Quantitative real-time PCR (qPCR) was done to estimate the expression level of miRNA-24 in serum. In addition, we measured the serum level of YKL-40 using ELISA.
Results: miR-24-fold change was found to be down-regulated, whereas serum YKL- 40 was up-regulated among SLE patients with observed significant and negative correlation between the two parameters.
Conclusion: Our study provided an insight about the role of miR-24 and its target serum YKL-40 protein in the development of SLE-related inflammation and atherosclerosis.
期刊介绍:
The Reports of Biochemistry & Molecular Biology (RBMB) is the official journal of the Varastegan Institute for Medical Sciences and is dedicated to furthering international exchange of medical and biomedical science experience and opinion and a platform for worldwide dissemination. The RBMB is a medical journal that gives special emphasis to biochemical research and molecular biology studies. The Journal invites original and review articles, short communications, reports on experiments and clinical cases, and case reports containing new insights into any aspect of biochemistry and molecular biology that are not published or being considered for publication elsewhere. Publications are accepted in the form of reports of original research, brief communications, case reports, structured reviews, editorials, commentaries, views and perspectives, letters to authors, book reviews, resources, news, and event agenda.