Synthetic Receptors Induce Anti Angiogenic and Stress Signaling on Human First Trimester Cytotrophoblast Cells

Pantho, Ahmed F; Price, Mason H.; Ashraf, Ahm Zuberi; Wajid, Umaima; Khansari, Maryam Emami; Jahan, Afsana; Afroze, Syeda H.; Rhaman, Mhahabubur; Johnson, Corey R.; Kuehl, Thomas J.; Hossain, Md. Alamgir; Uddin, Mohammad Nasir

doi:10.3390/ijerph14050517

“…Furthermore, MBG has been shown to regulate the permeability and gene expression of human brain microvascular endothelial cells in culture [31], increasing the interest in evaluating the possible role of MBG in cerebrovascular and other related vascular disease conditions. Recent studies have investigated the roles of MBG in angiogenic and stress signaling [32], modulation of oxidative stress [33] and neuroinflammation [11]. These findings support the earlier hypothesis that MBG activates endothelial NADPH oxidase [34].…”

Section: Discussionsupporting

confidence: 79%

Plasma Levels of the Cardiotonic Steroid Marinobufagenin in Ischemic Stroke Survivors and Treated Hypertensives: A Pilot Study

Estapé

¹

,

González-Sepúlveda

²

,

Wei

³

et al. 2018

Int Arch Transl Med

0

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Background: Numerous studies have demonstrated a strong relationship between circulating levels of marinobufagenin (MBG) and salt-sensitivity. Since salt-sensitive hypertensives have increased plasma levels of MBG and are known to be at a higher risk of having cardiovascular events, stroke and increased mortality, we evaluated the possibility of an association between MBG and ischemic stroke. In this pilot study, we determined plasma MBG levels in patients after surviving an ischemic stroke compared to similar age and gender groups of treated hypertensives and normotensive controls. Methods: We measured plasma MBG levels in a total of 40 participants subdivided into three groups: After an ischemic stroke STR (n = 13), participants with a diagnosis of hypertension receiving blood pressure medication HT (n = 14) and normotensive control subjects CTL (n = 13). We used inferential statistics (parametric or non-parametric) and ordered logistic regression models (unadjusted and adjusted) and all statistical analyses were performed using Stata 14. Results: We did not include a subject from the CTL group because of a diagnosis of glucose-6-phosphate dehydrogenase deficiency and an extreme plasma MBG value of 2,246 pmol/L. Participants’ mean age was 60.4 ± 11.5 years; 56% were male. There was no significant difference between study groups (p > 0.05) for gender, age, and body mass index. HbA1c levels were significantly higher in the STR as compared to the CTL p < 0.05). In the STR group MBG levels were below the normal range (< 200 pmol/L) in three (23%), eight (61%) were in the normal range (200–400 pmol/L), while two (16%) had increased MBG values (> 400 pmol/L). Also, among the STR, the plasma MBG levels did not differ between those receiving and not receiving thrombolytic therapy (p > 0.05). From the 14 HT participants, six (43%) had MBG plasma levels within the normal range, and eight (57%) had high concentrations (> 400 pmol/L). Four (29%) of the treated hypertensives had extreme MBG levels (> 1,000 pmol/L) and normal values of blood pressure. Conclusion: There was no significant elevation of plasma MBG in survivors 24 h or more after an ischemic stroke. The extreme values of plasma MBG in 29% of the treated hypertensives suggests the presence of salt-sensitivity and a possible side effect of a specific combination of medications. Both of these findings contribute new knowledge to the design of studies to define if there is an MBG molecular mechanism underlying the complex associations among salt-sensitivity, hypertension, and ischemic stroke.

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“…Furthermore, MBG has been shown to regulate the permeability and gene expression of human brain microvascular endothelial cells in culture [31], increasing the interest in evaluating the possible role of MBG in cerebrovascular and other related vascular disease conditions. Recent studies have investigated the roles of MBG in angiogenic and stress signaling [32], modulation of oxidative stress [33] and neuroinflammation [11]. These findings support the earlier hypothesis that MBG activates endothelial NA-DPH oxidase [34].…”

Section: Discussionsupporting

confidence: 76%

Untitled

2018

Int Arch Transl Med

0

View full text Add to dashboard Cite

Background: Numerous studies have demonstrated a strong relationship between circulating levels of marinobufagenin (MBG) and salt-sensitivity. Since salt-sensitive hypertensives have increased plasma levels of MBG and are known to be at a higher risk of having cardiovascular events, stroke and increased mortality, we evaluated the possibility of an association between MBG and ischemic stroke. In this pilot study, we determined plasma MBG levels in patients after surviving an ischemic stroke compared to similar age and gender groups of treated hypertensives and normotensive controls. Methods:We measured plasma MBG levels in a total of 40 participants subdivided into three groups: After an ischemic stroke STR (n = 13), participants with a diagnosis of hypertension receiving blood pressure medication HT (n = 14) and normotensive control subjects CTL (n = 13). We used inferential statistics (parametric or non-parametric) and ordered logistic regression models (unadjusted and adjusted) and all statistical analyses were performed using Stata 14.

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“…11,12 In the study of early pregnancy termination induced by artificial embryonic stem cells, researchers found that artificial embryonic stem cells may have anti-angiogenic effects. 13 Other studies have demonstrated that PAB can inhibit HUVEC proliferation and downregulate the expression of VEGF and HIF1α. 14,15 Therefore, the first part of this paper aims to explore the role of PAB in ESCC and its effect on the angiogenesis.…”

Section: Introductionmentioning

confidence: 97%

<p>Pseudolaric Acid B Inhibits Proliferation, Invasion, and Angiogenesis in Esophageal Squamous Cell Carcinoma Through Regulating CD147</p>

Yin

¹

,

Cai

²

,

Wang

³

et al. 2020

DDDT

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Background Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor of the digestive system. Studies have shown that pseudolaric acid B (PAB) has several pharmacological effects like anti-microtubule, anti-angiogenesis, and antitumor functions, while the effect and mechanism of PAB on esophageal cancer are still unclear. This study was designed to investigate the effects of PAB on ESCC. Methods To study the effects of PAB on the biological function through a series of in vitro and in vivo experiments. Results The results revealed that PAB inhibited the proliferation, invasion, and migration, but promoted the apoptosis of ESCC. Moreover, PAB restrained the growth of cancer cells in vivo and inhibited the angiogenesis of HUVEC in mice with ESCC. CD147 expression was increased in the esophageal squamous cell lines, and interference with CD147 hindered the proliferation, invasion, and migration of ESCC cells, and inhibited the growth and angiogenesis of the esophageal squamous cell line. PAB reduced the expression of CD147 in vivo and in vitro. The expression of MMP2, 3, and 9 was increased after overexpression of CD147, which provided the opportunity to reverse the role of PAB in inhibiting proliferation, invasion, migration, and angiogenesis of ESCC. Discussion The results revealed that PAB inhibited the proliferation, invasion, migration, and angiogenesis of ESCC in vitro and in vivo by CD147. PAB is a promising monomer for therapy of ESCC, providing references for future research on ESCC treatment.

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Synthetic Receptors Induce Anti Angiogenic and Stress Signaling on Human First Trimester Cytotrophoblast Cells

Cited by 5 publications

References 60 publications

Plasma Levels of the Cardiotonic Steroid Marinobufagenin in Ischemic Stroke Survivors and Treated Hypertensives: A Pilot Study

Plasma Levels of the Cardiotonic Steroid Marinobufagenin in Ischemic Stroke Survivors and Treated Hypertensives: A Pilot Study

Untitled

<p>Pseudolaric Acid B Inhibits Proliferation, Invasion, and Angiogenesis in Esophageal Squamous Cell Carcinoma Through Regulating CD147</p>

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