Optical coherence tomography in patients with  somatotropin-producing pituitary adenoma

Optical coherence tomography (OCT) is widely used in ophthalmological practice. The review presents the results of OCT in patients with somatotropin-producing pituitary adenoma, or somatotropinoma, which is a hormone-active tumor of the adenohypophysis, characterized by excessive production of somatotropic hormone (STH). It stimulates the secretion of type I insulin-like growth factor (IGF-I). The mechanisms of STH action (pro-angiogenic action, stimulation endothelial cell proliferation and migration, development of endothelial dysfunction and retinal edema) requires much attention to the results of examination of patients with somatotropinomas using modern diagnostic methods, such as OCT.

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SnoN facilitates ALK1–Smad1/5 signaling during embryonic angiogenesis

The Journal of Cell Biology ◽

10.1083/jcb.201208113 ◽

2013 ◽

Vol 202 (6) ◽

pp. 937-950 ◽

Cited By ~ 10

Author(s):

Qingwei Zhu ◽

Yong Hwan Kim ◽

Douglas Wang ◽

S. Paul Oh ◽

Kunxin Luo

Keyword(s):

Endothelial Cells ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Negative Regulator ◽

Endothelial Cell Proliferation ◽

Type I ◽

Positive Role ◽

And Migration ◽

Proliferation And Migration

In endothelial cells, two type I receptors of the transforming growth factor β (TGF-β) family, ALK1 and ALK5, coordinate to regulate embryonic angiogenesis in response to BMP9/10 and TGF-β. Whereas TGF-β binds to and activates ALK5, leading to Smad2/3 phosphorylation and inhibition of endothelial cell proliferation and migration, BMP9/10 and TGF-β also bind to ALK1, resulting in the activation of Smad1/5. SnoN is a negative regulator of ALK5 signaling through the binding and repression of Smad2/3. Here we uncover a positive role of SnoN in enhancing Smad1/5 activation in endothelial cells to promote angiogenesis. Upon ligand binding, SnoN directly bound to ALK1 on the plasma membrane and facilitated the interaction between ALK1 and Smad1/5, enhancing Smad1/5 phosphorylation. Disruption of this SnoN–Smad interaction impaired Smad1/5 activation and up-regulated Smad2/3 activity. This resulted in defective angiogenesis and arteriovenous malformations, leading to embryonic lethality at E12.5. Thus, SnoN is essential for TGF-β/BMP9-dependent biological processes by its ability to both positively and negatively modulate the activities of Smad-dependent pathways.

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Faculty Opinions recommendation of HLA class I molecules partner with integrin β4 to stimulate endothelial cell proliferation and migration.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.7711957.8463067 ◽

2011 ◽

Author(s):

Arthur Mercurio

Keyword(s):

Cell Proliferation ◽

Endothelial Cell ◽

Hla Class I ◽

Class I ◽

Endothelial Cell Proliferation ◽

Cell Proliferation And Migration ◽

Hla Class I Molecules ◽

Integrin Β4 ◽

And Migration ◽

Proliferation And Migration

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Bioinformatics-based approach for identifying peptide inhibitors of endothelial cell proliferation and migration

Science-Business eXchange ◽

10.1038/scibx.2008.788 ◽

2008 ◽

Vol 1 (32) ◽

pp. 788-788

Keyword(s):

Cell Proliferation ◽

Endothelial Cell ◽

Peptide Inhibitors ◽

Endothelial Cell Proliferation ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

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TIMP-2-derived 18-mer peptide inhibits endothelial cell proliferation and migration through cAMP/PKA-dependent mechanism

Cancer Letters ◽

10.1016/j.canlet.2013.10.037 ◽

2014 ◽

Vol 343 (2) ◽

pp. 210-216 ◽

Cited By ~ 19

Author(s):

Hyeon-Ju Kim ◽

Young-Rak Cho ◽

Soo Hyeon Kim ◽

Dong-Wan Seo

Keyword(s):

Cell Proliferation ◽

Endothelial Cell ◽

Endothelial Cell Proliferation ◽

Cell Proliferation And Migration ◽

And Migration ◽

Dependent Mechanism ◽

Proliferation And Migration

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miR-27b Suppresses Endothelial Cell Proliferation and Migration by Targeting Smad7 in Kawasaki Disease

Cellular Physiology and Biochemistry ◽

10.1159/000492354 ◽

2018 ◽

Vol 48 (4) ◽

pp. 1804-1814 ◽

Cited By ~ 9

Author(s):

Xing Rong ◽

Donghui Ge ◽

Danping Shen ◽

Xianda Chen ◽

Xuliang Wang ◽

...

Keyword(s):

Endothelial Cell ◽

Kawasaki Disease ◽

Therapeutic Target ◽

Umbilical Vein ◽

Luciferase Reporter ◽

Endothelial Cell Proliferation ◽

Cell Functions ◽

Potential Biomarker ◽

And Migration ◽

Proliferation And Migration

Background/Aims: Increasing evidence indicates that microRNAs (miRNAs) play important roles in Kawasaki disease (KD). Our previous study demonstrated that hsa-miR-27b-3p (miR-27b) was up-regulated in KD serum. However, the specific role of miR-27b in KD remains unclear. We aimed to investigate that miR-27b could be a biomarker and therapeutic target for KD treatment. As well, the specific mechanism of miR-27b effecting endothelial cell functions was studied. Methods: The expression of miR-27b and Smad7 was measured by qRT-PCR. Gain-of-function strategy was used to observe the effect of miR-27b on human umbilical vein endothelial cells (HUVECs) proliferation and migration. Bioinformatics analyses were applied to predict miR-27b targets and then we verified Smad7 by a luciferase reporter assay. Western blot was performed to detect the protein expression of Smad7, PCNA, MMP9, MMP12 and TGF-β-related genes. Results: We confirmed that miR-27b was shown to be dramatically up-regulated in KD serum and KD serum-treated HUVECs and that elevated expression of miR-27b suppressed the proliferation and migration of HUVECs. Furthermore, our results verified that miR-27b mediated cell functions by affecting the TGF-β via targeting Smad7 in HUVECs. Conclusion: These results suggested that up-regulated miR-27b had a protective role in HUVECs proliferation and migration via targeting Smad7 and affecting TGF-β pathway. Therefore, miR-27b represented a potential biomarker for KD and may serve as a promising therapeutic target for KD treatment.

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