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61.
Crisan M Yap S Casteilla L Chen CW Corselli M Park TS Andriolo G Sun B Zheng B Zhang L Norotte C Teng PN Traas J Schugar R Deasy BM Badylak S Buhring HJ Giacobino JP Lazzari L Huard J Péault B 《Cell Stem Cell》2008,3(3):301-313
Mesenchymal stem cells (MSCs), the archetypal multipotent progenitor cells derived in cultures of developed organs, are of unknown identity and native distribution. We have prospectively identified perivascular cells, principally pericytes, in multiple human organs including skeletal muscle, pancreas, adipose tissue, and placenta, on CD146, NG2, and PDGF-Rbeta expression and absence of hematopoietic, endothelial, and myogenic cell markers. Perivascular cells purified from skeletal muscle or nonmuscle tissues were myogenic in culture and in vivo. Irrespective of their tissue origin, long-term cultured perivascular cells retained myogenicity; exhibited at the clonal level osteogenic, chondrogenic, and adipogenic potentials; expressed MSC markers; and migrated in a culture model of chemotaxis. Expression of MSC markers was also detected at the surface of native, noncultured perivascular cells. Thus, blood vessel walls harbor a reserve of progenitor cells that may be integral to the origin of the elusive MSCs and other related adult stem cells. 相似文献
62.
63.
Caveolin-1 null mice develop cardiac hypertrophy with hyperactivation of p42/44 MAP kinase in cardiac fibroblasts 总被引:14,自引:0,他引:14
Cohen AW Park DS Woodman SE Williams TM Chandra M Shirani J Pereira de Souza A Kitsis RN Russell RG Weiss LM Tang B Jelicks LA Factor SM Shtutin V Tanowitz HB Lisanti MP 《American journal of physiology. Cell physiology》2003,284(2):C457-C474
Recently, development ofa caveolin-1-deficient (Cav-1 null) mouse model has allowed thedetailed analysis of caveolin-1's function in the context of awhole animal. Interestingly, we now report that the hearts ofCav-1 null mice are markedly abnormal, despite the fact that caveolin-1is not expressed in cardiac myocytes. However, caveolin-1 is abundantlyexpressed in the nonmyocytic cells of the heart, i.e., cardiacfibroblasts and endothelia. Quantitative imaging studies of Cav-1 nullhearts demonstrate a significantly enlarged right ventricular cavityand a thickened left ventricular wall with decreased systolic function.Histological analysis reveals myocyte hypertrophy withinterstitial/perivascular fibrosis. Because caveolin-1 is thought toact as a negative regulator of the p42/44 MAP kinase cascade, weperformed Western blot analysis with phospho-specific antibodies thatonly recognize activated ERK1/2. As predicted, the p42/44 MAP kinasecascade is hyperactivated in Cav-1 null heart tissue (i.e.,interstitial fibrotic lesions) and isolated cardiac fibroblasts. Inaddition, endothelial and inducible nitric oxide synthase levels aredramatically upregulated. Thus loss of caveolin-1 expression drivesp42/44 MAP kinase activation and cardiac hypertrophy. 相似文献
64.
Ronald E. Clawson Merrill J. Egorin Bonnie M. Fox Louis A. Ross Nicholas R. Bachur 《Life sciences》1981,28(10):1133-1137
The ability of rat liver microsomes and liver slices to metabolize the antineoplastic compound cyclophosphamide was studied at 37° and at elevated temperatures comparable to those used for human systemic hyperthermic antineoplastic therapy. Temperatures above 40.5° and 41.8° inhibited cyclophospamide metabolism by microsomes and liver slices respectively. Therefore, cyclophosphamide may not be a suitable drug for combination with systemic hyperthermia in cancer therapy. 相似文献
65.
Olivier Cohen Christine Cans Jean Louis Gilardi Hubert Roth Marie-Ange Mermet Pierre Jalbert Jacques Demongeot Martine Cuillel 《Human genetics》1996,97(5):659-667
Reciprocal translocations (rcp) are among the most common constitutional chromosomal aberrations in man. Using a European
database of 1574 families carrying autosomal rcp, a cartographic study was done on the breakpoints involved. The breakpoints
are non-randomly distributed along the different chromosomes, indicating “hot spots”. Breakpoints of rcp that result in descendants
that are unbalanced chromosomally at birth are more frequent in a distal position on chromosomal arms, and 65% of them are
localised in R-bands. Among the R-bands, bands rich in GC islands and poor in Alu repetitive sequences are more frequently
the site of breakpoints, as well as bands that include a fragile site. This result suggests that the variation in degree of
methylation in GC islands could be involved in chromosomal breakage and hence in chromosomal rearrangements.
Received: 10 April 1995 / Revised: 1 July 1995 相似文献
66.
67.
Palynological and sedimentological data from a core extracted from Lake Eteza shed new light on the Holocene vegetation and climate history in KwaZulu-Natal and can be linked to regional and global climate change. A 2072 cm core with nineteen radiocarbon dates and chronological extrapolation to the bottom of the sequence suggests that sedimentation started ca. 10 200 cal yrs BP. Between ca. 10 200 and 6800 cal yrs BP pollen indicators point to a change from intermediately humid conditions to comparatively drier grassy environments. This is in good agreement with Sea Surface Temperature (SST) fluctuations from a core in the Mozambique Channel which influence precipitation in coastal KwaZulu-Natal, and the beginning of the Holocene Thermal Maximum ca. 10 500 cal yrs BP. The lower section of the core corresponds to gradually increasing Holocene sea levels along the coast and development of freshwater or estuarine conditions at Lake Eteza. The middle Holocene (ca. 6800-3600 cal yrs BP), when the sea level reached its highest stand and SST peak, indicate humid climatic conditions that favoured an increase of forest trees, e.g. Podocarpus, and undergrowth plants like Issoglossa. As a consequence of higher precipitation and increase of the water table, conditions were favourable for the spread of mangrove, swamp and possibly riverine forest. During the late Holocene after ca. 3600 cal yrs BP a decrease of Podocarpus and other trees as well as an increase of Chenopodiaceae/Amaranthaceae, grasses and Phoenix coincide with a return to lower sea levels and drier conditions. The decrease of all trees including Phoenix at ca. 700 cal yrs BP, accompanied by rapid sedimentation rates, possibly reflect forest clearing and upland erosion induced by activities of Iron Age settlers. A dry period at the globally recognized onset of the Little Ice Age might have contributed to these changes. Late Iron Age settlers have probably already introduced Zea mays, which was detected in the profile since ca. 210 BP. The appearance of neophytes like Pinus, Casuarina and pollen of Ambrosia-type in the youngest sediments indicates increased disturbance of European settlements and land use since ca. 100 cal yrs BP. 相似文献
68.
Codd V Dolezel D Stehlik J Piccin A Garner KJ Racey SN Straatman KR Louis EJ Costa R Sauman I Kyriacou CP Rosato E 《Genetics》2007,177(3):1539-1551
The circadian mechanism appears remarkably conserved between Drosophila and mammals, with basic underlying negative and positive feedback loops, cycling gene products, and temporally regulated nuclear transport involving a few key proteins. One of these negative regulators is PERIOD, which in Drosophila shows very similar temporal and spatial regulation to TIMELESS. Surprisingly, we observe that in the housefly, Musca domestica, PER does not cycle in Western blots of head extracts, in contrast to the TIM protein. Furthermore, immunocytochemical (ICC) localization using enzymatic staining procedures reveals that PER is not localized to the nucleus of any neurons within the brain at any circadian time, as recently observed for several nondipteran insects. However, with confocal analysis, immunofluorescence reveals a very different picture and provides an initial comparison of PER/TIM-containing cells in Musca and Drosophila, which shows some significant differences, but many similarities. Thus, even in closely related Diptera, there is considerable evolutionary flexibility in the number and spatial organization of clock cells and, indeed, in the expression patterns of clock products in these cells, although the underlying framework is similar. 相似文献
69.
70.
Disruption of axonal transport by loss of huntingtin or expression of pathogenic polyQ proteins in Drosophila 总被引:6,自引:0,他引:6
Gunawardena S Her LS Brusch RG Laymon RA Niesman IR Gordesky-Gold B Sintasath L Bonini NM Goldstein LS 《Neuron》2003,40(1):25-40
We tested whether proteins implicated in Huntington's and other polyglutamine (polyQ) expansion diseases can cause axonal transport defects. Reduction of Drosophila huntingtin and expression of proteins containing pathogenic polyQ repeats disrupt axonal transport. Pathogenic polyQ proteins accumulate in axonal and nuclear inclusions, titrate soluble motor proteins, and cause neuronal apoptosis and organismal death. Expression of a cytoplasmic polyQ repeat protein causes adult retinal degeneration, axonal blockages in larval neurons, and larval lethality, but not neuronal apoptosis or nuclear inclusions. A nuclear polyQ repeat protein induces neuronal apoptosis and larval lethality but no axonal blockages. We suggest that pathogenic polyQ proteins cause neuronal dysfunction and organismal death by two non-mutually exclusive mechanisms. One mechanism requires nuclear accumulation and induces apoptosis; the other interferes with axonal transport. Thus, disruption of axonal transport by pathogenic polyQ proteins could contribute to early neuropathology in Huntington's and other polyQ expansion diseases. 相似文献