The Effect of Baicalin on the Expression Profiles of Long Non-Coding RNAs and mRNAs in Porcine Aortic Vascular Endothelial Cells Infected with Haemophilus parasuis

2020 ◽  
Vol 39 (5) ◽  
pp. 801-815 ◽  
Author(s):  
Ling Guo ◽  
Jun Liu ◽  
Yunfei Zhang ◽  
Shulin Fu ◽  
Yinsheng Qiu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Expression Profiles ◽  
Vascular Endothelial ◽  
Haemophilus Parasuis ◽  
Non Coding Rnas

scholarly journals Impact of Spaceflight and Artificial Gravity on the Mouse Retina: Biochemical and Proteomic Analysis

2018 ◽  
Vol 19 (9) ◽  
pp. 2546 ◽  
Author(s):  
Xiao Mao ◽  
Stephanie Byrum ◽  
Nina Nishiyama ◽  
Michael Pecaut ◽  
Vijayalakshmi Sridharan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Visual Acuity ◽  
Protein Expression ◽  
Proteomic Analysis ◽  
Vascular Endothelial Cells ◽  
Expression Profiles ◽  
Artificial Gravity ◽  
Ocular Tissue ◽  
Mouse Retina ◽  
Vascular Endothelial

Astronauts are reported to have experienced some impairment in visual acuity during their mission on the International Space Station (ISS) and after they returned to Earth. There is emerging evidence that changes in vision may involve alterations in ocular structure and function. To investigate possible mechanisms, changes in protein expression profiles and oxidative stress-associated apoptosis were examined in mouse ocular tissue after spaceflight. Nine-week-old male C57BL/6 mice (n = 12) were launched from the Kennedy Space Center on a SpaceX rocket to the ISS for a 35-day mission. The animals were housed in the mouse Habitat Cage Unit (HCU) in the Japan Aerospace Exploration Agency (JAXA) “Kibo” facility on the ISS. The flight mice lived either under an ambient microgravity condition (µg) or in a centrifugal habitat unit that produced 1 g artificial gravity (µg + 1 g). Habitat control (HC) and vivarium control mice lived on Earth in HCUs or normal vivarium cages, respectively. Quantitative assessment of ocular tissue demonstrated that the µg group induced significant apoptosis in the retina vascular endothelial cells compared to all other groups (p < 0.05) that was 64% greater than that in the HC group. Proteomic analysis showed that many key pathways responsible for cell death, cell repair, inflammation, and metabolic stress were significantly altered in µg mice compared to HC animals. Additionally, there were more significant changes in regulated protein expression in the µg group relative to that in the µg + 1 g group. These data provide evidence that spaceflight induces retinal apoptosis of vascular endothelial cells and changes in retinal protein expression related to cellular structure, immune response and metabolic function, and that artificial gravity (AG) provides some protection against these changes. These retinal cellular responses may affect blood–retinal barrier (BRB) integrity, visual acuity, and impact the potential risk of developing late retinal degeneration.

scholarly journals Negative correlation between endoglin levels and coronary atherosclerosis

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Haibin Chen ◽  
Yiping Wang ◽  
Bing Sun ◽  
Xunxia Bao ◽  
Yu Tang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Atherosclerosis ◽  
Transforming Growth Factor ◽  
Vascular Endothelial Cells ◽  
Expression Profiles ◽  
Receptor Protein ◽  
Inflammatory Factors ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Smad Pathway

Abstract Background Coronary artery disease (CAD) is a common cardiovascular disease, and abnormal blood lipid metabolism is an important risk factor. Transforming growth factor-ß (TGF-ß) and its receptor (TGF-ßR) can inhibit the release of inflammatory factors through the SMAD pathway-mediated immune response, thereby suppressing the progression of CAD. Endoglin (TGF-ßRIII), a TGF-ßR family homologous receptor protein, is directly involved in the immunoregulatory process, but the exact mechanism is unclear. This study aimed to clarify the pathophysiological effects of endoglin on the development of atherosclerosis and to explore the mechanism of the signalling pathway. Methods We downloaded the GEO dataset to perform a functional analysis of SMAD family activity and TGF-ß receptor protein expression in the monocyte expression profiles of patients with familial hyperlipidaemia (FH). The effect of endoglin on endothelial cell proliferation, migration, and apoptosis was examined by disrupting the endoglin gene in human umbilical vein endothelial cells (HUVECs) and validated by western blotting. The related genes and pathways regulated by endoglin were obtained by analysing the sequencing data. Results Research has shown that interference with endoglin can promote the proliferation and migration and significantly inhibit the apoptosis of vascular endothelial cells. Interference with endoglin particularly encourages the expression of VEGFB in vascular endothelial cells. Conclusion The endoglin gene in vascular endothelial cells regulates the PI3K-Akt, Wnt, TNF, and cellular metabolism pathways by activating the SMAD pathway. RAB26, MR1, CCL2, SLC29A4, IBTK, VEGFB, and GOLGA8B play critical roles. Endoglin interacts closely with 11 proteins such as CCL2 and SEPRINE1, which participate in the vital pathway of plaque formation. Interference with endoglin can alter the course of coronary atherosclerosis.

scholarly journals Long Non-Coding RNAs in Cardiac Remodeling

2017 ◽  
Vol 41 (5) ◽  
pp. 1830-1837 ◽  
Author(s):  
Shutong Shen ◽  
Huimin Jiang ◽  
Yihua Bei ◽  
Junjie Xiao ◽  
Xinli Li
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cardiac Remodeling ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Non Coding Rnas

Cardiac remodeling occurs after stress to the heart, manifested as pathological processes, including hypertrophy and apoptosis of cardiomyocytes, dysfunction of vascular endothelial cells and vascular smooth muscle cells as well as differentiation and proliferation of fibroblasts, ultimately resulting in progression of cardiovascular diseases. Emerging evidence has revealed that long non-coding RNAs (lncRNAs) acted as powerful and dynamic modifiers of cardiac remodeling. LncRNAs including Chaer, Chast, Mhrt, CHRF, ROR, H19, and MIAT have been implicated in cardiac hypertrophy while NRF, H19, APF, CARL, UCA, Mhrt and several other lncRNAs (n379599, n379519, n384640, n380433 and n410105) in cardiomyocyte loss and extracellular matrix remodeling. In addition, MALAT1 and TGFB2-OT1 have been reported to contribute to vascular endothelial cells dysfunction while lincRNA-p21 and lnc-Ang362 to vascular smooth muscle cells proliferation. Thus, manipulation of lncRNA expression levels through either the inhibition of disease-up-regulated lncRNAs or increasing disease-down-regulated lncRNAs represents novel therapeutic strategies for cardiac remodeling.

Unique Gene Expression Profiles of Donor-Matched Human Retinal and Choroidal Vascular Endothelial Cells

2007 ◽  
Vol 48 (6) ◽  
pp. 2676 ◽  
Author(s):  
Justine R. Smith ◽  
Dongseok Choi ◽  
Timothy J. Chipps ◽  
Yuzhen Pan ◽  
David O. Zamora ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Vascular Endothelial ◽  
Unique Gene
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