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41.
Mesenchymal stromal cells from amniotic fluid are less prone to senescence compared to those obtained from bone marrow: An in vitro study
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Nicola Alessio Caterina Pipino Domitilla Mandatori Pamela Di Tomo Angela Ferone Marco Marchiso Mariarosa A.B. Melone Gianfranco Peluso Assunta Pandolfi Umberto Galderisi 《Journal of cellular physiology》2018,233(11):8996-9006
Mesenchymal stromal cells (MSCs) are considered to be an excellent source in regenerative medicine. They contain several cell subtypes, including multipotent stem cells. MSCs are of particular interest as they are currently being tested using cell and gene therapies for a number of human diseases. They represent a rare population in tissues; for this reason, they require, before being transplanted, an in vitro amplification. This process may induce replicative senescence, thus affecting differentiation and proliferative capacities. Increasing evidence suggests that MSCs from fetal tissues are significantly more plastic and grow faster than MSCs from bone marrow. Here, we compare amniotic fluid mesenchymal stromal cells (AF‐MSCs) and bone marrow mesenchymal stromal cells (BM‐MSCs) in terms of cell proliferation, surface markers, multidifferentiation potential, senescence, and DNA repair capacity. Our study shows that AF‐MSCs are less prone to senescence with respect to BM‐MSCs. Moreover, both cell models activate the same repair system after DNA damage, but AF‐MSCs are able to return to the basal condition more efficiently with respect to BM‐MSCs. Indeed, AF‐MSCs are better able to cope with genotoxic stress that may occur either during in vitro cultivation or following transplantation in patients. Our findings suggest that AF‐MSCs may represent a valid alternative to BM‐MSCs in regenerative medicine, and, of great relevance, the investigation of the mechanisms involved in DNA repair capacity of both AF‐MSCs and BM‐MSCs may pave the way to their rational use in the medical field. 相似文献
42.
Effects of Elevated Temperature on the Shell Density of the Large Benthic Foraminifera Amphistegina lobifera
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This study investigated the effects of elevated temperature on shell density and Mg‐ATPase activity of Amphistegina lobifera. This species is abundant in shallow reef habitats, and can be vulnerable to daily physicochemical fluctuations. To assess potential responses and acclimation mechanisms of A. lobifera to changing temperature conditions, we performed a blocked‐design experiment exposing specimens collected from different reef sites (inshore and offshore) to three temperature treatments (Control: 24 °C, + 2 °C: 26 °C and + 5 °C: 29 °C) for 30 days. The final size and shell density of inshore reef foraminifera were unaffected by elevated temperature, and the enzyme activity in these individuals showed that they were able to acclimate to new temperature conditions. In contrast, offshore A. lobifera were more sensitive to changes in temperature, and heat stress caused growth impairment and inhibited Mg‐ATPase activity. However, newly added chambers were not affected. These results suggested that Mg‐ATPase plays an important role in regulating intracellular Mg2+ ions, but has little influence in the onset of calcification in A. lobifera. Moreover, it suggests that even though A. lobifera can regulate intracellular functions, local habitat seems to play a crucial role in determining how foraminifera respond to environmental changes. 相似文献
43.
Targeted Disruption of CDK4 Delays Cell Cycle Entry with Enhanced p27Kip1 Activity 总被引:16,自引:0,他引:16
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Tateki Tsutsui Bahar Hesabi David S. Moons Pier Paolo Pandolfi Kimberly S. Hansel Andrew Koff Hiroaki Kiyokawa 《Molecular and cellular biology》1999,19(10):7011-7019
The mechanism by which cyclin-dependent kinase 4 (CDK4) regulates cell cycle progression is not entirely clear. Cyclin D/CDK4 appears to initiate phosphorylation of retinoblastoma protein (Rb) leading to inactivation of the S-phase-inhibitory action of Rb. However, cyclin D/CDK4 has been postulated to act in a noncatalytic manner to regulate the cyclin E/CDK2-inhibitory activity of p27(Kip1) by sequestration. In this study we investigated the roles of CDK4 in cell cycle regulation by targeted disruption of the mouse CDK4 gene. CDK4(-/-) mice survived embryogenesis and showed growth retardation and reproductive dysfunction associated with hypoplastic seminiferous tubules in the testis and perturbed corpus luteum formation in the ovary. These phenotypes appear to be opposite to those of p27-deficient mice such as gigantism and gonadal hyperplasia. A majority of CDK4(-/-) mice developed diabetes mellitus by 6 weeks, associated with degeneration of pancreatic islets. Fibroblasts from CDK4(-/-) mouse embryos proliferated similarly to wild-type embryonic fibroblasts under conditions that promote continuous growth. However, quiescent CDK4(-/-) fibroblasts exhibited a substantial ( approximately 6-h) delay in S-phase entry after serum stimulation. This cell cycle perturbation by CDK4 disruption was associated with increased binding of p27 to cyclin E/CDK2 and diminished activation of CDK2 accompanied by impaired Rb phosphorylation. Importantly, fibroblasts from CDK4(-/-) p27(-/-) embryos displayed partially restored kinetics of the G(0)-S transition, indicating the significance of the sequestration of p27 by CDK4. These results suggest that at least part of CDK4's participation in the rate-limiting mechanism for the G(0)-S transition consists of controlling p27 activity. 相似文献
44.
Transcriptional repression of Stat6-dependent interleukin-4-induced genes by BCL-6: specific regulation of iepsilon transcription and immunoglobulin E switching.
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47.
A ceRNA hypothesis: the Rosetta Stone of a hidden RNA language? 总被引:4,自引:0,他引:4
48.
In vivo identification of tumor- suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma 总被引:6,自引:0,他引:6
49.
Sandra Münch Stefanie Weidtkamp-Peters Karolin Klement Paulius Grigaravicius Shamci Monajembashi Paolo Salomoni Pier Paolo Pandolfi Klaus Wei?hart Peter Hemmerich 《Molecular and cellular biology》2014,34(10):1733-1746
The PML tumor suppressor has been functionally implicated in DNA damage response and cellular senescence. Direct evidence for such a role based on PML knockdown or knockout approaches is still lacking. We have therefore analyzed the irradiation-induced DNA damage response and cellular senescence in human and mouse fibroblasts lacking PML. Our data show that PML nuclear bodies (NBs) nonrandomly associate with persistent DNA damage foci in unperturbed human skin and in high-dose-irradiated cell culture systems. PML bodies do not associate with transient γH2AX foci after low-dose gamma irradiation. Superresolution microscopy reveals that all PML bodies within a nucleus are engaged at Rad51- and RPA-containing repair foci during ongoing DNA repair. The lack of PML (i) does not majorly affect the DNA damage response, (ii) does not alter the efficiency of senescence induction after DNA damage, and (iii) does not affect the proliferative potential of primary mouse embryonic fibroblasts during serial passaging. Thus, while PML NBs specifically accumulate at Rad51/RPA-containing lesions and senescence-derived persistent DNA damage foci, they are not essential for DNA damage-induced and replicative senescence of human and murine fibroblasts. 相似文献