scholarly journals Small GTP-Binding Protein GDP Dissociation Stimulator Prevents Thoracic Aortic Aneurysm Formation and Rupture by Phenotypic Preservation of Aortic Smooth Muscle Cells

Circulation ◽  
2018 ◽  
Vol 138 (21) ◽  
pp. 2413-2433 ◽  
Author(s):  
Masamichi Nogi ◽  
Kimio Satoh ◽  
Shinichiro Sunamura ◽  
Nobuhiro Kikuchi ◽  
Taijyu Satoh ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Thoracic Aortic Aneurysm ◽  
Muscle Cells ◽  
Gtp Binding Protein ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Aneurysm Formation ◽  
Gtp Binding

Vasopressin activates phospholipase D through pertussis toxin-insensitive GTP-binding protein in aortic smooth muscle cells: function of Ca2+/calmodulin

1995 ◽  
Vol 73 (3-4) ◽  
pp. 191-199 ◽  
Author(s):  
Masaichi Miwa ◽  
Atsushi Suzuki ◽  
Yasuko Watanabe ◽  
Junji Shinoda ◽  
Yutaka Oiso ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Phospholipase D ◽  
Pertussis Toxin ◽  
Binding Protein ◽  
Muscle Cells ◽  
Gtp Binding Protein ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Gtp Binding

In the present study, we examined the effect of vasopressin (AVP) on phosphatidylcholine-hydrolyzing phospholipase D activity in primary cultured rat aortic smooth muscle cells. AVP stimulation of choline formation was dose dependent. The time-course was quite different from those of inositol phosphates. The effect of AVP on the formation of inositol phosphates (EC50 was 3 nM) was more potent than that on the formation of choline (EC50 was 30 nM). 12-O-Tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C (PKC), stimulated the formation of choline. However, 4α-phorbol 12,13-didecanoate, which is inactive for PKC, had little effect. Staurosporine, an inhibitor of protein kinases, which inhibited the TPA-induced formation of choline, had little effect on the AVP-induced formation of choline. Neither calphostin C, a highly specific PKC inhibitor, nor PKC down-regulation with TPA affected AVP-induced formation of choline. A combination of AVP and TPA additively stimulated the formation of choline. The depletion of extracellular Ca2+ by (ethylenebis(oxyethylenenitrilo))tetraacetic acid significantly reduced the AVP-induced formation of choline. W-7, an antagonist of calmodulin, inhibited the AVP-induced formation of choline in a dose-dependent manner. NaF, an activator for GTP-binding protein (G-protein), stimulated the formation of choline. However, the formation of choline by a combination of AVP and NaF was not additive. Pertussis toxin had little effect on the AVP-induced formation of choline. These results strongly suggest that AVP stimulates phospholipase D in a Ca2+/calmodulin-dependent manner in aortic smooth muscle cells, that a pertussis-toxin-insensitive G-protein is involved in the AVP-induced phospholipase D activation, and furthermore, that PKC is not essential for the activation.Key words: vasopressin, phospholipase D, protein kinase C, calmodulin, GTP-binding protein, aortic smooth muscle cells.

scholarly journals LncRNA LOXL1-AS is up-regulated in thoracic aortic aneurysm and regulated proliferation and apoptosis of aortic smooth muscle cells

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Ben Huang ◽  
Shuyang Lu ◽  
Hao Lai ◽  
Jun Li ◽  
Yongxin Sun ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Thoracic Aortic Aneurysm ◽  
Muscle Cells ◽  
Healthy Controls ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Proliferation And Apoptosis ◽  
Aortic Media

Abstract Long non-coding RNA LOXL1-AS is up-regulated in several types of cancers. The present study was carried out to explore the potential interactions between LOXL1-AS and lncRNA Giver in thoracic aortic aneurysm (TAA). We found that LOXL1-AS was up-regulated in TAA patients than in healthy controls in aortic media specimens. Altered expression levels of LOXL1-AS distinguished TAA patients from healthy controls. LncRNA Giver was also up-regulated in TAA patients than in healthy controls in aortic media specimens, and was positively correlated with LOXL1-AS. LOXL1-AS overexpression mediated the up-regulation of Giver in human aortic smooth muscle cells, while Giver overexpression failed to significantly affect LOXL1-AS. LOXL1-AS and Giver overexpression resulted in promoted proliferation and inhibited apoptosis of HAOSMC. Giver silencing played an opposite role and attenuated the effect of LOXL1-AS overexpression. Therefore, LOXL1-AS was up-regulated in TAA and regulated proliferation and apoptosis of LOXL1-AS by up-regulating Giver.

Active cytomegalovirus infection in aortic smooth muscle cells from patients with abdominal aortic aneurysm

2008 ◽  
Vol 87 (4) ◽  
pp. 347-356 ◽  
Author(s):  
Sara Gredmark-Russ ◽  
Mensur Dzabic ◽  
Afsar Rahbar ◽  
Anders Wanhainen ◽  
Martin Björck ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Cytomegalovirus Infection ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Abdominal Aortic
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