<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Reports of Biochemistry and Molecular Biology</title>
<title_fa></title_fa>
<short_title>rbmb.net</short_title>
<subject>Basic Sciences</subject>
<web_url>http://rbmb.net</web_url>
<journal_hbi_system_id>1</journal_hbi_system_id>
<journal_hbi_system_user>admin</journal_hbi_system_user>
<journal_id_issn>2322-3480</journal_id_issn>
<journal_id_issn_online>2322-3480</journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi>10.61882/rbmb</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid></journal_id_sid>
<journal_id_nlai></journal_id_nlai>
<journal_id_science></journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1401</year>
	<month>8</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2022</year>
	<month>11</month>
	<day>1</day>
</pubdate>
<volume>11</volume>
<number>3</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Can Micro RNA-24 Affect the Cardiovascular Morbidity in Systemic Lupus Erythematosus by Targeting YKL-40?</title>
	<subject_fa>بیوشیمی</subject_fa>
	<subject>Biochemistry</subject>
	<content_type_fa>مقالات اصلی</content_type_fa>
	<content_type>Original Article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;div style=&quot;text-align: justify;&quot;&gt;&lt;strong&gt;Background&lt;/strong&gt;: 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.&lt;br&gt;
&lt;br&gt;
&lt;strong&gt;Methods&lt;/strong&gt;: This work was conducted on 40 SLE patients and 40 healthy controls. Quantitative realtime 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.&lt;br&gt;
&lt;br&gt;
&lt;strong&gt;Results&lt;/strong&gt;: miR-24-fold change was found to be down-regulated, whereas serum YKL- 40 was upregulated among SLE patients with observed significant and negative correlation between the two parameters.&lt;br&gt;
&lt;br&gt;
&lt;strong&gt;Conclusions&lt;/strong&gt;: 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.&lt;/div&gt;</abstract>
	<keyword_fa></keyword_fa>
	<keyword>miRNA-24, SDC-1, SLE, VCAM, YKL-40.</keyword>
	<start_page>511</start_page>
	<end_page>523</end_page>
	<web_url>http://rbmb.net/browse.php?a_code=A-10-883-1&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Maha</first_name>
	<middle_name></middle_name>
	<last_name>Alhelf</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>100319475328460016760</code>
	<orcid>100319475328460016760</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Biotechnology School, Nile University, Giza, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Laila</first_name>
	<middle_name></middle_name>
	<last_name>Rashed</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>100319475328460016761</code>
	<orcid>100319475328460016761</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Cairo University,Cairo, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Sahar</first_name>
	<middle_name></middle_name>
	<last_name>Ahmed</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>100319475328460016762</code>
	<orcid>100319475328460016762</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Rheumatologyand Immunology Unit, Internal Medicine Department, Faculty ofMedicine, Cairo University, Cairo, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohamed</first_name>
	<middle_name></middle_name>
	<last_name>Mohamed</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>100319475328460016763</code>
	<orcid>100319475328460016763</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Endocrinology Unit, Internal Medicine Department, Faculty of Medicine, Cairo University, Cairo, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Marwa</first_name>
	<middle_name></middle_name>
	<last_name>Abdelgwad</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>Marwa.Soliman@kasralainy.edu.eg.</email>
	<code>100319475328460016764</code>
	<orcid>100319475328460016764</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>Medical Biochemistry and Molecular Biology Department, Faculty of Medicine, Cairo University,Cairo, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


	</article>
</articleset>
</journal>
