Role of Slit2/Robo1 in trophoblast invasion and vascular remodeling during ectopic tubal pregnancy

In humans, pregnancy maintenance depends on normal placental formation following trophoblast invasion into the endometrium and vascular remodeling. In the early stages of pregnancy, immune tolerance, inflammatory response and adaptation to hypoxia need to be precisely regulated in the placental microenvironment. Various types of cells, such as trophoblasts, endothelial cells, immune cells, mesenchymal stem cells (MSCs) and adipocytes, induce normal placental development via intercellular interactions through soluble factors. Extracellular vesicles (EVs) are used to diagnose various diseases because their constituents vary depending on the type of cell of origin and pathological characteristics. EV-derived microRNAs (miRNAs) and proteins in the placenta regulate inflammatory responses and the invasion of trophoblasts through intercellular delivery in the placental microenvironment. If the placenta does not adapt to the changed environment during early pregnancy, pregnancy disorders such as pre-eclampsia, preterm birth and gestational diabetes mellitus can occur. Thus, the important roles of EVs during pregnancy and development is fast emerging. This review describes the physiological role of EVs during placentation and their composition in the human placenta. It also suggests the possibility of finding EV markers that can diagnose pregnancy disorders. Furthermore, it describes the properties of EVs that affect pregnancy in livestock.

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A review of the mechanism for poor placentation in early-onset preeclampsia: the role of autophagy in trophoblast invasion and vascular remodeling

Journal of Reproductive Immunology ◽

10.1016/j.jri.2013.06.002 ◽

2014 ◽

Vol 101-102 ◽

pp. 80-88 ◽

Cited By ~ 102

Author(s):

Shigeru Saito ◽

Akitoshi Nakashima

Keyword(s):

Early Onset ◽

Vascular Remodeling ◽

Trophoblast Invasion ◽

Early Onset Preeclampsia

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Role of vip in trophoblast invasion, vascular remodeling and immunomodulation during early pregnancy

Placenta ◽

10.1016/j.placenta.2017.07.146 ◽

2017 ◽

Vol 57 ◽

pp. 267 ◽

Cited By ~ 1

Author(s):

Daniel Paparini ◽

Ruhul Choudhury ◽

Sarah Fin-Sell ◽

Magda Karolczack-Bayatti ◽

Daiana Vota ◽

...

Keyword(s):

Early Pregnancy ◽

Vascular Remodeling ◽

Trophoblast Invasion

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Endothelial cell-related autophagic pathways in Sugen/hypoxia-exposed pulmonary arterial hypertensive rats

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00527.2016 ◽

2017 ◽

Vol 313 (5) ◽

pp. L899-L915 ◽

Cited By ~ 8

Author(s):

Fumiaki Kato ◽

Seiichiro Sakao ◽

Takao Takeuchi ◽

Toshio Suzuki ◽

Rintaro Nishimura ◽

...

Keyword(s):

Flow Cytometry ◽

Endothelial Cell ◽

Vascular Remodeling ◽

Time Dependent ◽

Causative Role ◽

Dependent Manner ◽

Vascular Endothelial ◽

Pulmonary Vascular Remodeling ◽

Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is characterized by progressive obstructive remodeling of pulmonary arteries. However, no reports have described the causative role of the autophagic pathway in pulmonary vascular endothelial cell (EC) alterations associated with PAH. This study investigated the time-dependent role of the autophagic pathway in pulmonary vascular ECs and pulmonary vascular EC kinesis in a severe PAH rat model (Sugen/hypoxia rat) and evaluated whether timely induction of the autophagic pathway by rapamycin improves PAH. Hemodynamic and histological examinations as well as flow cytometry of pulmonary vascular EC-related autophagic pathways and pulmonary vascular EC kinetics in lung cell suspensions were performed. The time-dependent and therapeutic effects of rapamycin on the autophagic pathway were also assessed. Sugen/hypoxia rats treated with the vascular endothelial growth factor receptor blocker SU5416 showed increased right ventricular systolic pressure (RVSP) and numbers of obstructive vessels due to increased pulmonary vascular remodeling. The expression of the autophagic marker LC3 in ECs also changed in a time-dependent manner, in parallel with proliferation and apoptotic markers as assessed by flow cytometry. These results suggest the presence of cross talk between pulmonary vascular remodeling and the autophagic pathway, especially in small vascular lesions. Moreover, treatment of Sugen/hypoxia rats with rapamycin after SU5416 injection activated the autophagic pathway and improved the balance between cell proliferation and apoptosis in pulmonary vascular ECs to reduce RVSP and pulmonary vascular remodeling. These results suggested that the autophagic pathway can suppress PAH progression and that rapamycin-dependent activation of the autophagic pathway could ameliorate PAH.

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The role of ATG-7 contributes to pulmonary hypertension by impacting vascular remodeling

Journal of Molecular and Cellular Cardiology ◽

10.1016/j.yjmcc.2021.03.013 ◽

2021 ◽

Author(s):

Xi Yang ◽

Li Zhang ◽

Jian-qiang Ye ◽

Xiao-hui Wu ◽

Xi-xi Zeng ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Vascular Remodeling

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Role of NF-κB in Flow-Induced Vascular Remodeling

Antioxidants and Redox Signaling ◽

10.1089/ars.2008.2393 ◽

2009 ◽

Vol 11 (7) ◽

pp. 1641-1649 ◽

Cited By ~ 31

Author(s):

Yves Castier ◽

Bhama Ramkhelawon ◽

Stéphanie Riou ◽

Alain Tedgui ◽

Stephanie Lehoux

Keyword(s):

Vascular Remodeling

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Role of Endothelial Shear Stress in the Natural History of Coronary Atherosclerosis and Vascular Remodeling

Journal of the American College of Cardiology ◽

10.1016/j.jacc.2007.02.059 ◽

2007 ◽

Vol 49 (25) ◽

pp. 2379-2393 ◽

Cited By ~ 807

Author(s):

Yiannis S. Chatzizisis ◽

Ahmet Umit Coskun ◽

Michael Jonas ◽

Elazer R. Edelman ◽

Charles L. Feldman ◽

...

Keyword(s):

Shear Stress ◽

Natural History ◽

Vascular Remodeling ◽

Coronary Atherosclerosis ◽

History Of ◽

Endothelial Shear Stress

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The role of vascular remodeling and inflammation in the pathogenesis of intracranial aneurysms

Journal of Clinical Neuroscience ◽

10.1016/j.jocn.2013.07.004 ◽

2014 ◽

Vol 21 (1) ◽

pp. 28-32 ◽

Cited By ~ 45

Author(s):

David L. Penn ◽

Samantha R. Witte ◽

Ricardo J. Komotar ◽

E. Sander Connolly

Keyword(s):

Vascular Remodeling ◽

Intracranial Aneurysms

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MiR-22-3p Suppresses Vascular Remodeling and Oxidative Stress by Targeting CHD9 during the Development of Hypertension

Journal of Vascular Research ◽

10.1159/000514311 ◽

2021 ◽

pp. 1-11

Author(s):

Hanqing Chen ◽

Xiru Xu ◽

Zhengqing Liu ◽

Yong Wu

Keyword(s):

Oxidative Stress ◽

Vascular Remodeling ◽

Underlying Mechanism ◽

Inhibitory Effect ◽

Spontaneously Hypertensive ◽

Aortic Smooth Muscle ◽

Phenotype Switch ◽

And Oxidative Stress

Hypertension is considered a risk factor for a series of systematic diseases. Known factors including genetic predisposition, age, and diet habits are strongly associated with the initiation of hypertension. The current study aimed to investigate the role of miR-22-3p in hypertension. In this study, we discovered that the miR-22-3p level was significantly decreased in the thoracic aortic vascular tissues and aortic smooth muscle cells (ASMCs) of spontaneously hypertensive rats. Functionally, the overexpression of miR-22-3p facilitated the switch of ASMCs from the synthetic to contractile phenotype. To investigate the underlying mechanism, we predicted 11 potential target mRNAs for miR-22-3p. After screening, chromodomain helicase DNA-binding 9 (CHD9) was validated to bind with miR-22-3p. Rescue assays showed that the co-overexpression of miR-22-3p and CHD9 reversed the inhibitory effect of miR-22-3p mimics on cell proliferation, migration, and oxidative stress in ASMCs. Finally, miR-22-3p suppressed vascular remodeling and oxidative stress in vivo. Overall, miR-22-3p regulated ASMC phenotype switch by targeting CHD9. This new discovery provides a potential insight into hypertension treatment.

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