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  • 1
    Language: English
    In: Science (American Association for the Advancement of Science), 2004-03-05, Vol.303 (5663), p.1532-1535
    Description: Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria. These neutrophil extracellular traps (NETs) degrade virulence factors and kill bacteria. NETs are abundant in vivo in experimental dysentery and spontaneous human appendicitis, two examples of acute inflammation. NETs appear to be a form of innate response that binds microorganisms, prevents them from spreading, and ensures a high local concentration of antimicrobial agents to degrade virulence factors and kill bacteria.
    Subject(s): Animals ; Antibodies ; Antimicrobials ; Appendicitis - immunology ; Bacteria ; Bacterial Proteins - metabolism ; Biological and medical sciences ; Blood Bactericidal Activity ; Cellular biology ; Chemical properties ; Cytochalasin D - pharmacology ; Cytoplasmic Granules - metabolism ; DNA ; DNA - analysis ; DNA - metabolism ; Dysentery, Bacillary - immunology ; Endopeptidases - metabolism ; Fundamental and applied biological sciences. Psychology ; Histones ; Histones - analysis ; Histones - metabolism ; Humans ; Immune system ; Immunity, Innate ; Infections ; Inflammation ; Leucocytes ; Leukocyte Elastase - analysis ; Leukocyte Elastase - metabolism ; Microscopy, Electron ; Molecular and cellular biology ; Neuroendocrine tumors ; Neutrophil Activation ; Neutrophils ; Neutrophils - chemistry ; Neutrophils - immunology ; Neutrophils - physiology ; Neutrophils - ultrastructure ; Phagocytosis ; Physiological aspects ; Rabbits ; Reports ; Salmonella typhimurium - immunology ; Salmonella typhimurium - physiology ; Shigella flexneri - immunology ; Shigella flexneri - physiology ; Staphylococcus aureus - immunology ; Staphylococcus aureus - physiology ; Virulence factors ; Virulence Factors - metabolism
    ISSN: 0036-8075
    E-ISSN: 1095-9203
    Source: JSTOR Life Sciences
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: Get It Now
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  • 2
    Language: English
    In: PloS one, 2011, Vol.6 (11), p.e27352
    Description: Somatic cells reprogrammed into induced pluripotent stem cells (iPSCs) acquire features of human embryonic stem cells (hESCs) and thus represent a promising source for cellular therapy of debilitating diseases, such as age-related disorders. However, reprogrammed cell lines have been found to harbor various genomic alterations. In addition, we recently discovered that the mitochondrial DNA of human fibroblasts also undergoes random mutational events upon reprogramming. Aged somatic cells might possess high susceptibility to nuclear and mitochondrial genome instability. Hence, concerns over the oncogenic potential of reprogrammed cells due to the lack of genomic integrity may hinder the applicability of iPSC-based therapies for age-associated conditions. Here, we investigated whether aged reprogrammed cells harboring chromosomal abnormalities show resistance to apoptotic cell death or mitochondrial-associated oxidative stress, both hallmarks of cancer transformation. Four iPSC lines were generated from dermal fibroblasts derived from an 84-year-old woman, representing the oldest human donor so far reprogrammed to pluripotency. Despite the presence of karyotype aberrations, all aged-iPSCs were able to differentiate into neurons, re-establish telomerase activity, and reconfigure mitochondrial ultra-structure and functionality to a hESC-like state. Importantly, aged-iPSCs exhibited high sensitivity to drug-induced apoptosis and low levels of oxidative stress and DNA damage, in a similar fashion as iPSCs derived from young donors and hESCs. Thus, the occurrence of chromosomal abnormalities within aged reprogrammed cells might not be sufficient to over-ride the cellular surveillance machinery and induce malignant transformation through the alteration of mitochondrial-associated cell death. Taken together, we unveiled that cellular reprogramming is capable of reversing aging-related features in somatic cells from a very old subject, despite the presence of genomic alterations. Nevertheless, we believe it will be essential to develop reprogramming protocols capable of safeguarding the integrity of the genome of aged somatic cells, before employing iPSC-based therapy for age-associated disorders.
    Subject(s): Aberration ; Abnormalities ; Age ; Aged, 80 and over ; Aging ; Aging - genetics ; Aging - pathology ; Apoptosis ; Biochemistry ; Biology ; Cancer ; Cell death ; Cell Death - genetics ; Cellular Reprogramming ; Chromosome Aberrations ; Chromosomes ; Deoxyribonucleic acid ; Disorders ; DNA ; DNA damage ; Embryo cells ; Embryonic stem cells ; Female ; Fibroblasts ; Fibroblasts - cytology ; Genetic aspects ; Genomes ; Genomic instability ; Genomic Instability - genetics ; Genomics ; Humans ; Induced Pluripotent Stem Cells - cytology ; Induced Pluripotent Stem Cells - metabolism ; Induced Pluripotent Stem Cells - pathology ; Inhibitory postsynaptic potentials ; Integrity ; Karyotype ; Medicine ; Mitochondria - metabolism ; Mitochondria - pathology ; Mitochondrial DNA ; Mortality ; Oxidation resistance ; Oxidative stress ; Oxidative Stress - genetics ; Pluripotency ; Signal Transduction - genetics ; Skin ; Somatic cells ; Stability ; Stem cells ; Telomerase ; Therapy ; Tissue Donors ; Transformation ; Transplantation
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 3
    Language: English
    In: Nature communications, 2019-07-02, Vol.10 (1), p.2919-15
    Description: Oncogenic mutations in KRAS or BRAF are frequent in colorectal cancer and activate the ERK kinase. Here, we find graded ERK phosphorylation correlating with cell differentiation in patient-derived colorectal cancer organoids with and without KRAS mutations. Using reporters, single cell transcriptomics and mass cytometry, we observe cell type-specific phosphorylation of ERK in response to transgenic KRAS(G12V) in mouse intestinal organoids, while transgenic BRAF(V600E) activates ERK in all cells. Quantitative network modelling from perturbation data reveals that activation of ERK is shaped by cell type-specific MEK to ERK feed forward and negative feedback signalling. We identify dual-specificity phosphatases as candidate modulators of ERK in the intestine. Furthermore, we find that oncogenic KRAS, together with beta-Catenin, favours expansion of crypt cells with high ERK activity. Our experiments highlight key differences between oncogenic BRAF and KRAS in colorectal cancer and find unexpected heterogeneity in a signalling pathway with fundamental relevance for cancer therapy.
    Subject(s): Animals ; Cancer ; Cancer models ; Cell activation ; Cell differentiation ; Cell Line, Tumor ; Colon ; Colon cancer ; Colonic Neoplasms - enzymology ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Colorectal cancer ; Colorectal carcinoma ; Cytometry ; Differentiation (biology) ; Epithelium ; Extracellular signal-regulated kinase ; Gastrointestinal cancer ; Gene Expression Regulation, Neoplastic ; Heterogeneity ; Humans ; Intestinal Mucosa - enzymology ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Intestine ; Kinases ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinase Kinases - genetics ; Mitogen-Activated Protein Kinase Kinases - metabolism ; Modulators ; Morphogen signalling ; Multidisciplinary Sciences ; Mutation ; Negative feedback ; Network topology ; Oncogenes ; Organoids ; Perturbation methods ; Phosphorylation ; Proto-Oncogene Proteins B-raf - genetics ; Proto-Oncogene Proteins B-raf - metabolism ; Proto-Oncogene Proteins p21(ras) - genetics ; Proto-Oncogene Proteins p21(ras) - metabolism ; Science & Technology ; Science & Technology - Other Topics ; Signal transduction ; Signaling ; Species Specificity ; β-Catenin
    ISSN: 2041-1723
    E-ISSN: 2041-1723
    Source: Nature Open Access
    Source: Web of Science - Science Citation Index Expanded - 2019〈img src="http://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /〉
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 4
    Language: English
    In: Scientific reports, 2017-07-24, Vol.7 (1), p.6294-11
    Description: Induced pluripotent stem cells (iPSCs) are similar to embryonic stem cells and can be generated from somatic cells. We have generated episomal plasmid-based and integration-free iPSCs (E-iPSCs) from human fetal foreskin fibroblast cells (HFF1). We used an E-iPSC-line to model hepatogenesis in vitro. The HLCs were characterized biochemically, i.e. glycogen storage, ICG uptake and release, UREA and bile acid production, as well as CYP3A4 activity. Ultra-structure analysis by electron microscopy revealed the presence of lipid and glycogen storage, tight junctions and bile canaliculi- all typical features of hepatocytes. Furthermore, the transcriptome of undifferentiated E-iPSC, DE, HE and HLCs were compared to that of fetal liver and primary human hepatocytes (PHH). K-means clustering identified 100 clusters which include developmental stage-specific groups of genes, e.g. OCT4 expression at the undifferentiated stage, SOX17 marking the DE stage, DLK and HNF6 the HE stage, HNF4α and Albumin is specific to HLCs, fetal liver and adult liver (PHH) stage. We use E-iPSCs for modeling gene regulatory networks associated with human hepatogenesis and gastrulation in general.
    Subject(s): Acid production ; Bile Canaliculi - cytology ; Bile Canaliculi - metabolism ; Bile ducts ; Cell Lineage ; Cells, Cultured ; Electron microscopy ; Embryo cells ; Embryos ; Fetus - cytology ; Fetus - metabolism ; Fetuses ; Fibroblasts - cytology ; Fibroblasts - metabolism ; Foreskin - cytology ; Foreskin - metabolism ; Gastrulation ; Gene expression ; Gene Regulatory Networks ; Glycogen ; Hepatocytes ; Hepatocytes - cytology ; Hepatocytes - metabolism ; Humans ; Induced Pluripotent Stem Cells - cytology ; Induced Pluripotent Stem Cells - metabolism ; Infant, Newborn ; Inhibitory postsynaptic potentials ; Liver ; Male ; Oct-4 protein ; Pluripotency ; Somatic cells ; Stem cells ; Tight junctions ; Transcriptome ; Urea
    ISSN: 2045-2322
    E-ISSN: 2045-2322
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 5
    Language: English
    In: Stem cells and development, 2012-11-01, Vol.21 (16), p.2987-3000
    Description: Bone morphogenetic protein (BMP) signaling is known to support differentiation of human embryonic stem cells ( hESCs) into mesoderm and extraembryonic lineages, whereas other signaling pathways can largely influence this lineage specification. Here, we set out to reinvestigate the influence of ACTIVIN/NODAL and fibroblast growth factor (FGF) pathways on the lineage choices made by hESCs during BMP4-driven differentiation. We show that BMP activation, coupled with inhibition of both ACTIVIN/NODAL and FGF signaling, induces differentiation of hESCs, specifically to βhCG hormone-secreting multinucleated syncytiotrophoblast and does not support induction of embryonic and extraembryonic lineages, extravillous trophoblast, and primitive endoderm. It has been previously reported that FGF2 can switch BMP4-induced hESC differentiation outcome to mesendoderm. Here, we show that FGF inhibition alone, or in combination with either ACTIVIN/NODAL inhibition or BMP activation, supports hESC differentiation to hCG-secreting syncytiotrophoblast. We show that the inhibition of the FGF pathway acts as a key in directing BMP4-mediated hESC differentiation to syncytiotrophoblast.
    Subject(s): Activins - metabolism ; Animals ; Autocrine Communication - drug effects ; Autocrine Communication - genetics ; Benzamides - pharmacology ; Bone Morphogenetic Protein 4 - pharmacology ; Bone morphogenetic proteins ; CDX2 Transcription Factor ; Cell differentiation ; Cell Differentiation - drug effects ; Cell Differentiation - genetics ; Cell Fusion ; Cell Line ; Cellular signal transduction ; Chorionic Gonadotropin, beta Subunit, Human - metabolism ; Dioxoles - pharmacology ; Embryonic stem cells ; Embryonic Stem Cells - cytology ; Embryonic Stem Cells - drug effects ; Embryonic Stem Cells - metabolism ; Endoderm - cytology ; Endoderm - drug effects ; Endoderm - metabolism ; Female ; Fibroblast growth factors ; Fibroblast Growth Factors - antagonists & inhibitors ; Fibroblast Growth Factors - metabolism ; Gene Expression Regulation - drug effects ; Genetic aspects ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Humans ; Mesoderm - cytology ; Mesoderm - drug effects ; Mesoderm - metabolism ; Mice ; Models, Biological ; Nodal Protein - antagonists & inhibitors ; Nodal Protein - metabolism ; Original Research Reports ; Placenta - drug effects ; Placenta - metabolism ; Pregnancy ; Pyrroles - pharmacology ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Trophoblasts - cytology ; Trophoblasts - drug effects ; Trophoblasts - metabolism ; Wnt Proteins - metabolism
    ISSN: 1547-3287
    E-ISSN: 1557-8534
    Source: Alma/SFX Local Collection
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  • 6
    Language: English
    In: The Journal of biological chemistry, 2014-07-18, Vol.289 (29), p.20182-20191
    Description: Although soluble species of the amyloid-β peptide Aβ42 correlate with disease symptoms in Alzheimer disease, little is known about the biological activities of amyloid-β (Aβ). Here, we show that Aβ peptides varying in lengths from 38 to 43 amino acids are internalized by cultured neuroblastoma cells and can be found in the nucleus. By three independent methods, we demonstrate direct detection of nuclear Aβ42 as follows: (i) biochemical analysis of nuclear fractions; (ii) detection of biotin-labeled Aβ in living cells by confocal laser scanning microscopy; and (iii) transmission electron microscopy of Aβ in cultured cells, as well as brain tissue of wild-type and transgenic APPPS1 mice (overexpression of amyloid precursor protein and presenilin 1 with Swedish and L166P mutations, respectively). Also, this study details a novel role for Aβ42 in nuclear signaling, distinct from the amyloid precursor protein intracellular domain. Chromatin immunoprecipitation showed that Aβ42 specifically interacts as a repressor of gene transcription with LRP1 and KAI1 promoters. By quantitative RT-PCR, we confirmed that mRNA levels of the examined candidate genes were exclusively decreased by the potentially neurotoxic Aβ42 wild-type peptide. Shorter peptides (Aβ38 or Aβ40) and other longer peptides (nontoxic Aβ42 G33A substitution or Aβ43) did not affect mRNA levels. Overall, our data indicate that the nuclear translocation of Aβ42 impacts gene regulation, and deleterious effects of Aβ42 in Alzheimer disease pathogenesis may be influenced by altering the expression profiles of disease-modifying genes. Background: Biological activities of nontoxic Aβ42 peptides remain unclear in Alzheimer disease. Results: Aβ species are taken up in the nucleus of cells by a nonregulated mechanism, but only Aβ42 plays a role in gene transcription. Conclusion: Aβ42 may act as a transcriptional regulator, similar to the cytoplasmic fragment AICD. Significance: Genes regulated by nuclear Aβ42 could represent alternative targets for therapeutic approaches.
    Subject(s): Active Transport, Cell Nucleus ; Alzheimer Disease ; Alzheimer Disease - metabolism ; Amino Acid Substitution ; Amyloid ; Amyloid beta-Peptides - chemistry ; Amyloid beta-Peptides - genetics ; Amyloid beta-Peptides - metabolism ; Amyloid beta-Protein Precursor - deficiency ; Amyloid beta-Protein Precursor - genetics ; Amyloid beta-Protein Precursor - metabolism ; Amyloid β42 Toxicity ; Amyloid β42-Chromatin Interaction ; Animals ; Cell Line ; Chromatin Immunoprecipitation (ChiP) ; Gene Expression Regulation ; Gene Regulation ; HEK293 Cells ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Models, Molecular ; Molecular Bases of Disease ; Mutagenesis, Site-Directed ; Neurons - metabolism ; Neurons - ultrastructure ; Nuclear Amyloid β Peptides ; Peptide Fragments - chemistry ; Peptide Fragments - genetics ; Peptide Fragments - metabolism ; Presenilin-1 - deficiency ; Presenilin-1 - genetics ; Presenilin-1 - metabolism ; Protein Multimerization ; Recombinant Proteins - chemistry ; Recombinant Proteins - genetics ; Recombinant Proteins - metabolism ; RNA ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Static Electricity
    ISSN: 0021-9258
    E-ISSN: 1083-351X
    Source: HighWire Press (Free Journals)
    Source: PubMed Central
    Source: Alma/SFX Local Collection
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  • 7
    Language: English
    In: iScience, 2020-10-23, Vol.23 (10), p.101615-101615
    Description: Mononuclear cells are the first line of defense against microbial infection. Yet, several viruses have evolved different mechanisms to overcome host defenses to ensure their spread. Here, we show unique mechanisms of how equid herpesvirus-1 manipulates peripheral blood mononuclear cells (PBMC) to travel further in the body. (1) “PBMC-hitching”: at the initial contact, herpesviruses lurk in the extracellular matrix (ECM) of PBMC without entering the cells. The virus exploits the components of the ECM to bind, transport, and then egress to infect other cells. (2) “Intracellular delivery”: transendothelial migration is a physiological mechanism where mononuclear cells can transmigrate through the endothelial cells. The virus was intangible and probably did not interfere with such a mechanism where the infected PBMC can probably deliver the virus inside the endothelium. (3) “Classical-fusion”: this process is well mastered by herpesviruses due to a set of envelope glycoproteins that facilitate cell-cell fusion and virus spread. [Display omitted] •Several viral proteins facilitate rapid and efficient virus cell-to-cell spread•Viruses can evade face-off engagement with host defenses via cell-to-cell spread•The ECM of PBMC ensures safe transmission of viruses to target cells•Viruses can be transmitted during a transendothelial migration process of PBMC Virology; Cell Biology
    Subject(s): Cell Biology ; Virology
    ISSN: 2589-0042
    E-ISSN: 2589-0042
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 8
    Language: English
    In: Nature communications, 2013, Vol.4 (1), p.1531-1531
    Description: Centrosome morphology and number are frequently deregulated in cancer cells. Here, to identify factors that are functionally relevant for centrosome abnormalities in cancer cells, we established a protein-interaction network around 23 centrosomal and cell-cycle regulatory proteins, selecting the interacting proteins that are deregulated in cancer for further studies. One of these components, LGALS3BP, is a centriole- and basal body-associated protein with a dual role, triggering centrosome hypertrophy when overexpressed and causing accumulation of centriolar substructures when downregulated. The cancer cell line SK-BR-3 that overexpresses LGALS3BP exhibits hypertrophic centrosomes, whereas in seminoma tissues with low expression of LGALS3BP, supernumerary centriole-like structures are present. Centrosome hypertrophy is reversed by depleting LGALS3BP in cells endogenously overexpressing this protein, supporting a direct role in centrosome aberration. We propose that LGALS3BP suppresses assembly of centriolar substructures, and when depleted, causes accumulation of centriolar complexes comprising CPAP, acetylated tubulin and centrin.
    Subject(s): Animals ; Antigens, Neoplasm - genetics ; Antigens, Neoplasm - metabolism ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Cell Line, Tumor ; Centrioles - metabolism ; Centrioles - pathology ; Centrioles - ultrastructure ; Chromatography, Affinity ; Extracellular Matrix Proteins - metabolism ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Glycoproteins - genetics ; Glycoproteins - metabolism ; HEK293 Cells ; Humans ; Hypertrophy ; Male ; Microtubules - metabolism ; Microtubules - ultrastructure ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Protein Interaction Maps ; Protein Transport ; Protein-Serine-Threonine Kinases - metabolism ; Rats ; Rats, Sprague-Dawley ; RNA, Small Interfering - metabolism ; Seminoma - genetics ; Seminoma - pathology ; Spindle Apparatus - metabolism ; Spindle Apparatus - ultrastructure
    ISSN: 2041-1723
    E-ISSN: 2041-1723
    Source: Nature Open Access
    Source: PubMed Central
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  • 9
    Language: English
    In: iScience, 2020-11-20, Vol.23 (11), p.101683-101683
    Description: Estrogens play an important role in the development and progression of human cancers, particularly in breast cancer. Breast cancer progression depends on the malignant destabilization of adherens junctions (AJs) and disruption of tissue integrity. We found that estrogen receptor alpha (ERα) inhibition led to a striking spatial reorganization of AJs and microclustering of E-Cadherin (E-Cad) in the cell membrane of breast cancer cells. This resulted in increased stability of AJs and cell stiffness and a reduction of cell motility. These effects were actomyosin-dependent and reversible by estrogens. Detailed investigations showed that the ERα target gene and epidermal growth factor receptor (EGFR) ligand Amphiregulin (AREG) essentially regulates AJ reorganization and E-Cad microclustering. Our results not only describe a biological mechanism for the organization of AJs and the modulation of mechanical properties of cells but also provide a new perspective on how estrogens and anti-estrogens might influence the formation of breast tumors. [Display omitted] •ERα inhibition causes adherens junction (AJ) reorganization through AREG and EGFR•AJ reorganization coincides with microclustering of E-Cadherin at cell membranes•AJ reorganization and microclustering of E-Cadherin are actomyosin dependent•AJ reorganization correlates with increased cell stiffness and reduced motility Cell Biology; Cancer
    Subject(s): Cancer ; Cell Biology
    ISSN: 2589-0042
    E-ISSN: 2589-0042
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 10
    Language: English
    In: Stem cells (Dayton, Ohio), 2010-04, Vol.28 (4), p.721-733
    Description: The ability of stem cells to propagate indefinitely is believed to occur via the fine modulation of pathways commonly involved in cellular senescence, including the telomerase, the p53, and the mitochondrial/oxidative stress pathways. Induced pluripotent stem cells (iPSCs) are a novel stem cell population obtained from somatic cells through forced expression of a set of genes normally expressed in embryonic stem cells (ESCs). These reprogrammed cells acquire self‐renewal properties and appear almost undistinguishable from ESCs in terms of morphology, gene expression, and differentiation potential. Accordingly, iPSCs exhibit alterations of the senescence‐related telomerase and p53 signaling pathways. However, although treatments with antioxidants have been recently shown to enhance cellular reprogramming, detailed information regarding the state of the mitochondrial/oxidative stress pathway in iPSCs is still lacking. Mitochondria undergo specific changes during organismal development and aging. Thus, addressing whether somatic mitochondria within iPSCs acquire ESC‐like features or retain the phenotype of the parental cell is an unanswered but relevant question. Herein, we demonstrate that somatic mitochondria within human iPSCs revert to an immature ESC‐like state with respect to organelle morphology and distribution, expression of nuclear factors involved in mitochondrial biogenesis, content of mitochondrial DNA, intracellular ATP level, oxidative damage, and lactate generation. Upon differentiation, mitochondria within iPSCs and ESCs exhibited analogous maturation and anaerobic‐to‐aerobic metabolic modifications. Overall, the data highlight that human iPSCs and ESCs, although not identical, share similar mitochondrial properties and suggest that cellular reprogramming can modulate the mitochondrial/oxidative stress pathway, thus inducing a rejuvenated state capable of escaping cellular senescence. STEM CELLS 2010;28:721–733
    Subject(s): Aging ; Anaerobiosis ; Cells, Cultured ; Cellular Senescence ; Differentiation ; DNA, Mitochondrial - genetics ; Embryonic stem cells ; Gene Dosage ; Gene expression ; Gene Expression Profiling ; Glycolysis ; Humans ; Induced pluripotency ; Induced Pluripotent Stem Cells - metabolism ; iPS ; Karyotyping ; Microscopy, Electron, Transmission ; Mitochondria - metabolism ; Mitochondria - ultrastructure ; Oxidative Stress ; Reprogramming ; Transcription, Genetic
    ISSN: 1066-5099
    E-ISSN: 1549-4918
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Wiley-Blackwell Full Collection 2014
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