Monocyte adhesion to decidual endothelial cells is increased in pregnancies complicated by type 1 diabetes but not by gestational diabetes.

نویسندگان

  • Anoula Galettis
  • Suzanne Campbell
  • Jonathan M Morris
  • Christopher J Jackson
  • Steven M Twigg
  • Eileen D M Gallery
چکیده

T ype 1 diabetes complicates 1 of every 200 pregnancies and gestational diabetes a further 2–3% of pregnancies (1). Systemic atheromatous vascular disease can develop or accelerate during diabetic pregnancy. We and others (2) have observed similar vascular lesions in placental bed vessels (Fig. 1A) associated with impaired placental function and fetal growth. Genesis of atheroma involves adherence of peripheral blood monocytes to endothelium (3–5). To determine whether a similar process underlies the placental bed vasculopathy of diabetes, we examined cell adhesion in an in vitro coculture system using decidual endothelial cells from normal pregnancies and monocytes from both normal and diabetic pregnancies.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Homing Receptor Expression Is Deviated on CD56+ Blood Lymphocytes during Pregnancy in Type 1 Diabetic Women

Type 1 Diabetes Mellitus (T1DM) is characterized by an augmented pro-inflammatory immune state. This contributes to the increased risk for gestational complications observed in T1DM mothers. In normal pregnancies, critical immunological changes occur, including the massive recruitment of lymphocytes, particularly CD56bright NK cells, into early decidua basalis and a 2nd trimester shift towards ...

متن کامل

Dysregulation of Placental Endothelial Lipase in Obese Women With Gestational Diabetes Mellitus

OBJECTIVE This study addressed the hypothesis that placental endothelial lipase (EL) expression is affected by pregnancies complicated by obesity and gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS EL expression in placental tissues from pregnancies complicated by obesity, GDM, or obesity combined with GDM (obese-GDM) was analyzed by quantitative RT-PCR. Moreover, primary pla...

متن کامل

Gestational diabetes leads to down-regulation of CDK4-pRB-E2F1 pathway genes in pancreatic islets of rat offspring

Objective(s): The link between a hyperglycemic intrauterine environment and the development of diabetes later in life has been observed in offspring exposed to gestational diabetes mellitus (GDM), but the underlying mechanisms for this phenomenon are still not clear. Reduced β-cells mass is a determinant in the development of diabetes (type 1 and type 2 diabetes). Some recent studies have provi...

متن کامل

The effect of microRNA-125 on the adhesion molecule expression of integrin beta2 and adhesive determination of endothelial cells isolated from human aorta to monocyte

Background: The immune-mediated responses in vascular cells may include the increased expression of endothelial adhesion molecules, leukocyte rolling and infiltration, cellular lipid dysregulation and vascular smooth muscle cells (VSMCs) differentiation. Investigating the cellular and molecular events involved in the rolling process is useful for treatment or prevention of the vessel stenosis es...

متن کامل

Placental Lipases in Pregnancies Complicated by Gestational Diabetes Mellitus (GDM)

Infants of women with gestational diabetes mellitus (GDM) are more likely to be born large for gestational age with a higher percentage body fat. Elevated maternal lipids may contribute to this. Placental lipases such as lipoprotein lipase (LPL), endothelial lipase (EL) and hormone sensitive lipase (HSL) are involved in transferring lipids from mother to fetus. Previous studies of expression of...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Diabetes care

دوره 27 10  شماره 

صفحات  -

تاریخ انتشار 2004