![](/images/graphics-bg.png)
Identification of SMAD3 as a Novel Mediator of Inflammation in Human Myometrium In Vitro
المؤلف
المصدر
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-09-27
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Preterm birth remains the primary cause of early neonatal death and is a major determinant for long-term health consequences.
Aberrant intrauterine inflammation and infection are known to augment the synthesis of proinflammatory cytokines and induce uterine contractions, which can subsequently lead to preterm birth.
The transforming growth factor-β (TGF-β) superfamily members regulate numerous cellular processes through the activation of intracellular mediators known as mothers against decapentaplegic homolog (SMADs).
Studies in nongestational tissues have shown that SMAD3 plays a role in immune regulation and inflammation; however, its role in human labour remains unknown.
Thus, the present study aimed at (i) characterising the expression of SMAD3 in the human myometrium; (ii) determining the effect of bacterial and viral products and proinflammatory cytokines on SMAD3 transcriptional activity in primary human myometrial cells; and (iii) investigating the effect of SMAD3 siRNA knockdown on the production of prolabour mediators in primary human myometrial cells.
Phosphorylated (i.e., active) SMAD3 protein expression was lower in the myometrium after spontaneous term labour compared to the myometrium from nonlabouring women.
Using a luciferase assay, the proinflammatory cytokines IL-1β and TNF, and viral analogue polyinosinic : polycytidylic acid (poly(I : C)) significantly reduced SMAD3 transcriptional activity in human primary myometrial cells.
Loss-of-function studies found that SMAD3 knockdown in myometrial cells significantly increased IL-1β- and poly(I : C)-induced proinflammatory cytokines (IL-1A, IL-6), chemokines (IL-8, MCP-1), the adhesion molecule ICAM-1, COX-2 mRNA expression, and subsequent PGF2α release.
In conclusion, SMAD3 deficiency is associated with increased production of proinflammatory and prolabour mediators in the human myometrium.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Lappas, Martha. 2018. Identification of SMAD3 as a Novel Mediator of Inflammation in Human Myometrium In Vitro. Mediators of Inflammation،Vol. 2018, no. 2018, pp.1-11.
https://search.emarefa.net/detail/BIM-1203530
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Lappas, Martha. Identification of SMAD3 as a Novel Mediator of Inflammation in Human Myometrium In Vitro. Mediators of Inflammation No. 2018 (2018), pp.1-11.
https://search.emarefa.net/detail/BIM-1203530
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Lappas, Martha. Identification of SMAD3 as a Novel Mediator of Inflammation in Human Myometrium In Vitro. Mediators of Inflammation. 2018. Vol. 2018, no. 2018, pp.1-11.
https://search.emarefa.net/detail/BIM-1203530
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1203530
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
![](/images/ebook-kashef.png)
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر
![](/images/kashef-image.png)