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Caveolae-mediated membrane transport - Preface

ADVANCED DRUG DELIVERY REVIEWS 2001年第3期49卷 217-221页

作者： Gumbleton, M Cardiff Univ Welsh Sch Pharm Cardiff CF10 3XF S Glam Wales

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Caveolin-1 binding to endoplasmic reticulum membranes and entry into the regulated secretory pathway are regulated by serine phosphorylation - Protein sorting at the level of the endoplasmic reticulum

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第6期276卷 4398-4408页

作者： Schlegel, A Arvan, P Lisanti, MP Yeshiva Univ Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Div Endocrinol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Dev & Mol Biol Bronx NY 10461 USA

Caveolin-1 serves as the main coat protein of caveolae membranes, as an intracellular cholesterol shuttle, and as a regulator of diverse signaling molecules. Of the 12 residues conserved across all caveolin isoforms from all species examined to date, only Ser(80) and Ser(168) could serve as phosphorylation sites. me show here that mimicking chronic phosphorylation of Ser(80) by mutation to Glu tie. Cav-1(S80E), blocks phosphate incorporation. However, Cav-1(S168E) is phosphorylated to the same extent as wild-type caveolin-1. Cav-1(S80E) targets to the endoplasmic reticulum membrane, remains oligomeric, and maintains normal membrane topology. In contrast, Cav-1(S80A), which cannot be phosphorylated, targets to caveolae membranes. Some exocrine cells secrete caveolin-1 in a regulated manner. Cav-1(S80A) is not secreted by AR42J pancreatic adenocarcinoma cells even in the presence of dexamethasone, an agent that induces the secretory phenotype. Conversely, Cav-1(S80E) is secreted to a greater extent than wildtype caveolin-1 following dexamethasone treatment. We conclude that caveolin-1 phosphorylation on invariant serine residue 80 is required for endoplasmic reticulum retention and entry into the regulated secretory pathway.

关键词：氨基酸序列窖蛋白1 细胞质膜微囊蛋白/化学细胞质膜微囊蛋白/遗传学细胞质膜微囊蛋白/代谢细胞系内质网/代谢分子序列数据诱变磷酰化沉淀素试验蛋白质结合蛋白质转运序列同源性氨基酸丝氨酸/代谢动物狗人类

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Caveolin-1 knockout mice show an impaired angiogenic response to exogenous stimuli

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AMERICAN JOURNAL OF PATHOLOGY 2003年第6期162卷 2059-2068页

作者： Woodman, SE Ashton, AW Schubert, W Lee, H Williams, TM Medina, FA Wyckoff, JB Combs, TP Lisanti, MP Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA Albert Einstein Coll Med Dept Cardiol Bronx NY 10461 USA Albert Einstein Coll Med Dept Anat & Struct Biol Bronx NY 10461 USA Albert Einstein Coll Med Dept Cell Biol Bronx NY 10461 USA Albert Einstein Coll Med Albert Einstein Canc Ctr Bronx NY 10461 USA

Recent studies have shown that caveolin-1 (Cav-1) plays an important role as a regulator of angiogenesis in vitro. Here, we use Cav-1 knockout (KO) mice as a model system to examine the in vivo relevance of these findings. A primary mediator of angiogenesis is basic fibroblast growth factor (bFGF). Thus, we studied bFGF-induced angiogenesis in Cav-1 KO mice using a reconstituted basement membrane system, ie, Matrigel plugs, supplemented with bFGF. In Cav-1 KO mice, implanted Matrigel plugs showed a dramatic reduction in both vessel infiltration and density, as compared with identical plugs implanted in wild-type control mice. We also examined the necessity of Cav-1 to support the angiogenic response of an exogenous;tumor by subcutaneously injecting Cav-1 KO mice with the melanoma cell line, B16-F10. We show that tumor weight, volume, and vessel density are all reduced in Cav-1 KO mice, consistent with diminished angiogenesis. Ultrastructural analysis of newly formed capillaries within the exogenous tumors reveals a lack of endothelial caveolae and incomplete capillary formation in Cav-1 KO mice. These results provide novel evidence that Cav-1 and caveolae play an important positive role in the process of pathological angiogenesis in vivo. (Am J Pathol 2003, 162:2059-2068)

关键词：毛细血管/病理学毛细血管/超微结构细胞质膜微囊/病理学细胞质膜微囊/超微结构窖蛋白1 窖蛋白2 细胞质膜微囊蛋白/遗传学细胞质膜微囊蛋白/代谢胶原复方合剂内皮血管/病理学内皮血管/超微结构成纤维细胞生长因子2/药理学基因型层黏连蛋白小鼠近交C57BL 小鼠基因敲除显微镜检查共焦/方法显微镜检查电子肿瘤移植肿瘤实验性/血液供给肿瘤实验性/遗传学肿瘤实验性/预防和控制新生血管化病理性/病理学新生血管化病理性/预防和控制新生血管化生理性/药物作用蛋白聚糖类肿瘤细胞培养的动物小鼠

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PC12 cells have caveolae that contain TrkA -: Caveolae-disrupting drugs inhibit nerve growth factor-induced, but not epidermal growth factor-induced, MAPK phosphorylation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第48期275卷 37846-37852页

作者： Peiró, S Comella, JX Enrich, C Martín-Zanca, D Rocamora, N Inst Catala Oncol Lab Biol Mol Barcelona 08907 Spain Univ Barcelona Fac Med IDIBAPS Inst Invest Biomed August Pi & SunyerDept Biol C Barcelona 08036 Spain Univ Lleida Fac Med Dept Ciencias Med Basiques Grp Neurobiol Mol Lleida 25198 Spain Univ Salamanca CSIC Inst Microbiol Bioquim Salamanca 37007 Spain

Nerve growth factor (NGF) induces survival and differentiation of the neural crest-derived PC12 cell line. Caveolae are cholesterol-enriched, caveolin-containing plasma membrane microdomains involved in vesicular transport and signal transduction. Here we demonstrate the presence of caveolae in PC12 cells and their involvement in NGF signaling. Our results showed the expression of caveolin-1 by Western blot and confocal immuno-microscopy. The presence of plasma membrane caveolae was directly shown by rapid-freeze deep-etching electron microscopy. Moreover, combined deep-etching and immunogold techniques revealed the presence of the NGF receptor TrkA in the caveolae of PC12 cells. These data together with the cofractionation of Shc, Ras, caveolin, and TrkA in the caveolae fraction supported a role for these plasma membrane microdomains in NGF signaling. To approach this hypothesis, caveolae were disrupted by treatment of PC12 cells with cholesterol binding drugs. Either filipin or cyclodextrin treatment increased basal levels of MAPK phosphorylation. in contrast, pretreatment of PC12 cells with these drugs inhibited the NGF- but not the epidermal growth factor-induced MAPK phosphorylation without affecting the TrkA autophosphorylation. Taken together, our results demonstrate the presence of caveolae in PC12 cells, which contain the high affinity NGF receptor TrkA, and the specific involvement of these cholesterol-enriched plasma membrane microdomains in the propagation of the NGF-induced signal.

关键词：窖蛋白1 细胞质膜微囊蛋白/代谢胆固醇/代谢表皮生长因子/药理学显微镜检查电子丝裂原激活蛋白激酶类/代谢神经生长因子/代谢神经生长因子/药理学 PC12细胞磷酰化受体 trkA/代谢信号传导动物大鼠

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Caveolin-1 is down-regulated in human ovarian carcinoma and acts as a candidate tumor suppressor gene

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AMERICAN JOURNAL OF PATHOLOGY 2001年第5期159卷 1635-1643页

作者： Kai, WC Diatchenko, L Agoulnik, A Scharff, KM Schober, H Arlt, K Zhumabayeva, B Siebert, PD Dietel, M Schäfer, R Sers, C Humboldt Univ Charite Inst Pathol Lab Mol Tumor Pathol D-10117 Berlin Germany Clontech Labs Inc Palo Alto CA USA Baylor Coll Med Dept Obstet & Gynecol Houston TX 77030 USA

To identify novel markets differentially expressed in ovarian cancer versus normal ovary, we hybridized microarrays with cDNAs derived from normal human ovaries and advanced stage ovarian carcinomas. This analysis revealed down-regulation of the caveolin-1 gene (CAV1) in ovarian carcinoma samples. Suppression of CAV1 in ovarian carcinomas was confirmed using a tumor tissue army consisting of 68 cDNA pools from different matched human tumor and normal tissues. Immunohistochemistry demonstrated expression of caveolin-1 in normal and benign ovarian epithelial cells, but loss of expression in serous ovarian carcinomas. In low-grade carcinomas, redistribution of caveolin-1 from a membrane-associated pattern observed in normal epithelium to a cytoplasmic localization pattern was observed. No expression of caveolin-1 was detectable in four of six ovarian carcinoma cell lines investigated. In SKOV-3 and ES-2 carcinoma cells, which express high levels of the caveolin-1 protein, phosphorylation of the 22-kd caveolin-1 isoform was detected. Inhibition of both DNA methylation and histone deacetylation using 5-aza-2'deoxycytidine and Trichostatin A, respectively, relieves down-regulation of caveolin-1 in OAW42 and OVCAR-3 cells which is in part mediated by direct regulation at the mRNA level. Expression of CAV1 in the ovarian carcinoma cell line OVCAR-3, resulted in suppression of tumor cell survival in vitro, suggesting that the CAV1 gene is likely to act as a tumor suppressor gene in human ovarian epithelium.

关键词：癌/遗传学癌/代谢癌/病理学窖蛋白1 细胞质膜微囊蛋白/遗传学细胞质膜微囊蛋白/代谢细胞存活/生理学减量调节基因肿瘤抑制/生理学甲基化寡核苷酸序列分析卵巢肿瘤/遗传学卵巢肿瘤/代谢卵巢肿瘤/病理学磷酰化肿瘤细胞培养的女(雌)性人类

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Caveolin-3 directly interacts with the C-terminal tail of β-dystroglycan -: Identification of a central WW-like domain within caveolin family members

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第48期275卷 38048-38058页

作者： Sotgia, F Lee, JK Das, K Bedford, M Petrucci, TC Macioce, P Sargiacomo, M Bricarelli, FD Minetti, C Sudol, M Lisanti, MP Yeshiva Univ Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Albert Einstein Canc Ctr Bronx NY 10461 USA Univ Genoa Ist Gaslini Serv Malattie Neuro Muscolari I-16147 Genoa Italy Yeshiva Univ Albert Einstein Coll Med Dept Cell Biol Bronx NY 10461 USA Harvard Univ Sch Med Dept Genet Boston MA 02115 USA Ist Super Sanita Biol Cellulaire Lab I-00161 Rome Italy Ist Super Sanita Dept Hematol Oncol I-00161 Rome Italy CUNY Mt Sinai Sch Med Dept Biochem & Mol Biol New York NY 10029 USA EO Osped Galliera Lab Genet Umana I-16128 Genoa Italy

Caveolin-3, the most recently recognized member of the caveolin gene family, is muscle-specific and is found in both cardiac and skeletal muscle, as well as smooth muscle cells. Several independent lines of evidence indicate that caveolin-3 is localized to the sarcolemma, where it associates with the dystrophin-glycoprotein complex. However, it remains unknown which component of the dystrophin complex interacts with caveolin-3. Here, we demonstrate that caveolin-3 directly interacts with beta -dystroglycan, an integral membrane component of the dystrophin complex. Our results indicate that caveolin-3 co-localizes, co-fractionates, and coimmunoprecipitates with a fusion protein containing the cytoplasmic tail of beta -dystroglycan. In addition, we show that a novel WW-like domain within caveolin-3 directly recognizes the extreme C terminus of beta -dystroglycan that contains a PPXY motif. As the WW domain of dystrophin recognizes the same site within beta -dystroglycan, we also demonstrate that caveolin-3 can effectively block the interaction of dystrophin with beta -dystroglycan. In this regard, interaction of caveolin-3 with beta -dystroglycan may competitively regulate the recruitment of dystrophin to the sarcolemma. We discuss the possible implications of our findings in the context of Duchenne muscular dystrophy.

关键词： 3T3细胞氨基酸序列结合部位窖蛋白3 细胞质膜微囊蛋白/化学细胞质膜微囊蛋白/代谢细胞支架蛋白质类/化学细胞支架蛋白质类/代谢肌营养不良蛋白聚糖类膜糖蛋白类/化学膜糖蛋白类/代谢分子序列数据沉淀素试验蛋白质结合序列同源性氨基酸动物小鼠

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Absence of caveolin-1 sensitizes mouse skin to carcinogen-induced epidermal hyperplasia and tumor formation

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AMERICAN JOURNAL OF PATHOLOGY 2003年第6期162卷 2029-2039页

作者： Capozza, F Williams, TM Schubert, W McClain, S Bouzahzah, B Sotgia, F Lisanti, MP Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA Albert Einstein Coll Med Albert Einstein Canc Ctr Bronx NY 10461 USA Albert Einstein Coll Med Dept Pathol Bronx NY 10461 USA Montefiore Med Ctr Bronx NY 10467 USA Albert Einstein Coll Med Div Cardiol Dept Med Bronx NY 10461 USA Albert Einstein Coll Med Div Infect Dis Dept Med Bronx NY 10461 USA

Caveolin-1 is the principal Protein component of caveolae membrane domains, which are located at the cell surface in most cell types. Evidence has accumulated suggesting that caveolin-1 may function as a suppressor of cell transformation in cultured cells. The human CAV-1 gene is located at a putative tumor suppressor locus (7q31.1/D7S522) and a known fragile site (FRA7G) that is deleted in a variety of epithelial-derived tumors. Mechanistically, caveolin-1 is known to function as a negative regulator of the Ras-p42/44 MAP kinase cascade and as a transcriptional repressor of cyclin D1, possibly explaining its transformation suppressor activity in cultured cells. However, it remains unknown whether caveolin-1 functions as a tumor suppressor gene in vivo. Here, we examine the tumor suppressor function of caveolin-1 using Cav-1 (-/-) null mice as a model system. Cav-1 null mice and their wild-type counterparts were subjected to carcinogen-induced skin tumorigenesis, using 7,12-dimethylbenzanthracene (DMBA). Mice were monitored weekly for the development of tumors. We demonstrate that Cav-1 null mice are dramatically more susceptible to carcinogen-induced tumorigenesis, as they develop skin tumors at an increased rate. After 16 weeks of DMBA-treatment, Cav-1 null mice showed a 10-fold increase in tumor incidence, a 15-fold increase in tumor number per mouse (multiplicity), and a 35-fold increase in tumor area per mouse, as compared with wild-type litter-mate mice. Moreover, before the development of tumors, DMBA-treatment induced severe epidermal hyperplasia in Cav-1 null mice. Both the basal cell layer and the suprabasal cell layers were expanded in treated Cav-1 null mice, as evidenced by immunostaining with cell-type specific differentiation markers (keratin-10 and keratin-14). In addition, cyclin D1 and phospho-ERK1/2 levels were up-regulated during epidermal hyperplasia, suggesting a possible mechanism for the increased susceptibility of Cav-1 null mice to tumorige

关键词： 9 10-二甲基-1 2-苯并蒽/毒性致癌物/毒性窖蛋白1 细胞质膜微囊蛋白/遗传学细胞质膜微囊蛋白/代谢细胞分裂/药物作用细胞周期蛋白D1/代谢表皮/药物作用表皮/病理学增生免疫组织化学角蛋白细胞/药物作用角蛋白细胞/代谢角蛋白细胞/超微结构小鼠近交C57BL 小鼠基因敲除显微镜检查电子丝裂原活化蛋白激酶1/代谢丝裂原活化蛋白激酶3 丝裂原激活蛋白激酶类/代谢肿瘤实验性/化学诱导肿瘤实验性/病理学磷酰化皮肤/药物作用皮肤/病理学皮肤/超微结构时间因素增量调节动物小鼠

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Constitutive and growth factor-regulated phosphorylation of caveolin-1 occurs at the same site (Tyr-14) in vivo:: Identification of a c-Src/Cav-1/Grb7 signaling cassette

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MOLECULAR ENDOCRINOLOGY 2000年第11期14卷 1750-1775页

作者： Lee, H Volonte, D Galbiati, F Iyengar, P Lublin, DM Bregman, DB Wilson, MT Campos-Gonzalez, R Bouzahzah, B Pestell, RG Scherer, PE Lisanti, MP Yeshiva Univ Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Albert Einstein Canc Ctr Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Cell Biol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Pathol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Dev & Mol Biol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Med Bronx NY 10461 USA Washington Univ Sch Med Dept Pathol St Louis MO 63110 USA BD Transduct Labs Lexington KY 40511 USA

Caveolin-1 was first identified as a phosphoprotein in Rous sarcoma virus (RSV)-transformed chicken embryo fibroblasts. Tyrosine 14 is now thought to be the principal site for recognition by c-Src kinase;however, little is known about this phosphorylation event. Here, we generated a monoclonal antibody (mAb) probe that recognizes only tyrosine 14-phosphorylated caveolin-1. Using this approach, we show that caveolin-1 (Y14) is a specific tyrosine kinase substrate that is constitutively phosphorylated in Src- and Abl-transformed cells and transiently phosphorylated in a regulated fashion during growth factor signaling. We also provide evidence that tyrosine-phosphorylated caveolin-1 is localized at the major sites of tyrosine-kinase signaling, i.e. focal adhesions. By analogy with other signaling events, we hypothesized that caveolin-1 could serve as a docking site for pTyr-binding molecules. In support of this hypothesis, we show that phosphorylation of caveolin-1 on tyrosine 14 confers binding to Grb7 (an SH2-domain containing protein) both in vitro and in vivo. Furthermore, we demonstrate that binding of Grb7 to tyrosine 14-phosphorylated caveolin-1 functionally augments anchorage-independent growth and epidermal growth factor (EGF)-stimulated cell migration. We discuss the possible implications of our findings in the context of signal transduction.

关键词： 3T3细胞脂细胞/药物作用氨基酸序列抗体单克隆/药理学细胞质膜微囊/代谢窖蛋白1 细胞质膜微囊蛋白/遗传学细胞质膜微囊蛋白/免疫学细胞质膜微囊蛋白/代谢细胞黏附/生理学细胞分裂/生理学细胞运动/生理学表皮生长因子/药理学 GRB7衔接蛋白质生长物质/代谢胰岛素/代谢胰岛素/药理学脂类代谢小鼠近交BALBC 分子序列数据磷酰化/药物作用蛋白质类/代谢受体表皮生长因子/代谢信号传导酪氨酸/代谢钒酸盐类/药理学 src族激酶类/代谢动物女(雌)性人类小鼠

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Caveolin-1在人雄激素非依赖性前列腺癌细胞系中的表达

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中国医师杂志 2009年第9期11卷 1262-1263页

作者：廖海球杨罗艳湖南省娄底市中心医院泌尿外科湖南娄底417000 中南大学湘雅二医院泌尿外科

目的研究人雄激素非依赖性前列腺癌PC-3和PC-3m细胞中Caveolin-1 mRNA的表达，分析Caveolin—1与前列腺癌发生发展的关系，探讨Caveolin—1表达在PC-3m具有高侵袭性和转移性中的作用。方法以PC-3和PC-3m细胞系为研究对象，采用RT-PCR检... 详细信息

目的研究人雄激素非依赖性前列腺癌PC-3和PC-3m细胞中Caveolin-1 mRNA的表达，分析Caveolin—1与前列腺癌发生发展的关系，探讨Caveolin—1表达在PC-3m具有高侵袭性和转移性中的作用。方法以PC-3和PC-3m细胞系为研究对象，采用RT-PCR检测PC-3和PC-3m细胞系中Caveolin-1 mRNA的表达。结果PC-3、PC-3m细胞中均有Caveolin-1 mRNA的表达，其在PC-3m细胞中的表达水平明显高于PC-3细胞，两者差异有统计学意义（P〈0．01）。结论Caveolin-1在人前列腺癌的侵袭和转移过程中发挥作用。

关键词：细胞质膜微囊蛋白/代谢前列腺肿瘤/代谢雄激素类

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