排序方式: 共有49条查询结果,搜索用时 9 毫秒
41.
Federica Corallini Paola Secchiero Antonio Paolo Beltrami Daniela Cesselli Elisa Puppato Roberto Ferrari Carlo Alberto Beltrami Giorgio Zauli 《Cellular and molecular life sciences : CMLS》2010,67(8):1307-1314
The number of circulating mesenchymal stem cells (MSC), analyzed after acute myocardial infarction (AMI), was lower in AMI
patients who developed heart failure (HF) in the follow-up. Conversely, the circulating levels of tumor necrosis factor (TNF)-α,
and osteoprotegerin (OPG) were higher in AMI patients who developed HF with respect to the patients who did not develop HF.
In vitro exposure to TNF-α enhanced the migration of MSC in response to TNF-related apoptosis-inducing ligand (TRAIL) and
significantly increased the release of OPG by endothelial cells. On the contrary, OPG dose-dependently neutralized the in
vitro pro-migratory activity of TRAIL. Thus, TNF-α exhibits opposite effects on MSC migration driven by TRAIL: it is capable
of potentiating MSC migration as well as of inhibiting MSC migration as an indirect consequence of OPG induction, which might
result in a suboptimal recruitment of circulating MSC after AMI in those patients who develop HF in the follow-up. 相似文献
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Morgado M Cairrão E Santos-Silva AJ Verde I 《Cellular and molecular life sciences : CMLS》2012,69(2):247-266
Vascular smooth muscle tone is controlled by a balance between the cellular signaling pathways that mediate the generation
of force (vasoconstriction) and release of force (vasodilation). The initiation of force is associated with increases in intracellular
calcium concentrations, activation of myosin light-chain kinase, increases in the phosphorylation of the regulatory myosin
light chains, and actin-myosin crossbridge cycling. There are, however, several signaling pathways modulating Ca2+ mobilization and Ca2+ sensitivity of the contractile machinery that secondarily regulate the contractile response of vascular smooth muscle to
receptor agonists. Among these regulatory mechanisms involved in the physiological regulation of vascular tone are the cyclic
nucleotides (cAMP and cGMP), which are considered the main messengers that mediate vasodilation under physiological conditions.
At least four distinct mechanisms are currently thought to be involved in the vasodilator effect of cyclic nucleotides and
their dependent protein kinases: (1) the decrease in cytosolic calcium concentration ([Ca2+]c), (2) the hyperpolarization of the smooth muscle cell membrane potential, (3) the reduction in the sensitivity of the contractile
machinery by decreasing the [Ca2+]c sensitivity of myosin light-chain phosphorylation, and (4) the reduction in the sensitivity of the contractile machinery
by uncoupling contraction from myosin light-chain phosphorylation. This review focuses on each of these mechanisms involved
in cyclic nucleotide-dependent relaxation of vascular smooth muscle under physiological conditions. 相似文献
43.
Comino-Méndez I Gracia-Aznárez FJ Schiavi F Landa I Leandro-García LJ Letón R Honrado E Ramos-Medina R Caronia D Pita G Gómez-Graña A de Cubas AA Inglada-Pérez L Maliszewska A Taschin E Bobisse S Pica G Loli P Hernández-Lavado R Díaz JA Gómez-Morales M González-Neira A Roncador G Rodríguez-Antona C Benítez J Mannelli M Opocher G Robledo M Cascón A 《Nature genetics》2011,43(7):663-667
Hereditary pheochromocytoma (PCC) is often caused by germline mutations in one of nine susceptibility genes described to date, but there are familial cases without mutations in these known genes. We sequenced the exomes of three unrelated individuals with hereditary PCC (cases) and identified mutations in MAX, the MYC associated factor X gene. Absence of MAX protein in the tumors and loss of heterozygosity caused by uniparental disomy supported the involvement of MAX alterations in the disease. A follow-up study of a selected series of 59 cases with PCC identified five additional MAX mutations and suggested an association with malignant outcome and preferential paternal transmission of MAX mutations. The involvement of the MYC-MAX-MXD1 network in the development and progression of neural crest cell tumors is further supported by the lack of functional MAX in rat PCC (PC12) cells and by the amplification of MYCN in neuroblastoma and suggests that loss of MAX function is correlated with metastatic potential. 相似文献
44.
Elisa Rossi Christilla Bachelot-Loza Dominique Pidard Pascale Gaussem Sonia Poirault-Chassac Francisco J. Blanco Carmen Langa Consuelo González-Manchón Jose M. Lopez Novoa David M. Smadja Carmelo Bernabeu 《Cellular and molecular life sciences : CMLS》2018,75(7):1269-1284
Complex interactions between platelets and activated endothelium occur during the thrombo-inflammatory reaction at sites of vascular injuries and during vascular hemostasis. The endothelial receptor endoglin is involved in inflammation through integrin-mediated leukocyte adhesion and transmigration; and heterozygous mutations in the endoglin gene cause hereditary hemorrhagic telangiectasia type 1. This vascular disease is characterized by a bleeding tendency that is postulated to be a consequence of telangiectasia fragility rather than a platelet defect, since platelets display normal functions in vitro in this condition. Here, we hypothesize that endoglin may act as an adhesion molecule involved in the interaction between endothelial cells and platelets through integrin recognition. We find that the extracellular domain of human endoglin promotes specific platelet adhesion under static conditions and confers resistance of adherent platelets to detachment upon exposure to flow. Also, platelets adhere to confluent endothelial cells in an endoglin-mediated process. Remarkably, Chinese hamster ovary cells ectopically expressing the human αIIbβ3 integrin acquire the capacity to adhere to myoblast transfectants expressing human endoglin, whereas platelets from Glanzmann’s thrombasthenia patients lacking the αIIbβ3 integrin are defective for endoglin-dependent adhesion to endothelial cells. Furthermore, the bleeding time, but not the prothrombin time, is significantly prolonged in endoglin-haplodeficient (Eng +/?) mice compared to Eng +/+ animals. These results suggest a new role for endoglin in αIIbβ3 integrin-mediated adhesion of platelets to the endothelium, and may provide a better understanding on the basic cellular mechanisms involved in hemostasis and thrombo-inflammatory events. 相似文献
45.
VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche 总被引:4,自引:0,他引:4
Kaplan RN Riba RD Zacharoulis S Bramley AH Vincent L Costa C MacDonald DD Jin DK Shido K Kerns SA Zhu Z Hicklin D Wu Y Port JL Altorki N Port ER Ruggero D Shmelkov SV Jensen KK Rafii S Lyden D 《Nature》2005,438(7069):820-827
The cellular and molecular mechanisms by which a tumour cell undergoes metastasis to a predetermined location are largely unknown. Here we demonstrate that bone marrow-derived haematopoietic progenitor cells that express vascular endothelial growth factor receptor 1 (VEGFR1; also known as Flt1) home to tumour-specific pre-metastatic sites and form cellular clusters before the arrival of tumour cells. Preventing VEGFR1 function using antibodies or by the removal of VEGFR1(+) cells from the bone marrow of wild-type mice abrogates the formation of these pre-metastatic clusters and prevents tumour metastasis, whereas reconstitution with selected Id3 (inhibitor of differentiation 3)-competent VEGFR1+ cells establishes cluster formation and tumour metastasis in Id3 knockout mice. We also show that VEGFR1+ cells express VLA-4 (also known as integrin alpha4beta1), and that tumour-specific growth factors upregulate fibronectin--a VLA-4 ligand--in resident fibroblasts, providing a permissive niche for incoming tumour cells. Conditioned media obtained from distinct tumour types with unique patterns of metastatic spread redirected fibronectin expression and cluster formation, thereby transforming the metastatic profile. These findings demonstrate a requirement for VEGFR1+ haematopoietic progenitors in the regulation of metastasis, and suggest that expression patterns of fibronectin and VEGFR1+VLA-4+ clusters dictate organ-specific tumour spread. 相似文献
46.
The specification of both the germ line and abdomen in Drosophila depends on the localization of oskar messenger RNA to the posterior of the oocyte. This localization requires several trans-acting factors, including Barentsz and the Mago-Y14 heterodimer, which assemble with oskar mRNA into ribonucleoprotein particles (RNPs) and localize with it at the posterior pole. Although Barentsz localization in the germ line depends on Mago-Y14, no direct interaction between these proteins has been detected. Here, we demonstrate that the translation initiation factor eIF4AIII interacts with Barentsz and is a component of the oskar messenger RNP localization complex. Moreover, eIF4AIII interacts with Mago-Y14 and thus provides a molecular link between Barentsz and the heterodimer. The mammalian Mago (also known as Magoh)-Y14 heterodimer is a component of the exon junction complex. The exon junction complex is deposited on spliced mRNAs and functions in nonsense-mediated mRNA decay (NMD), a surveillance mechanism that degrades mRNAs with premature translation-termination codons. We show that both Barentsz and eIF4AIII are essential for NMD in human cells. Thus, we have identified eIF4AIII and Barentsz as components of a conserved protein complex that is essential for mRNA localization in flies and NMD in mammals. 相似文献
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Stefania Fadda Simonetta Sangiorgi Elisa Pieragostini 《Cellular and molecular life sciences : CMLS》1979,35(11):1441-1442
Summary G6PD isozyme variation inDrosophila melanogaster is investigated in the larval stage through electrophoretic and genetic analyses. As current structural models for this gene-enzyme system fail to apply in these laboratory populations, the authors suggest a regulatory hypothesis to explain their observations. 相似文献