Role of GADD153 (growth arrest- and DNA damage-inducible gene 153) in vascular smooth muscle cell apoptosis

2001 ◽  
Vol 100 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Michiya IGASE ◽  
Takafumi OKURA ◽  
Michitsugu NAKAMURA ◽  
Yasunori TAKATA ◽  
Yutaka KITAMI ◽  
...  
Keyword(s):  
Dna Damage ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Molecular Mechanisms ◽  
Growth Arrest ◽  
Cell Contact ◽  
Inducible Gene

GADD153 (growth arrest- and DNA damage-inducible gene 153) is expressed at very low levels in growing cells, but is markedly induced in response to a variety of cellular stresses, including glucose deprivation, exposure to genotoxic agents and other growth-arresting situations. Forced expression of GADD153 induces cell cycle arrest in many types of cells. It is also reported that GADD153 is directly associated with apoptosis. Recently we have reported that platelet-derived growth factor (PDGF)-BB induces apoptosis in cultured vascular smooth muscle cells (VSMC), but only when 100% confluency is reached. These results suggested that cell–cell contact inhibition (cell growth arrest) may be a critical factor for induction of VSMC apoptosis by PDGF-BB. In the present study, we explored the role of GADD153, one of a number of growth-arrest-related gene products, in the molecular mechanisms of VSMC apoptosis in vitro and in vivo. GADD153 was markedly induced at both the mRNA and protein levels, in parallel with the induction of VSMC apoptosis, after treatment with PDGF-BB. Moreover, overexpression of GADD153 in VSMC significantly reduced cell viability and induced apoptosis. In the carotid artery balloon injury model in rats, GADD153 protein was expressed in apoptotic VSMC which were positively stained by in situ DNA labelling. These results demonstrate an important role for GADD153 in the molecular mechanisms of VSMC apoptosis.

Role of GADD153 (growth arrest- and DNA damage-inducible gene 153) in vascular smooth muscle cell apoptosis

2001 ◽  
Vol 100 (3) ◽  
pp. 275 ◽  
Author(s):  
Michiya IGASE ◽  
Takafumi OKURA ◽  
Michitsugu NAKAMURA ◽  
Yasunori TAKATA ◽  
Yutaka KITAMI ◽  
...  
Keyword(s):  
Dna Damage ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cell Apoptosis ◽  
Growth Arrest ◽  
Muscle Cell Apoptosis ◽  
Inducible Gene

scholarly journals Induction of the growth arrest and DNA damage-inducible gene GADD153 by cisplatin in vitro and in vivo

1994 ◽  
Vol 70 (6) ◽  
pp. 1102-1106 ◽  
Author(s):  
DP Gately ◽  
JA Jones ◽  
R Christen ◽  
RM Barton ◽  
G Los ◽  
...  
Keyword(s):  
Dna Damage ◽  
Growth Arrest ◽  
Inducible Gene

scholarly journals Anti-Inflammatory Role of Cilostazol in Vascular Smooth Muscle Cells In vitro and In vivo

2010 ◽  
Vol 17 (5) ◽  
pp. 503-509 ◽  
Author(s):  
Chie Aoki ◽  
Yoshiyuki Hattori ◽  
Atsuko Tomizawa ◽  
Teruo Jojima ◽  
Kikuo Kasai
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Anti Inflammatory

Role of Na(+)-Ca2+ exchange in the regulation of vascular smooth muscle tension

1993 ◽  
Vol 264 (4) ◽  
pp. H1028-H1040 ◽  
Author(s):  
E. D. Motley ◽  
R. J. Paul ◽  
M. A. Matlib
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Nerve Terminal ◽  
Muscle Tension ◽  
Second Phase ◽  
Nerve Terminals ◽  
Free Solution

To determine the role of the Na(+)-Ca2+ exchange systems of nerve terminal and sarcolemmal membrane on development of tension in rabbit aortic rings, internal or external Na+ concentration was changed with either ouabain or Na(+)-free solution, respectively. Ouabain produced a verapamil-insensitive but external Na(+)- and Ca(2+)-dependent biphasic tension with distinct lag periods both of which were shortened by depolarization with KCl. The first phase of tension was inhibited by prazosin, phentolamine, in vitro neurolysis with 6-hydroxydopamine and in vivo treatment with reserpine to deplete catecholamines in nerve terminals. Therefore, first phase of tension was attributed to catecholamines released from nerve terminals induced by increased axoplasmic Ca2+ concentration mediated by the neural Na(+)-Ca2+ exchanger due to the increased axoplasmic Na+ concentration resulting from inhibition of the Na(+)-Ka+ pump with ouabain. In the absence of the first phase of tension, the second phase of tension was enhanced by caffeine, presumably by preventing sequestration of the sarcolemmal Na(+)-Ca2+ exchanger-mediated increase in cytosolic Ca2+ concentration in vascular smooth muscle cells. The prazosin-insensitive tension was dependent on the external Na+ concentration and was also attributed to the sarcolemmal Na(+)-Ca2+ exchanger of vascular smooth muscle. The magnitude of the increase in tension with ouabain or Na(+)-free solution attributed to the sarcolemmal Na(+)-Ca2+ exchanger of vascular smooth muscle was larger than that mediated by the exchanger of the nerve terminal. It was concluded that the Na(+)-Ca2+ exchange systems of both the nerve terminal and the vascular smooth muscle sarcolemma contribute to the development of tension by different mechanisms and to different extents when internal or external Na+ concentration was changed.

A review of changes in vascular smooth muscle functions in hypertension: isolated tissue versus in vivo studies

1985 ◽  
Vol 63 (4) ◽  
pp. 355-365 ◽  
Author(s):  
C. R. Triggle ◽  
I. Laher
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Function ◽  
Spontaneously Hypertensive Rat ◽  
In Vivo Studies ◽  
Neuronal Uptake ◽  
Smooth Muscle Function

The role of altered vascular smooth muscle function in the etiology of essential hypertension has been extensively studied by a number of investigators. The results obtained from in vivo studies do not always correlate with results from in vitro studies and it is not always apparent whether the results reflect differences related to hypertension or to the genetic background of the animal model. In vitro and perfused vascular bed studies in our laboratory have utilized the spontaneously hypertensive rat (SHR), the normotensive Wistar Kyoto rat (WKY), genetically related crossbred rats (F1, F2, and BC1), and also Dahl salt-sensitive (DS) and salt-resistant (DR) rats. The role of altered smooth muscle function in relation to the development of the elevated blood pressure (BP) of the SHR or DS rat was studied and emphasis was placed on determining the role of altered neuronal uptake1 (U1) in hypertensives in masking elevated postsynaptic sensitivity to noradrenaline. In addition, the relationship between postsynaptic sensitivity to cations and BP was assessed. Such studies have indicated that alterations in postsynaptic sensitivity, U1 activity, and sensitivity to cations are not entirely consistent with the etiology of hypertension in the SHR and DS rat but may simply reflect genetic strain differences between the hypertensive and normotensive animals.

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