Academic literature on the topic 'Caveoli-1 (Cav1)'
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Journal articles on the topic "Caveoli-1 (Cav1)"
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Li, Zhen, Shu Feng, Vanessa Lopez, Gina Elhammady, Matthew L. Anderson, Elena M. Kaftanovskaya, and Alexander I. Agoulnik. "Uterine Cysts in Female Mice Deficient for Caveolin-1 and Insulin-Like 3 Receptor RXFP2." Endocrinology 152, no. 6 (April 5, 2011): 2474–82. http://dx.doi.org/10.1210/en.2010-1015.
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Gene mutations of insulin-like 3 (INSL3) peptide or its G protein-coupled receptor RXFP2 (relaxin family peptide receptor 2) lead to cryptorchidism. The role of INSL3 in adult females is less known, although INSL3 expression has been described in female reproductive organs. Caveolin-1 (CAV1), the main component of caveoli cell membrane invaginations, has been shown to play an important role in epithelial organization and stromal-epithelial interactions. We created a null allele of Cav1 mice by deleting its second exon through embryonic stem cell targeting. Immunohistochemical analysis demonstrated that CAV1 expression was primarily localized to endothelial blood vessel cells and the myometrium uterus, whereas the strongest expression of Rxfp2 was detected in the endometrial epithelium. By 12 months of age approximately 18% of Cav1−/− females developed single or multiple dilated endometrial cysts lined by a flattened, simple low epithelium. A deficiency for Rxfp2 on Cav1-deficient background led to more than a 2-fold increase in the incidence of uterine cysts (54–58%). Appearance of cysts led to a severe disorganization of uterine morphology. We have found that the cysts had an increased expression of β-catenin and estrogen receptor β in endometrial stromal and epithelial cells and increased epithelial proliferation. An analysis of simple dilated cysts in human patients for CAV1 expression did not show appreciable differences with control regardless of menstrual phase, suggesting an involvement of additional factors in human disease. The results of this study suggest a novel synergistic role of INSL3/RXFP2 and CAV1 in structural maintenance of the uterus.
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Hayer, Arnold, Miriam Stoeber, Danilo Ritz, Sabrina Engel, Hemmo H. Meyer, and Ari Helenius. "Caveolin-1 is ubiquitinated and targeted to intralumenal vesicles in endolysosomes for degradation." Journal of Cell Biology 191, no. 3 (November 1, 2010): 615–29. http://dx.doi.org/10.1083/jcb.201003086.
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Caveolae are long-lived plasma membrane microdomains composed of caveolins, cavins, and a cholesterol-rich membrane. Little is known about how caveolae disassemble and how their coat components are degraded. We studied the degradation of caveolin-1 (CAV1), a major caveolar protein, in CV1 cells. CAV1 was degraded very slowly, but turnover could be accelerated by compromising caveolae assembly. Now, CAV1 became detectable in late endosomes (LE) and lysosomes where it was degraded. Targeting to the degradative pathway required ubiquitination and the endosomal sorting complex required for transport (ESCRT) machinery for inclusion into intralumenal vesicles in endosomes. A dual-tag strategy allowed us to monitor exposure of CAV1 to the acidic lumen of individual, maturing LE in living cells. Importantly, we found that “caveosomes,” previously described by our group as independent organelles distinct from endosomes, actually correspond to late endosomal compartments modified by the accumulation of overexpressed CAV1 awaiting degradation. The findings led us to a revised model for endocytic trafficking of CAV1.
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Joshi, Bharat, Michele Bastiani, Scott S. Strugnell, Cecile Boscher, Robert G. Parton, and Ivan R. Nabi. "Phosphocaveolin-1 is a mechanotransducer that induces caveola biogenesis via Egr1 transcriptional regulation." Journal of Cell Biology 199, no. 3 (October 22, 2012): 425–35. http://dx.doi.org/10.1083/jcb.201207089.
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Caveolin-1 (Cav1) is an essential component of caveolae whose Src kinase-dependent phosphorylation on tyrosine 14 (Y14) is associated with regulation of focal adhesion dynamics. However, the relationship between these disparate functions remains to be elucidated. Caveola biogenesis requires expression of both Cav1 and cavin-1, but Cav1Y14 phosphorylation is dispensable. In this paper, we show that Cav1 tyrosine phosphorylation induces caveola biogenesis via actin-dependent mechanotransduction and inactivation of the Egr1 (early growth response-1) transcription factor, relieving inhibition of endogenous Cav1 and cavin-1 genes. Cav1 phosphorylation reduces Egr1 binding to Cav1 and cavin-1 promoters and stimulates their activity. In MDA-231 breast carcinoma cells that express elevated levels of Cav1 and caveolae, Egr1 regulated Cav1, and cavin-1 promoter activity was dependent on actin, Cav1, Src, and Rho-associated kinase as well as downstream protein kinase C (PKC) signaling. pCav1 is therefore a mechanotransducer that acts via PKC to relieve Egr1 transcriptional inhibition of Cav1 and cavin-1, defining a novel feedback regulatory loop to regulate caveola biogenesis.
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Jung, WooRam, Emma Sierecki, Michele Bastiani, Ailis O’Carroll, Kirill Alexandrov, James Rae, Wayne Johnston, et al. "Cell-free formation and interactome analysis of caveolae." Journal of Cell Biology 217, no. 6 (May 1, 2018): 2141–65. http://dx.doi.org/10.1083/jcb.201707004.
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Caveolae have been linked to the regulation of signaling pathways in eukaryotic cells through direct interactions with caveolins. Here, we describe a cell-free system based on Leishmania tarentolae (Lt) extracts for the biogenesis of caveolae and show its use for single-molecule interaction studies. Insertion of expressed caveolin-1 (CAV1) into Lt membranes was analogous to that of caveolin in native membranes. Electron tomography showed that caveolins generate domains of precise size and curvature. Cell-free caveolae were used in quantitative assays to test the interaction of membrane-inserted caveolin with signaling proteins and to determine the stoichiometry of interactions. Binding of membrane-inserted CAV1 to several proposed binding partners, including endothelial nitric-oxide synthase, was negligible, but a small number of proteins, including TRAF2, interacted with CAV1 in a phosphorylation-(CAV1Y14)–stimulated manner. In cells subjected to oxidative stress, phosphorylated CAV1 recruited TRAF2 to the early endosome forming a novel signaling platform. These findings lead to a novel model for cellular stress signaling by CAV1.
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Aravamudan, Bharathi, Sarah K. VanOosten, Lucas W. Meuchel, Pawan Vohra, Michael Thompson, Gary C. Sieck, Y. S. Prakash, and Christina M. Pabelick. "Caveolin-1 knockout mice exhibit airway hyperreactivity." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 8 (October 15, 2012): L669—L681. http://dx.doi.org/10.1152/ajplung.00018.2012.
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Caveolae are flask-shaped plasma membrane invaginations expressing the scaffolding caveolin proteins. Although caveolins have been found in endothelium and epithelium (where they regulate nitric oxide synthase activity), their role in smooth muscle is still under investigation. We and others have previously shown that caveolae of human airway smooth muscle (ASM), which express caveolin-1, contain Ca2+ and force regulatory proteins and are involved in mediating the effects of inflammatory cytokines such as TNF-α on intracellular Ca2+ concentration responses to agonist. Accordingly, we tested the hypothesis that in vivo, absence of caveolin-1 leads to reduced airway hyperresponsiveness, using a knockout (KO) (Cav1 KO) mouse and an ovalbumin-sensitized/challenged (OVA) model of allergic airway hyperresponsiveness. Surprisingly, airway responsiveness to methacholine, tested by use of a FlexiVent system, was increased in Cav1 KO control (CTL) as well as KO OVA mice, which could not be explained by a blunted immune response to OVA. In ASM of wild-type (WT) OVA mice, expression of caveolin-1, the caveolar adapter proteins cavins 1–3, and caveolae-associated Ca2+ and force regulatory proteins such as Orai1 and RhoA were all increased, effects absent in Cav1 KO CTL and OVA mice. However, as with WT OVA, both CTL and OVA Cav1 KO airways showed signs of enhanced remodeling, with high expression of proliferation markers and increased collagen. Separately, epithelial cells from airways of all three groups displayed lower endothelial but higher inducible nitric oxide synthase and arginase expression. Arginase activity was also increased in these three groups, and the inhibitor nor-NOHA ( N-omega-nor-l-arginine) enhanced sensitivity of isolated tracheal rings to ACh, especially in Cav1 KO mice. On the basis of these data disproving our original hypothesis, we conclude that caveolin-1 has complex effects on ASM vs. epithelium, resulting in airway hyperreactivity in vivo mediated by altered airway remodeling and bronchodilation.
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Tagawa, Akiko, Anna Mezzacasa, Arnold Hayer, Andrea Longatti, Lucas Pelkmans, and Ari Helenius. "Assembly and trafficking of caveolar domains in the cell." Journal of Cell Biology 170, no. 5 (August 29, 2005): 769–79. http://dx.doi.org/10.1083/jcb.200506103.
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Using total internal reflection fluorescence microscopy (TIR-FM), fluorescence recovery after photobleaching (FRAP), and other light microscopy techniques, we analyzed the dynamics, the activation, and the assembly of caveolae labeled with fluorescently tagged caveolin-1 (Cav1). We found that when activated by simian virus 40 (SV40), a nonenveloped DNA virus that uses caveolae for cell entry, the fraction of mobile caveolae was dramatically enhanced both in the plasma membrane (PM) and in the caveosome, an intracellular organelle that functions as an intermediate station in caveolar endocytosis. Activation also resulted in increased microtubule (MT)-dependent, long-range movement of caveolar vesicles. We generated heterokaryons that contained GFP- and RFP-tagged caveolae by fusing cells expressing Cav1-GFP and -RFP, respectively, and showed that even when activated, individual caveolar domains underwent little exchange of Cav1. Only when the cells were subjected to transient cholesterol depletion, did the caveolae domain exchange Cav1. Thus, in contrast to clathrin-, or other types of coated transport vesicles, caveolae constitute stable, cholesterol-dependent membrane domains that can serve as fixed containers through vesicle traffic. Finally, we identified the Golgi complex as the site where newly assembled caveolar domains appeared first.
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Gerstenberger, Wladimir, Michaela Wrage, Eeva Kettunen, Klaus Pantel, Sisko Anttila, Stefan Steurer, and Harriet Wikman. "Stromal Caveolin-1 and Caveolin-2 Expression in Primary Tumors and Lymph Node Metastases." Analytical Cellular Pathology 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/8651790.
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The expression of caveolin-1 (CAV1) in both tumor cell and cancer-associated fibroblasts (CAFs) has been found to correlate with tumor aggressiveness in different epithelial tumor entities, whereas less is known for caveolin-2 (CAV2). The aim of this study was to investigate the clinicopathological significance and prognostic value of stromal CAV1 and CAV2 expression in lung cancer. The expression of these two genes was investigated at protein level on a tissue microarray (TMA) consisting of 161 primary tumor samples. 50.7% of squamous cell lung cancer (SCC) tumors showed strong expression of CAV1 in the tumor-associated stromal cells, whereas only 15.1% of adenocarcinomas (AC) showed a strong CAV1 expression (p<0.01). A strong CAV2 stromal expression was found in 46.0% of the lung tumor specimens, with no significant difference between the subtypes. Neither CAV1 nor CAV2 stromal expression was associated with any other clinicopathological factor including survival. When the stromal expression in matched primary tumors and lymph node metastases was compared, both CAV1 and CAV2 expressions were frequently found lost in the corresponding stroma of the lymph node metastasis (40.6%, p=0.003 and 38.4%, p=0.001, resp.). Loss of stromal CAV2 in the lymph node metastases was also significantly associated with earlier death (p=0.011). In conclusion, in contrast to the expression patterns in the tumor tissue of lung cancer, stromal expression of CAV1 in primary tumors was not associated with clinical outcome whereas the stromal expression of especially CAV2 in the metastatic lymph nodes could be associated with lung cancer pathogenesis.
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Copeland, Courtney A., Bing Han, Ajit Tiwari, Eric D. Austin, James E. Loyd, James D. West, and Anne K. Kenworthy. "A disease-associated frameshift mutation in caveolin-1 disrupts caveolae formation and function through introduction of a de novo ER retention signal." Molecular Biology of the Cell 28, no. 22 (November 2017): 3095–111. http://dx.doi.org/10.1091/mbc.e17-06-0421.
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Caveolin-1 (CAV1) is an essential component of caveolae and is implicated in numerous physiological processes. Recent studies have identified heterozygous mutations in the CAV1 gene in patients with pulmonary arterial hypertension (PAH), but the mechanisms by which these mutations impact caveolae assembly and contribute to disease remain unclear. To address this question, we examined the consequences of a familial PAH-associated frameshift mutation in CAV1, P158PfsX22, on caveolae assembly and function. We show that C-terminus of the CAV1 P158 protein contains a functional ER-retention signal that inhibits ER exit and caveolae formation and accelerates CAV1 turnover in Cav1–/– MEFs. Moreover, when coexpressed with wild-type (WT) CAV1 in Cav1–/– MEFs, CAV1-P158 functions as a dominant negative by partially disrupting WT CAV1 trafficking. In patient skin fibroblasts, CAV1 and caveolar accessory protein levels are reduced, fewer caveolae are observed, and CAV1 complexes exhibit biochemical abnormalities. Patient fibroblasts also exhibit decreased resistance to a hypo-osmotic challenge, suggesting the function of caveolae as membrane reservoir is compromised. We conclude that the P158PfsX22 frameshift introduces a gain of function that gives rise to a dominant negative form of CAV1, defining a new mechanism by which disease-associated mutations in CAV1 impair caveolae assembly.
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Păunescu, Teodor G., Hua A. J. Lu, Leileata M. Russo, Núria M. Pastor-Soler, Mary McKee, Margaret M. McLaughlin, Bianca E. Bartlett, Sylvie Breton, and Dennis Brown. "Vasopressin induces apical expression of caveolin in rat kidney collecting duct principal cells." American Journal of Physiology-Renal Physiology 305, no. 12 (December 15, 2013): F1783—F1795. http://dx.doi.org/10.1152/ajprenal.00622.2012.
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Caveolin (Cav)1 is expressed in the basolateral membrane domain of renal collecting duct (CD) principal cells (PCs), where it is associated with caveolae. To reveal any potential involvement of Cav1 in vasopressin signaling, we used specific monoclonal and polyclonal antibodies to examine its localization in CD PCs of Brattleboro (BB) rats treated with vasopressin (DDAVP). Compared with controls, immunofluorescence revealed a time-dependent increase in Cav1 expression in the apical membrane domain of PCs, where it overlapped with aquaporin-2 (AQP2). After 24 h of DDAVP treatment, Cav1 was visible as an increased number of small apical spots. The staining gradually became more extensive, and, after 2 wk of DDAVP, it occupied the majority of the apical membrane domain of many PCs. Cav1 also assumed an apical localization in PCs of DDAVP-treated Sprague-Dawley and Long-Evans rats. Similarly, Cav2 appeared at the apical pole of PCs after DDAVP treatment of BB, Sprague-Dawley, and Long-Evans rats. Immunogold electron microscopy confirmed bipolar Cav1 membrane expression in DDAVP-treated BB rats, whereas caveolae were only detected on the basolateral membrane. Immunoblot analysis of BB rat whole kidney homogenates revealed no significant increase in Cav1 levels in DDAVP-treated rats, suggesting that DDAVP induces Cav1 relocalization or modifies its targeting. We conclude that Cav1 and Cav2 trafficking and membrane localization are dramatically altered by the action of DDAVP. Importantly, the absence of apical caveolae indicates that while Cavs may have an as yet undetermined role in vasopressin-regulated signaling processes, this is probably unrelated to AQP2 internalization by caveolae.
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Zimnicka, Adriana M., Yawer S. Husain, Ayesha N. Shajahan, Maria Sverdlov, Oleg Chaga, Zhenlong Chen, Peter T. Toth, et al. "Src-dependent phosphorylation of caveolin-1 Tyr-14 promotes swelling and release of caveolae." Molecular Biology of the Cell 27, no. 13 (July 2016): 2090–106. http://dx.doi.org/10.1091/mbc.e15-11-0756.
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Caveolin 1 (Cav1) is a required structural component of caveolae, and its phosphorylation by Src is associated with an increase in caveolae-mediated endocytosis. Here we demonstrate, using quantitative live-cell 4D, TIRF, and FRET imaging, that endocytosis and trafficking of caveolae are associated with a Cav1 Tyr-14 phosphorylation-dependent conformational change, which spatially separates, or loosens, Cav1 molecules within the oligomeric caveolar coat. When tracked by TIRF and spinning-disk microscopy, cells expressing phosphomimicking Cav1 (Y14D) mutant formed vesicles that were greater in number and volume than with Y14F-Cav1-GFP. Furthermore, we observed in HEK cells cotransfected with wild-type, Y14D, or Y14F Cav1-CFP and -YFP constructs that FRET efficiency was greater with Y14F pairs than with Y14D, indicating that pY14-Cav1 regulates the spatial organization of Cav1 molecules within the oligomer. In addition, albumin-induced Src activation or direct activation of Src using a rapamycin-inducible Src construct (RapR-Src) led to an increase in monomeric Cav1 in Western blots, as well as a simultaneous increase in vesicle number and decrease in FRET intensity, indicative of a Src-mediated conformational change in CFP/YFP-tagged WT-Cav1 pairs. We conclude that phosphorylation of Cav1 leads to separation or “spreading” of neighboring negatively charged N-terminal phosphotyrosine residues, promoting swelling of caveolae, followed by their release from the plasma membrane.
Dissertations / Theses on the topic "Caveoli-1 (Cav1)"
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Burgy, Mickaël. "Intérêt pronostic et thérapeutique de l'axe miR-30a/e-3p -Cav1 dans les carcinomes épidermoïdes de la tête et du cou." Electronic Thesis or Diss., Strasbourg, 2025. http://www.theses.fr/2025STRAJ002.
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Le pronostic péjoratif des carcinomes épidermoïdes de la tête et du cou (CETEC) tient en partie aux mécanismes encore non élucidés de résistances aux thérapies actuelles. De plus l’absence de biomarqueurs complique le développement de stratégies thérapeutiques reposant actuellement sur le stade de la maladie excluant les caractéristiques biologiques tumorales. Dans ce projet de recherche translationnelle, nous avons identifié la cavéoline-1 (Cav1) et les miR-30a/e-3p comme des biomarqueurs pronostiques de la survie et de la récidive tumorale. Nous avons validé l’implication de l’axe CAV1/EREG/YAP dans la résistance au Cetuximab et à la radiothérapie. Nous avons également identifié miR-30a/e-3p à la fois comme des régulateurs de la voie du TGF-β via la répression de TGFBR1 et BMPR2 à l‘origine d’une diminution de l’agressivité tumorale, et également comme des immunomodulateurs favorisant l’activité phagocytaire des macrophages envers les cellules tumorales. Enfin nous avons pu développer un modèle de tumoroïdes issus de pièces opératoires de patients atteints de CETEC ayant permis de valider certains de nos résultats et destiné à un projet de recherche de drug-testingThe poor prognosis of head and neck squamous cell carcinomas (HNSCC) patients is partly attributed to resistance mechanisms against current therapies, which remain poorly understood. Furthermore, the absence of biomarkers complicates the development of therapeutic strategies currently based on disease staging, excluding the tumor's biological characteristics. In this translational research project, we identified caveolin-1 (Cav1) and miR-30a/e-3p as prognostic biomarkers for survival and recurrence. We validated the involvement of the CAV1/EREG/YAP axis in the resistance to Cetuximab and radiotherapy. We also identified miR-30a/e-3p both as regulators of the TGF-β pathway through the repression of TGFBR1 and BMPR2 leading to reduced tumor cell aggressiveness and as immunomodulators promoting the phagocytic activities of macrophages towards tumor cells. Finally, we developed a tumoroid model derived from resected tissue of HNSCC patients which confirmed several of our results and will be used in a drug-testing research project
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Wong, Kevin L. "Caveolae and Caveolin-1 are important for Vitamin D signalling." Thesis, Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/37086.
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The most active form of Vitamin D, 1alpha,25(OH)2D3, modulates cells via receptor mediated mechanisms. While studies have elucidated the pathway via the classical nuclear Vitamin D Receptor (VDR), little is known about the membrane-associated Vitamin D Receptor (ERp60). Caveolae and its characteristic protein Caveolin-1 have been involved in many signaling pathways due to its specific structure and physical configuration. Other studies have shown that many components of the Vitamin D pathway have been found in caveolae. This study hypothesizes that caveolae and Caveolin-1 are important for the effects of 1,25 Vitamin D signaling via ERp60. Research up to date have shown that in rat and mouse growth zone chondrocytes, cells deprived of intact caveolae either through disruption through beta-Cyclodextrin or genetic knockout do not exhibit the characteristic responses to Vitamin D through ERp60 when compared to chondrocytes with functional caveolae. Studies using immunofluorescence co-localization and caveolae fractionation have shown that ERp60 is localized in the caveolae domains. Cellular fractionation was also performed to examine the localization of the ERp60 receptor in lipid rafts and caveolae. Histology and transmission electron microscopy were also used to examine the physiological importance of caveolae and Caveolin-1 in growth plate morphology and cellular characteristics.
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Zampier, Carolina da Paz. "Papel de caveolina-1 na produção de mediadores inflamatórios." Instituto Oswaldo Cruz, 2012. https://www.arca.fiocruz.br/handle/icict/7031.
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Submitted by Alessandra Portugal (alessandradf@ioc.fiocruz.br) on 2013-10-01T21:53:22Z
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Carolina da Paz Zampier.pdf: 2134379 bytes, checksum: d822f378a88e2cf44b02c5ea60f52ea0 (MD5)Made available in DSpace on 2013-10-01T21:53:22Z (GMT). No. of bitstreams: 1 Carolina da Paz Zampier.pdf: 2134379 bytes, checksum: d822f378a88e2cf44b02c5ea60f52ea0 (MD5) Previous issue date: 2012
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
A caveolina-1 (Cav-1), uma proteína essencial para a formação de cavéolas, apresenta atividade na modulação da sinalização intracelular. Cav-1 é capaz de interagir com diversas proteínas através de seu domínio CSD (caveolin scaffolding domain) e, em geral, essa interação leva à inibição das proteínas associadas. O peptídeo CSD tem sido utilizado como um mimético de Cav-1 em relação à sua capacidade modulatória sobre a atividade de outras proteínas. Recentemente, tem sido mostrado que Cav-1 é capaz de modular a resposta inflamatória em diversos aspectos. Neste trabalho, examinamos o papel de Cav-1 na regulação da síntese de mediadores inflamatórios por macrófagos. O lipopolissacarídeo (LPS) de E.coli, um protótipo de estímulo inflamatório, foi capaz de induzir a expressão de Cav-1 e Cox-2 em macrófagos peritoneais in vitro. Estas proteínas são induzidas em um curso temporal semelhante, sendo detectadas por Western blot a partir de 3h com níveis de expressão crescentes até 18h. Por imunofluorescência, observamos que Cav-1 e Cox-2 apresentam um padrão de expressão mutualmente exclusivo em macrófagos estimulados com LPS. Mostramos por Western blot que a expressão de Cox-2 é induzida por LPS e que o tratamento com CSD leva à inibição da expressão de Cox- 2, mas não de Cox-1. Observamos, também, a redução parcial dos níveis de PGE2 no sobrenadante de macrófagos estimulados com LPS e tratados com CSD. O tratamento com o peptídeo CSD também foi capaz de reduzir os níveis de IL-1, IL- 6, e IL-12 induzidos por LPS. O LPS induz o aumento da expressão e fosforilação de STAT-1. A fosforilação de STAT-1 foi diminuída após o tratamento com CSD, indicando que Cav-1 modula negativamente a ativação de STAT-1. Estudos posteriores são necessários para complementar os dados obtidos até o momento para esclarecer os mecanismos de modulação da síntese de mediadores inflamatórios por Cav-1. Em conclusão, Cav-1 apresenta uma atividade inibitória sobre a expressão de Cox-2 e produção dos mediadores inflamatórios PGE2, IL1, IL-6, e IL-12 em macrófagos estimulados com LPS in vitro. O mecanismo de inibição possivelmente envolve inibição da ativação de STAT-1.
Caveolin-1 (Cav-1), a protein essential for the formation of caveolae, shows activity in the modulation of intracellular signaling. Cav-1 can interact with several proteins by its caveolin scaffolding domain (CSD) and, in general, this interaction leads to inhibition of associated proteins. The peptide CSD has been used as a Cav- 1 mimetic in relation to its capacity on the modulatory activity of other proteins. Recently, it has been shown that Cav-1 can modulate the inflammatory response in several respects. We examined the role of Cav-1 in regulating the synthesis of inflammatory mediators by macrophages. Lipopolysaccharide (LPS) from E. coli, a prototype of inflammatory stimulus, was able to induce the expression of Cav-1 and Cox-2 in peritoneal macrophages in vitro. These proteins are induced in a similar time course, being detected by Western blot at 3 hours with increasing levels of expression up to 18 hours. By immunofluorescence, we observed that Cav-1 and Cox-2 have a mutually exclusive pattern of expression in macrophages stimulated with LPS. Western blot analysis showed that the expression of Cox-2 is induced by LPS and that treatment with CSD leads to inhibition of Cox-2 but not Cox-1. We also observed the partial reduction of PGE2 levels in supernatants of macrophages stimulated with LPS and treated with CSD. Treatment with CSD peptide was also able to reduce the levels of IL1, IL-6 and IL-12 induced by LPS. LPS induces increased expression and phosphorylation of STAT-1. The phosphorylation of STAT- 1 was decreased after treatment with the CSD, indicating that a Cav-1 negatively modulates activation of STAT-1. Further studies are needed to supplement the data obtained so far to clarify the mechanisms of modulation of the synthesis of inflammatory mediators by Cav-1. In conclusion, Cav-1 shows an inhibitory activity on Cox-2 expression and production of the inflammatory mediators PGE2, IL1β, IL-6 and IL-12 in macrophages stimulated with LPS in vitro. The mechanism of inhibition possibly involves inhibition of STAT-1 activation.
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Comajoan, von Arend Pau. "Efecte de l'administració de l'rt-PA en condicions isquèmiques in vitro i in vivo: Cav-1 com a potencial biomarcador de volum d'infart." Doctoral thesis, Universitat de Girona, 2019. http://hdl.handle.net/10803/669184.
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Recombinant tissue plasminogen activator (rt-PA) is currently the only FDA-approved drug for the treatment of acute ischaemic stroke. However, the application of this therapy is limited to <5-7% of patients due to the associated increased risk of haemorrhagic transformation (HT). Although it is known that HT is related to rt-PA-induced blood brain barrier (BBB) disruption, the underlying mechanisms are not well established. The obtained results show that long-term studies are needed to elucidate time-dependent molecular mechanisms associated to BBB breakdown, and to explore protective BBB therapies after ischaemic stroke and rt-PA treatment. On the other hand, it has been demonstrated that OGD induces significant alterations to loading control proteins for Western Blot analysis proposing Stain-Free technology as an alternative normalization method to traditional housekeeping proteins. Finally, serum Cav-1 levels could represent a potential biomarker predicting the ischaemic outcome before rt-PA administrationL'rt-PA és l’únic fàrmac aprovat per tractar l’ictus isquèmic agut. No obstant, l’estreta finestra terapèutica, deguda al risc associat de transformació hemorràgica (TH) provoca que només s’apliqui a <5-7% dels pacients. La TH està relacionada amb la disrupció de la barrera hematoencefàlica (BHE) deguda a l’rt-PA però els mecanismes subjacents encara no estan del tot establerts. Els resultats obtinguts mostren que es requereixen estudis a llarg termini per tal de dilucidar els mecanismes dependents del temps associats a la disrupció de la BHE, i explorar noves teràpies protectores per al tractament de l’ictus isquèmic. S’ha demostrat que la POG provoca canvis significatius en els nivells proteics de controls de càrrega per “Western blot” i es presenta la tecnologia “Stain-Free” com a una alternativa a la normalització tradicional. Finalment, els nivells sèrics de Cav-1 podrien representar un potencial biomarcador predictor del pronòstic després d’una isquèmia en absència d’rt-PA
S'ha extret el capítol de resultats del pdf de la tesi fins a la seva publicació en forma d'article. Results chapter removed from pdf file until publication
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Jehl, Aude. "Cavéoline-1 prédictive de la métastase et de la rechute locorégionale des cancers des voies aérodigestives supérieures." Thesis, Strasbourg, 2022. http://www.theses.fr/2022STRAJ070.
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Ce projet de recherche translationnelle sur les cancers des voies aérodigestives supérieures (VADS) a permis d’identifier la cavéoline-1 (Cav1) comme un biomarqueur pronostique de l’évolution d’une tumeur primitive des VADS. En effet, une surexpression de cette protéine favorise une rechute locorégionale alors qu’un déficit de Cav1 engage la tumeur vers un processus métastatique. De plus, nous avons mis en évidence l’implication de l’axe Cav1 / EREG / YAP dans la résistance au traitement (cétuximab et radiothérapie). Enfin, nous avons identifié l’épireguline (EREG) comme la protéine clé de la résistance au cétuximab. Ainsi, un déficit d’EREG sensibilise les cellules au cétuximab par activation de la ferroptose et l’association de cette thérapie ciblée à la molécule de RSL3 ou à la metformine restreint drastiquement la survie cellulaire en accentuant cette mort cellulaire programmée. Ces derniers résultats ont pu être confirmés grâce à un modèle 3D complexe récapitulant l’hétérogénéité intra- et inter-tumorale, à savoir le modèle tumoroïde établi à partir de pièces opératoires de patients atteints d’un cancer des VADSThis translational research project on head and neck cancers has identified caveolin-1 (Cav1) as a prognostic biomarker for the evolution of a primary tumor of these cancers. Indeed, an overexpression of this protein favors a locoregional relapse whereas a deficiency of Cav1 engages the tumor towards a metastatic process. Moreover, we have highlighted the involvement of the Cav1 / EREG / YAP axis in the resistance to treatment (cetuximab and radiotherapy). Finally, we identified epiregulin (EREG) as the key protein in cetuximab resistance. Thus, a deficiency of EREG sensitizes cells to cetuximab by activation of ferroptosis and the association of this target therapy with the RSL3 molecule or metformin drastically restricts cell survival by accentuating this programmed cell death. These last results could be confirmed thanks to a complex 3D model recapitulating the intra- and inter-tumoral heterogeneity, namely the tumoroid model established from surgical parts of patients with head and neck cancer
Book chapters on the topic "Caveoli-1 (Cav1)"
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Hadinnapola, Charaka, and Nicholas Morrell. "Heritable pulmonary arterial hypertension." In ESC CardioMed, edited by Marc Humbert, 2527–28. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0590.
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Heritable pulmonary arterial hypertension (PAH) is diagnosed in patients presenting with PAH who have a family history of the disease or carry a mutation in a gene known to be associated with PAH. Heterozygous mutations in the gene encoding the bone morphogenetic protein receptor type 2 (BMPR2) are the most common genetic defects seen in heritable PAH. Mutations in BMPR2 are found in 82% of patients with a family history of PAH and 17% of patients presenting with no family history of the disease. Other causal genes include members of the transforming growth factor beta pathway, including activing receptor-like kinase 1 (ACVRL1) and endoglin (ENG), as well as caveolin 1 (CAV1) and the potassium two-pore domain channel subfamily K member 3 (KCNK3).
Conference papers on the topic "Caveoli-1 (Cav1)"
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Hynes, TS, S. Basu, AJ Halayko, and R. Mitchell. "Caveolin-1 (Cav-1) Orchestrates Allergic Airways Inflammation & Hyperresponsiveness in a Mouse Model of Allergic Asthma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2421.
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Mitchell, RW, Y. Bai, T. Hynes, S. Basu, MJ Sanderson, and AJ Halayko. "Airway Smooth Muscle (ASM) from Caveolin-1 Knockout (Cav-1 KO) Mice Exhibits Gs-Coupled β2-Receptor Hyperresponsiveness In Vitro." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2052.
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Yamaguchi, Tomoya, Can Lu, Lisa Ida, Kiyoshi Yanagisawa, Jiro Usukura, Jinglei Cheng, Naoe Hotta, et al. "Abstract 4585: ROR1 sustains caveolae and RTK-mediated survival signaling as a scaffold of cavin-1 and CAV1 in lung cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4585.
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Nho, Richard, and Polla Hergert. "Caveolin-1 (Cav-1) Alteration By Aberrant Forkhead Box O3a (FoxO3a) Activity Confers A Highly Proliferative And An Anti-Apoptotic IPF Fibroblast Phenotypes On Type I Collagen Matrix." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3497.
Full textReports on the topic "Caveoli-1 (Cav1)"
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Chanvorachote, Pithi. Roles of nitric oxide, reactive oxygen species, and their derivatives in regulation of lung cancer cell metastasis. Chulalongkorn University, 2013. https://doi.org/10.58837/chula.res.2013.28.
Full textAbstract:
The capability of cancer cells to resist to anoikis, migrate and invade surrounding tissues is associated with high metastatic potential and advanced stage of cancers. Recently, caveolin-1 (Cav-1) protein has garnered increased attention in implicating the aggressive behavior of cancer cells. We demonstrate herein that nitric oxide and hydrogen peroxide play a role in inhibiting anoikis process of lung cancer cells via caveolin-1 dependent mechanism. The Cav-1 function in inhibition of anoikis was demonstrated to be cause through Mcl-1 dependent mechanism. The present study demonstrated that Cav-1 regulates Mcl-1 through protein-protein interaction and inhibits its down-regulation during cell anoikis. Immunoprecipitation and immunocytochemistry studies showed that Cav-1 interacted with Mcl-1 and prevented it from degradation via the ubiquitin-proteasome pathway. Mcl-1 and Mcl-1-Cav-1 complex were highly elevated in Cav-1-overexpressing cells but were greatly reduced in Cav-1 knockdown cells. Consistent with this finding, we found that Mcl-1 ubiquitination was significantly attenuated by Cav-1 overexpression but increased by Cav-1 knockdown. Furthermore, we revealed herein that Cav-1 plays an important role in the migration and invasion of human lung carcinoma H460 cells and that these effects are differentially regulated by cellular ROS. Superoxide anion and hydrogen peroxide down-regulated Cav-1 expression and inhibited cell migration and invasion, whereas hydroxyl radical up-regulated the Cav-1 expression and promoted cell migration and invasion. The down-regulating effect of superoxide anion and hydrogen peroxide on Cav-1 is mediated through a transcription-independent mechanism that involves protein degradation via the ubiquitin-proteasome pathway.