Expressions and Roles of AMIGO Gene Family in Vascular Endothelial Cells

Hossain, Sharmin; Ahmed, Minhaz Uddin; Alam, Shamiul; Watanabe, Akuo; Harashima, Ai; Yonekura, Hideto; Yamamoto, Hiroshi

doi:10.7763/ijbbb.2012.v2.58

Cited by 4 publications

(4 citation statements)

References 9 publications

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“…Additionally, we saw upregulation of genes associated with angiogenesis and vascular sprouting, such as Ccl5 (Rantes), Tnf, Tspan18, and Amigo2, which is known to protect vascular ECs that are undergoing oxidative stress. [ 37–40 ] This data is reflective of the neovascularization modulation seen in acute MI in which the iECM upregulated genes such as Vegfa, Bmp7, Nrg1, and Fgf2 via NanoString analysis. [ 12 ] These mechanisms may provide insight into the interaction between iECM and vascular repair.…”

Section: Resultsmentioning

confidence: 94%

Infusible Extracellular Matrix Biomaterial Promotes Vascular Integrity and Modulates the Inflammatory Response in Acute Traumatic Brain Injury

Diaz

Kandell

et al. 2023

Adv Healthcare Materials

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Traumatic brain injury (TBI) affects millions of people each year and, in many cases, results in long‐term disabilities. Once a TBI has occurred, there is a significant breakdown of the blood−brain barrier resulting in increased vascular permeability and progression of the injury. In this study, the use of an infusible extracellular matrix‐derived biomaterial (iECM) for its ability to reduce vascular permeability and modulate gene expression in the injured brain is investigated. First, the pharmacokinetics of iECM administration in a mouse model of TBI is characterized, and the robust accumulation of iECM at the site of injury is demonstrated. Next, it is shown that iECM administration after injury can reduce the extravasation of molecules into the brain, and in vitro, iECM increases trans‐endothelial electrical resistance across a monolayer of TNFα‐stimulated endothelial cells. In gene expression analysis of brain tissue, iECM induces changes that are indicative of downregulation of the proinflammatory response 1‐day post‐injury/treatment and neuroprotection at 5 days post‐injury/treatment. Therefore, iECM shows potential as a treatment for TBI.

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Section: Resultsmentioning

confidence: 94%

Infusible Extracellular Matrix Biomaterial Promotes Vascular Integrity and Modulates the Inflammatory Response in Acute Traumatic Brain Injury

Diaz

Kandell

et al. 2023

Adv Healthcare Materials

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“…It has been reported that in ECs and in gastric adenocarcinoma cell lines the inhibition of AMIGO2 affected the ability to adhere to extracellular matrix components ( 34 , 36 ). Moreover, Hossain et al demonstrated the presence of AMIGO2 in human microvascular ECs and pericytes, pointing to an interaction between these cells in vascular remodeling ( 58 ). In mechanically stressed SVPs the up-regulation of AMIGO2 could confer a firmer adhesion to adhesion substrates but also enhance their sensitivity to modifications of the extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

Mechanical Strain Induces Transcriptomic Reprogramming of Saphenous Vein Progenitors

Maselli

Garoffolo

Cassanmagnago

et al. 2022

Front. Cardiovasc. Med.

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Intimal hyperplasia is the leading cause of graft failure in aortocoronary bypass grafts performed using human saphenous vein (SV). The long-term consequences of the altered pulsatile stress on the cells that populate the vein wall remains elusive, particularly the effects on saphenous vein progenitors (SVPs), cells resident in the vein adventitia with a relatively wide differentiation capacity. In the present study, we performed global transcriptomic profiling of SVPs undergoing uniaxial cyclic strain in vitro. This type of mechanical stimulation is indeed involved in the pathology of the SV. Results showed a consistent stretch-dependent gene regulation in cyclically strained SVPs vs. controls, especially at 72 h. We also observed a robust mechanically related overexpression of Adhesion Molecule with Ig Like Domain 2 (AMIGO2), a cell surface type I transmembrane protein involved in cell adhesion. The overexpression of AMIGO2 in stretched SVPs was associated with the activation of the transforming growth factor β pathway and modulation of intercellular signaling, cell-cell, and cell-matrix interactions. Moreover, the increased number of cells expressing AMIGO2 detected in porcine SV adventitia using an in vivo arterialization model confirms the upregulation of AMIGO2 protein by the arterial-like environment. These results show that mechanical stress promotes SVPs' molecular phenotypic switching and increases their responsiveness to extracellular environment alterations, thus prompting the targeting of new molecular effectors to improve the outcome of bypass graft procedure.

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“…AMIGO2 is a leucine‐rich repeat (LRR)‐containing cell adhesion molecule initially identified as a neurite outgrowth factor. 11 , 12 Further investigations suggest that AMIGO2 is implicated in neuronal survival and regulation, 13 vascular development and angiogenesis, 14 , 15 as well as ischemia protection and immune regulation. 16 , 17 Recently, AMIGO2 has been found to play a potential etiologic role in carcinogenesis and tumour progression.…”

Section: Introductionmentioning

confidence: 99%

AMIGO2 attenuates innate cisplatin sensitivity by suppression of GSDME‐conferred pyroptosis in non‐small cell lung cancer

Chen

Lin

Xie

et al. 2023

J Cellular Molecular Medi

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Non‐small cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer. Cisplatin is commonly used in the treatment of many malignant tumours including NSCLC. The innate drug sensitivity greatly affects the clinical efficacy of cisplatin‐based chemotherapy. As a plasma membrane adhesion molecule, amphoterin‐induced gene and ORF‐2 (AMIGO2) initially identified as a neurite outgrowth factor has been recently found to play a crucial role in cancer occurrence and progression. However, it is still unclear whether AMIGO2 is involved in innate cisplatin sensitivity. In the present study, we provided the in vitro and in vivo evidences indicating that the alteration of AMIGO2 expression triggered changes of innate cisplatin sensitivity as well as cisplatin‐induced pyroptosis in NSCLC. Further results revealed that AMIGO2 might inhibit cisplatin‐induced activation of (caspase‐8 and caspase‐9)/caspase‐3 via stimulating PDK1/Akt (T308) signalling axis, resulting in suppression of GSDME cleavage and the subsequent cell pyroptosis, thereby decreasing the sensitivity of NSCLC cells to cisplatin treatment. The results provided a new insight that AMIGO2 regulated the innate cisplatin sensitivity of NSCLC through GSDME‐mediated pyroptosis.

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Expressions and Roles of AMIGO Gene Family in Vascular Endothelial Cells

Cited by 4 publications

References 9 publications

Infusible Extracellular Matrix Biomaterial Promotes Vascular Integrity and Modulates the Inflammatory Response in Acute Traumatic Brain Injury

Infusible Extracellular Matrix Biomaterial Promotes Vascular Integrity and Modulates the Inflammatory Response in Acute Traumatic Brain Injury

Mechanical Strain Induces Transcriptomic Reprogramming of Saphenous Vein Progenitors

AMIGO2 attenuates innate cisplatin sensitivity by suppression of GSDME‐conferred pyroptosis in non‐small cell lung cancer

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