Caveolin-3 and eNOS colocalize and interact in ciliated airway epithelial cells in the rat

Krasteva, Gabriela; Pfeil, Uwe; Filip, Ana-Maria; Lips, Katrin Susanne; Kummer, Wolfgang; König, Peter

doi:10.1016/j.biocel.2006.10.019

Cited by 18 publications

(19 citation statements)

References 24 publications

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“…In resting vascular endothelial cells, NOS is maintained in an inactive state through interaction with caveolin proteins: caveolin-1 and -3, but not caveolin-2 inhibit the catalytic activity of nNOS, iNOS and eNOS, by direct binding of the CSD to a caveolin binding motif in the NOS proteins [66]. In ciliated airway epithelial cells of the rat, a similar interaction was recently described for caveolin-3 and eNOS, suggesting that regulatory caveolin-NOS interactions also exist in the airway epithelium [31]. Negative allosteric modulation of eNOS by caveolin-1 and-3 competes with positive allosteric modulation of eNOS by Ca 2+ /calmodulin and hsp90 complexes.…”

Section: Nitric Oxide Metabolismmentioning

confidence: 68%

“…Caveolin-2 immunoreactivity showed a similar distribution pattern though caveolin-2 was in very low abundance in tracheal epithelial cells [30]. Though absent from human lung tissue, caveolin-3 was expressed in the rat airway epithelium throughout the bronchial tree [31]. This broad and heterogeneous expression profile in the lung suggests an important, but cell-type specific role for caveolae and caveolins in determining cellular responses in health and disease; this is confirmed by studies showing that caveolin-1 and caveolin-2 knockout mice have severe pulmonary abnormalities [6,23,32], and by other studies showing that aberrant caveolin-1/2 expression is involved in diseases such as idiopathic pulmonary fibrosis, lung cancer and pulmonary hypertension [33][34][35].…”

Section: Caveolin Expression In the Lungmentioning

confidence: 72%

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Caveolae and Caveolins in the Respiratory System

Gosens¹,

Mutawe²,

Martin³

et al. 2008

CMM

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Caveolae are flask-shaped invaginations of the plasma membrane that are present in most structural cells. They owe their characteristic Omega-shape to complexes of unique proteins, the caveolins, which indirectly tether cholesterol and sphingolipid-enriched membrane microdomains to the cytoskeleton. Caveolins possess a unique scaffolding domain that anchors receptors, ion channels, second messenger producing enzymes, and effector kinases, thereby sequestering them to caveolae, and modulating cellular signaling and vesicular transport. The lungs express numerous caveolae and high levels of caveolins; therefore they likely play an important role in lung physiology. Indeed, recent and ongoing studies indicate important roles for caveolae and caveolins in the airway epithelium, airway smooth muscle, airway fibroblasts, airway inflammatory cells and the pulmonary vasculature. We review the role of caveolae and caveolins in lung cells and discuss their involvement in cellular signaling associated with asthma, COPD, lung cancer, idiopathic pulmonary fibrosis and pulmonary vascular defects.

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Section: Nitric Oxide Metabolismmentioning

confidence: 68%

Section: Caveolin Expression In the Lungmentioning

confidence: 72%

Caveolae and Caveolins in the Respiratory System

Gosens¹,

Mutawe²,

Martin³

et al. 2008

CMM

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“…Up until now, the presence of Cav-3 in ASMC has only been described in tracheal muscle in rat (19). Whereas these findings suggest Cav-3 to be distributed throughout all mammalian species, other groups reported an absence of Cav-3 in Fig.…”

Section: Discussionmentioning

confidence: 85%

“…Three Cav isoforms have been identified, Cav-1, Cav-2, and Cav-3, among which the presence of either Cav-1 or Cav-3 is essential for the formation of caveolae (33). Cav-1 is widely expressed, including ASMC (13,19,31), whereas Cav-3 is found primarily in striated (skeletal and cardiac) muscle and certain SMC (35). In the heart and urinary bladder, MR subtypes are functionally coupled to caveolins.…”

mentioning

confidence: 99%

Muscarinic receptor-mediated bronchoconstriction is coupled to caveolae in murine airways

Schlenz

Kummer

Jositsch

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Cholinergic bronchoconstriction is mediated by M(2) and M(3) muscarinic receptors (MR). In heart and urinary bladder, MR are linked to caveolin-1 or -3, the structural proteins of caveolae. Caveolae are cholesterol-rich, omega-shaped invaginations of the plasma membrane. They provide a scaffold for multiple G protein receptors and membrane-bound enzymes, thereby orchestrating signaling into the cell interior. Hence, we hypothesized that airway MR signaling pathways are coupled to caveolae as well. To address this issue, we determined the distribution of caveolin isoforms and MR subtype M2R in murine and human airways and investigated protein-protein associations by fluorescence resonance energy transfer (FRET)-confocal laser scanning microscopy (CLSM) analysis in immunolabeled murine tissue sections. Bronchoconstrictor responses of murine bronchi were recorded in lung-slice preparations before and after caveolae disruption by methyl-β-cyclodextrin, with efficiency of this treatment being validated by electron microscopy. KCl-induced bronchoconstriction was unaffected after treatment, demonstrating functional integrity of the smooth muscle. Caveolae disruption decreased muscarine-induced bronchoconstriction in wild-type and abolished it in M2R(-/-) and M3R(-/-) mice. Thus M2R and M3R signaling pathways require intact caveolae. Furthermore, we identified a presumed skeletal and cardiac myocyte-specific caveolin isoform, caveolin-3, in human and murine bronchial smooth muscle and found it to be associated with M2R in situ. In contrast, M2R was not associated with caveolin-1, despite an in situ association of caveolin-1 and caveolin-3 that was detected. Here, we demonstrated that M2R- and M3R-mediated bronchoconstriction is caveolae-dependent. Since caveolin-3 is directly associated with M2R, we suggest caveolin-3 as novel regulator of M2R-mediated signaling.

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“…The expression of Cav3 has been also reported in smooth muscle cells, astroglial cells (Ikezu et al, 1998), sinus endothelial cells in spleen (Uehara and Miyoshi, 2002), ciliated airway epithelial cells of the trachea and bronchial tree (Krasteva et al, 2007), and chondrocytes in the limb cartilage (Schwab et al, 1999(Schwab et al, , 2000. Although the precise function of Cav3 remains unclear, mutations or alterations of Cav3-expression are responsible for specific diseases such as cardiomyopathy, myodystrophy, and Alzheimer's disease (for review, see Quest et al, 2004).…”

mentioning

confidence: 99%

Immunocytochemical Localization of Caveolin‐3 in the Synoviocytes of the Rat Temporomandibular Joint During Development

Niwano¹,

Nozawa-Inoue²,

Suzuki³

et al. 2008

The Anatomical Record

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Caveolins-caveolin-1, -2, -3 (Cav1, 2, 3)-are major components of caveolae, which have diverse functions. Our recent study on the temporomandibular joint (TMJ) revealed expressions of Cav1 and muscle-specific Cav3 in some synovial fibroblast-like type B cells with well-developed caveolae. However, the involvement of Cav3 expression in the differentiation and maturation of type B cells remains unclear. The present study therefore examined the chronological alterations in the localization of Cav3 in the synovial lining cells of the rat TMJ during postnatal development by immunocytochemical techniques. Observations showed immature type B cells possessed a few caveolae with Cav1 but lacked Cav3 protein at postnatal day 5 (P5). At P14, Cav3-immunopositive type B cells first appeared in the synovial lining layer. They increased in number and immunointensity from P14 to P21 as occlusion became active. In immunoelectron microscopy and double immunolabeling with heat shock protein 25 (Hsp25) and Cav3, coexpressed type B cells developed rough endoplasmic reticulum and numerous caveolae, while the Cav3-immunonegative type B cell with Hsp25 immunoreaction possessed few of these. Results suggest that Cav3 expression, which is closely related to added functional stimuli, reflects the differentiation of the type B synoviocytes. Anat Rec,

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Caveolin-3 and eNOS colocalize and interact in ciliated airway epithelial cells in the rat

Cited by 18 publications

References 24 publications

Caveolae and Caveolins in the Respiratory System

Caveolae and Caveolins in the Respiratory System

Muscarinic receptor-mediated bronchoconstriction is coupled to caveolae in murine airways

Immunocytochemical Localization of Caveolin‐3 in the Synoviocytes of the Rat Temporomandibular Joint During Development

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