The Evolving Role of MicroRNAs in Endothelial Cell Dysfunction in Response to Infection

AbstractThe microRNAs are short noncoding RNA molecules responsible for translational repression and silencing of target genes via binding to the mRNA. They are found in all eukaryotic cells and play a critical role in virtually all physiological processes, including within the cardiovascular system where they influence cellular development, differentiation, cardiovascular function, hemostasis, and programmed cell death. Dysregulated microRNA expression is associated with several conditions ranging from cancer and autoimmune disease to infection. Progressively, it has become increasingly clear that microRNAs are important components of the host response to microbes. The cardiovascular system, coupled with cells of the innate immune system, provide the initial interaction and first response to microbial infection, respectively. This review presents the current state of knowledge regarding the role of microRNAs with emphasis on their role in controlling endothelial cell function.

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Enhanced Vascular Endothelial Cell Function on Nanostructured Titanium Surface Features: The Role of Nano to Submicron Roughness

MRS Proceedings ◽

10.1557/proc-1136-dd04-04 ◽

2008 ◽

Vol 1136 ◽

Cited By ~ 2

Author(s):

Jing Lu ◽

Dongwoo Khang ◽

Thomas J. Webster

Keyword(s):

Cell Adhesion ◽

Endothelial Cell ◽

Cell Function ◽

Vascular Endothelial Cell ◽

Vascular Endothelial ◽

Endothelial Cell Function ◽

Titanium Surfaces ◽

Endothelial Cell Adhesion

ABSTRACTTo study the contribution of different surface feature properties in improving vascular endothelial cell adhesion, rationally designed nano/sub-micron patterns with various dimensions were created on titanium surfaces in this study. In vitro results indicated that endothelial cell adhesion was improved when the titanium pattern dimensions decreased into the nano-scale. Specifically, endothelial cells preferred to adhere on sub-micron and nano rough titanium substrates compared to flat titanium. Moreover, titanium with nano and sub-micron roughness and with the same chemistry as compared to flat titanium, had significantly greater surface energy. Thus, the present study indicated the strong potential of surface nanotopography and nano/sub-micron roughness for improving current vascular stent design.

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FKBPL and SIRT-1, key angiogenesis proteins, are downregulated by diabetes in pregnancy

10.1101/2020.10.06.20208116 ◽

2020 ◽

Cited By ~ 1

Author(s):

Abdelrahim Alqudah ◽

Kelly-Ann Eastwood ◽

Djurdja Jerotic ◽

Naomi Todd ◽

Denise Hoch ◽

...

Keyword(s):

Endothelial Cell ◽

Protein Expression ◽

Gestational Age ◽

High Glucose ◽

Cell Function ◽

First Trimester ◽

Diabetes In Pregnancy ◽

Endothelial Cell Function ◽

In Pregnancy

AbstractContextDiabetes in pregnancy is associated with numerous complications, however the mechanisms are still poorly understood.ObjectiveTo investigate the role of new angiogenesis markers, FKBPL and SIRT-1, in pre-gestational (type 1 diabetes, T1D) and gestational diabetes (GDM).Design and interventionPlacental FKBPL, SIRT-1, PlGF and VEGF-R1 protein expression was determined from pregnant women with GDM or T1D, and in first trimester trophoblast cells exposed to high glucose and varying oxygen concentrations. Endothelial cell function was assessed in high glucose conditions and FKBPL overexpression.Settings and ParticipantsHuman placental samples from pregnant women with GDM (n=6) or T1D (n=8) were collected to assess FKBPL and SIRT-1 protein expression compared to non-diabetic controls.Main outcome measuresTo determine the role of placental FKBPL and/or SIRT-1 in diabetic pregnancies, in first trimester trophoblasts and endothelial cell function in high-glucose environment.ResultsPlacental FKBPL protein expression was downregulated in T1D (FKBPL; p<0.05) whereas PlGF/VEGF-R1 were upregulated (p<0.05); correlations adjusted for gestational age were also significant. In the presence of GDM, only SIRT-1 (p<0.001) was significantly downregulated even when adjusted for gestational age (r=-0.92, p=0.001). FKBPL and SIRT-1 were also downregulated in ACH-3P cells in high glucose conditions and 6.5%/2.5% oxygen concentrations (p<0.05). FKBPL overexpression in HUVECs reduced tubule formation compared to empty vector control, in high glucose conditions (junctions; p<0.01, branches; p<0.05).ConclusionsFKBPL and/or SIRT-1 downregulation in response to diabetes may have a role in the development of vascular dysfunction in pregnancy, and associated complications such as preeclampsia.

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Syk expression in endothelial cells and their morphologic defects in embryonic Syk-deficient mice

Blood ◽

10.1182/blood.v98.9.2869 ◽

2001 ◽

Vol 98 (9) ◽

pp. 2869-2871 ◽

Cited By ~ 50

Author(s):

Shigeru Yanagi ◽

Ryoko Inatome ◽

Junyi Ding ◽

Hironori Kitaguchi ◽

Victor L. J. Tybulewicz ◽

...

Keyword(s):

Endothelial Cells ◽

Endothelial Cell ◽

Cell Function ◽

Critical Role ◽

Microscopic Analysis ◽

Electron Microscopic ◽

Vascular Integrity ◽

Endothelial Cell Function ◽

Deficient Mice

Abstract Mice deficient in the Syk tyrosine kinase showed severe petechiae in utero and died shortly after birth. The mechanism of this bleeding, however, remains unknown. Here it is shown that this bleeding is caused by morphologic defects of Syk-deficient endothelial cells during embryogenesis. Immunoblot and reverse transcriptase–polymerase chain reaction Northern blot analysis indicated that Syk is expressed in several endothelial cell lines. Immunocytochemical analysis also confirmed that Syk is expressed in the normal embryonic endothelial cells and is absent in Syk-deficient mice. Furthermore, electron microscopic analysis of Syk-deficient mice revealed an abnormal morphogenesis and a decreased number of endothelial cells. The results indicate a critical role for Syk in endothelial cell function and in maintaining vascular integrity in vivo.

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