Caveolin-1 inhibits matrix metalloproteinase-2 activity in the heart

Chow, Ava K.; Cena, Jonathan; El-Yazbi, Ahmed F.; Crawford, Bryan D.; Holt, Andrew; Cho, W.J.; Daniel, E. E.; Schulz, Richard

doi:10.1016/j.yjmcc.2007.01.008

Cited by 74 publications

(62 citation statements)

References 26 publications

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“…Indeed, an association between glucose-induced damage in endothelial cells and altered vasoactive factors, such as increased ET-1 expression and decreased NO bioavailability, has already been shown previously [4]. Furthermore, MMP-2 is colocalized with caveolae on the endothelial cells [47], while Cav-1 overexpression can lead to a decrease in MMP-2 activity [48]. Therefore, an increased Cav-1 level and decreased levels of MMP-2 and MMP-9 in aortas from diabetic rats are supporting the above hypothesis.…”

Section: Discussionmentioning

confidence: 84%

“…6 Schematic illustration for the putative mechanisms leading to diabetic endothelial vascular dysfunction. Sustained hyperglycemia causes several alterations in vasculature including its direct effect on increase in oxidative stress as well as decrease in antioxidant defence system [3, 7-10, 15, 16, 22, 32-35, 37, 39-41], changes in function and density of receptors [7,10,13,17,23,31,40], increased expression levels of Cav-1 [5,6,23,31,47,48], ET-1 [4,13,33], activation of PKC [10, 39-42, 45, 46], and degradation of MMPs [11,12,15,16,43,[47][48][49]. In addition, according to literature, most of these components are also affected with increased oxidative stress and unbalanced oxidants/antioxidants ratio, as well as altered cellular redox state.…”

Section: Discussionmentioning

confidence: 99%

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Doxycycline Ameliorates Vascular Endothelial and Contractile Dysfunction in the Thoracic Aorta of Diabetic Rats

2011

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Studies have shown that tetracycline class antibiotics exhibit an ameliorating action with its antioxidant property on increased oxidative stress in tissues, including heart. Since endothelial vascular dysfunction in diabetes is associated with increased oxidative stress and prevented with antioxidants, herein, we aimed to test a hypothesis whether a low-dose doxycycline treatment of diabetic rats for 4 weeks can ameliorate endothelial vascular dysfunction of thoracic aortas. Results of the present study shows that both direct and alpha receptor-mediated contractile responses as well as endothelium-dependent and endothelium-independent vasodilatory responses were preserved with low-dose doxycycline treatment (30 μmol/kg, daily; for 4 weeks) compared with untreated diabetic group. Furthermore, doxycycline treatment normalized increased lipid peroxidation and cellular glutathione level measured in plasma and prevented diabetes-induced impaired body weight gain without significant effect on high blood glucose level. Increased membrane protein level of caveolin-1, elevated ratio of PKC in particulate and cytosolic fraction, and increased protein level of cytosolic endothelin-1 in diabetic rats were also significantly prevented with doxycycline treatment. Moreover, diabetes-induced another type of oxidative stress markers in rats, matrix metalloproteinases, MMP-2, and MMP-9 were also normalized with doxycycline treatment in blood. Taken together, our data address that amelioration and/or prevention of vascular endothelial and contractile dysfunction by doxycycline is accompanied by a clear reduction in oxidative stress markers of diabetes, which provides evidence for doxycycline's potential antioxidant action as a therapeutic agent for amelioration and/or prevention of vascular disorders in diabetic subjects.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Doxycycline Ameliorates Vascular Endothelial and Contractile Dysfunction in the Thoracic Aorta of Diabetic Rats

2011

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“…Recently, Williams et al reported that overexpression of Cav1 in metastatic breast cancer cells reduced cell invasion capacity, which might be mediated partly through inhibition of MMP2 and MMP9 activities [22]. Moreover, Chow et al found the colocalization of MMP2 and Cav1 on the plasma membrane of cardiomyocytes and Cav1 interacted with MMP2 via its scaffolding domain, which was responsible for the inhibition of MMP2 activity in the heart [23]. However, whether Cav1 directly regulates the activity of MMP2, or whether other signal molecules participate in this process, needs further investigations.…”

Section: Discussionmentioning

confidence: 99%

Caveolin-1 Regulating the Invasion and Expression of Matrix Metalloproteinase (MMPs) in Pancreatic Carcinoma Cells

Han

Zhu

2010

Journal of Surgical Research

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“…The activation of MMP2 increases SMC proliferation and migration. Importantly, membrane type 1-MMP, a physiological activator of pro-MMP2, is preferentially localized in caveolae, and caveolin-1 negatively regulates membrane type 1-MMP and MMP2 activity and inhibits cell migration (4,19,92). The increased expression and activity of MMP2 in the presence of enhanced expression of caveolin-1 in SMCs suggest that caveolin-1 has lost its inhibitory function.…”

Section: Enhanced Expression Of Caveolin-1 In Smcs Loss Of Endothelimentioning

confidence: 99%

Pathogenesis of pulmonary hypertension: a case for caveolin-1 and cell membrane integrity

Mathew

2014

American Journal of Physiology-Heart and Circulatory Physiology

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Mathew R. Pathogenesis of pulmonary hypertension: a case for caveolin-1 and cell membrane integrity. Am J Physiol Heart Circ Physiol 306: H15-H25, 2014. First published October 25, 2013 doi:10.1152/ajpheart.00266.2013.-Pulmonary hypertension (PH) is a progressive disease with a high morbidity and mortality rate. Despite important advances in the field, the precise mechanisms leading to PH are not yet understood. Main features of PH are loss of vasodilatory response, the activation of proliferative and antiapoptotic pathways leading to pulmonary vascular remodeling and obstruction, elevated pressure and right ventricular hypertrophy, resulting in right ventricular failure and death. Experimental studies suggest that endothelial dysfunction may be the key underlying feature in PH. Caveolin-1, a major protein constituent of caveolae, interacts with several signaling molecules including the ones implicated in PH and modulates them. Disruption and progressive loss of endothelial caveolin-1 with reciprocal activation of proliferative pathways occur before the onset of PH, and the rescue of caveolin-1 inhibits proliferative pathways and attenuates PH. Extensive endothelial damage/loss occurs during the progression of the disease with subsequent enhanced expression of caveolin-1 in smooth muscle cells. This caveolin-1 in smooth muscle cells switches from being an antiproliferative factor to a proproliferative one and participates in cell proliferation and cell migration, possibly leading to irreversible PH. In contrast, the disruption of endothelial caveolin-1 is not observed in the hypoxia-induced PH, a reversible form of PH. However, proliferative pathways are activated in this model, indicating caveolin-1 dysfunction. Thus disruption or dysfunction of endothelial caveolin-1 leads to PH, and the status of caveolin-1 may determine the reversibility versus irreversibility of PH. This article reviews the role of caveolin-1 and cell membrane integrity in the pathogenesis and progression of PH.caveolin-1; endothelial cells; pulmonary hypertension; smooth muscle cells THIS ARTICLE is part of a collection on Pathophysiology of Hypertension. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http://ajpheart.physiology.org/.In 1891, Ernst von Romberg, a German physician, described histological changes in pulmonary hypertension (PH) as pulmonary vascular sclerosis (30). Since then remarkable advances have been made in the understanding of PH, but the pathogenesis of PH still remains elusive, partly because a number of diseases can lead to PH and multiple signaling pathways are implicated in PH. Furthermore, not all signaling pathways are activated in a given patient, and their activation may depend on the stage of the disease. Experimental data suggest that the vascular changes occur before the onset of PH (47,48). Therefore, it is not surprising that by the time the diagnosis of PH is made, most patients have significant pathological changes in pulmonary vasculatu...

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Caveolin-1 inhibits matrix metalloproteinase-2 activity in the heart

Cited by 74 publications

References 26 publications

Doxycycline Ameliorates Vascular Endothelial and Contractile Dysfunction in the Thoracic Aorta of Diabetic Rats

Doxycycline Ameliorates Vascular Endothelial and Contractile Dysfunction in the Thoracic Aorta of Diabetic Rats

Caveolin-1 Regulating the Invasion and Expression of Matrix Metalloproteinase (MMPs) in Pancreatic Carcinoma Cells

Pathogenesis of pulmonary hypertension: a case for caveolin-1 and cell membrane integrity

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