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  1. Article ; Online: Apoptosis-related gene expression in glioblastoma (LN-18) and medulloblastoma (Daoy) cell lines.

    Wybranska, Iwona / Polus, Anna / Mikolajczyk, Magdalena / Knapp, Anna / Sliwa, Agnieszka / Zapala, Barbara / Staszel, Teresa / Dembinska-Kiec, Aldona

    Human cell

    2013  Volume 26, Issue 4, Page(s) 137–148

    Abstract: The expression of apoptosis genes in a commercial pre-designed low-density array from Applied Biosystems was evaluated in two human brain cancer cell models, LN-18 and Daoy (HTB-186™) in comparison to the reference human primary endothelial cells under ... ...

    Abstract The expression of apoptosis genes in a commercial pre-designed low-density array from Applied Biosystems was evaluated in two human brain cancer cell models, LN-18 and Daoy (HTB-186™) in comparison to the reference human primary endothelial cells under basic conditions. Analysis of the gene expression in the cancer cell lines compared to the normal control revealed features reflecting anti-apoptotic and inflammatory characteristics of the former. There was an overall downregulation of apoptosis-stimulating genes in both cancer cell lines, along with an upregulation of certain apoptosis inhibitors. A number of genes demonstrated statistically significant changes in their expressions, including BAX (BCL2-associated X protein); the CARD4/NLR family, CARD domain containing 4; CASP10 (caspase 10, apoptosis-related cysteine peptidase); DAP1 (death-associated protein kinase 1), and BIRC5 (baculoviral IAP repeat-containing 5). Anti-apoptotic potential in both cell lines was demonstrated by changes in the Bax:Bcl-2 ratio and downregulation of the APAF1 gene in LN18 cells. There was also significant downregulation of extrinsic signals and the TNF/FADD/inflammatory cascade, and upregulation of caspase inhibitors (IAPs). These results provided a novel molecular characterization of important human cancer cell lines, which might provide a useful research tool for investigating the experimental model of the CNS cell.
    MeSH term(s) Apoptosis/genetics ; Apoptosis Regulatory Proteins/genetics ; Apoptotic Protease-Activating Factor 1/genetics ; Caspase 10/genetics ; Cell Line, Tumor ; Down-Regulation/genetics ; Fas-Associated Death Domain Protein/genetics ; Glioblastoma/genetics ; Glioblastoma/pathology ; Humans ; Inhibitor of Apoptosis Proteins/genetics ; Medulloblastoma/genetics ; Medulloblastoma/pathology ; Nod1 Signaling Adaptor Protein/genetics ; Survivin ; Tumor Necrosis Factor-alpha/genetics ; Up-Regulation/genetics ; bcl-2-Associated X Protein/genetics
    Chemical Substances APAF1 protein, human ; Apoptosis Regulatory Proteins ; Apoptotic Protease-Activating Factor 1 ; BIRC5 protein, human ; DAP protein, human ; FADD protein, human ; Fas-Associated Death Domain Protein ; Inhibitor of Apoptosis Proteins ; NOD1 protein, human ; Nod1 Signaling Adaptor Protein ; Survivin ; Tumor Necrosis Factor-alpha ; bcl-2-Associated X Protein ; Caspase 10 (EC 3.4.22.-) ; CASP10 protein, human (EC 3.4.22.63)
    Language English
    Publishing date 2013-09-15
    Publishing country Japan
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1149134-6
    ISSN 1749-0774 ; 0914-7470
    ISSN (online) 1749-0774
    ISSN 0914-7470
    DOI 10.1007/s13577-011-0029-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Humanina i jej analogi jako peptydy o potencjalnym działaniu antyapoptotycznym i potwierdzonych właściwościach neuroprotekcyjnych.

    Zapała, Barbara / Staszel, Teresa / Kieć-Wilk, Beata / Polus, Anna / Knapp, Anna / Wybrańska, Iwona / Kaczyński, Łukasz / Dembińska-Kieć, Aldona

    Przeglad lekarski

    2011  Volume 68, Issue 7, Page(s) 372–377

    Abstract: Humanin (HN) is a newly discovered 24-amino acid peptide, which may suppress neuronal cell death. HN cDNA includes the open reading frame (HN-ORF) of 75 bases, located 950 bases downstream of the 5' end of the HN cDNA. It was demonstrated that HN cDNA is ...

    Title translation Humanin and its derivatives as peptides with potential antiapoptotic and confirmed neuroprotective activities.
    Abstract Humanin (HN) is a newly discovered 24-amino acid peptide, which may suppress neuronal cell death. HN cDNA includes the open reading frame (HN-ORF) of 75 bases, located 950 bases downstream of the 5' end of the HN cDNA. It was demonstrated that HN cDNA is 99% identical with mitochondrial DNA (mtDNA) sequence. HN homologues have been identified as expressed sequence tags (ESTs) in rat and nematode. Certain regions homologous to the HN cDNA exist on human chromosomes. HN forms homodimers and multimers and this seems to be essential for the peptide functions. HN acts as a ligand for formyl peptide receptor-like 1 (FPRL1) and 2 (FPRL2). It was demonstrated that HN plays a protective role by an antiapoptotic activity interfering with Bax activation, and suppressing Bax-dependent apoptosis. HN is also shown to suppress the c-Jun N-terminal kinase (JNK) and ASK/JNK-mediated neuronal cell death. Several studies also confirm that HN could be important in prevention of angiopathy-associated Alzheimer's disease dementia, diseases related to mitochondrial dysfunction (MELAS), and other types of beta-amyloid accumulation associated neurodegeneration. A very recent study demonstrated a pluripotent cytoprotective effect and mechanisms of HNs in cells other than from the CNS, such as germ cells, or panreatic b-cells, and potent physiological consequences that result from HN interaction with IGFBP3 and STAT3. The in vivo studies suggest that humanin may protect against cognitive impairment, also due to ischemia/reperfusion injury.
    MeSH term(s) Animals ; Apoptosis/physiology ; Base Sequence ; Cognitive Dysfunction/physiopathology ; Cognitive Dysfunction/prevention & control ; Cytoprotection/physiology ; DNA, Complementary ; DNA, Mitochondrial/chemistry ; Humans ; Intracellular Signaling Peptides and Proteins/chemistry ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Neuroprotective Agents/metabolism ; Reperfusion Injury/physiopathology ; Reperfusion Injury/prevention & control ; Sequence Homology
    Chemical Substances DNA, Complementary ; DNA, Mitochondrial ; Intracellular Signaling Peptides and Proteins ; Neuroprotective Agents ; humanin
    Language Polish
    Publishing date 2011
    Publishing country Poland
    Document type Journal Article ; Review
    ZDB-ID 414053-9
    ISSN 0033-2240 ; 0860-0422
    ISSN 0033-2240 ; 0860-0422
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Humanins, the neuroprotective and cytoprotective peptides with antiapoptotic and anti-inflammatory properties.

    Zapała, Barbara / Kaczyński, Łukasz / Kieć-Wilk, Beata / Staszel, Teresa / Knapp, Anna / Thoresen, G Hege / Wybrańska, Iwona / Dembińska-Kieć, Aldona

    Pharmacological reports : PR

    2010  Volume 62, Issue 5, Page(s) 767–777

    Abstract: Humanin (HN) is a newly discovered 24-amino acid peptide, which may suppress neuronal cell death. HN cDNA includes an open reading frame (HN-ORF) of 75 bases located 950 bases downstream of the 5' end of the HN cDNA. It has been demonstrated that HN cDNA ...

    Abstract Humanin (HN) is a newly discovered 24-amino acid peptide, which may suppress neuronal cell death. HN cDNA includes an open reading frame (HN-ORF) of 75 bases located 950 bases downstream of the 5' end of the HN cDNA. It has been demonstrated that HN cDNA is 99% identical to the mitochondrial DNA (mtDNA) sequence. HN homologs have been identified as expressed sequence tags (ESTs) in both rats and nematodes. Certain regions that are homologous to the HN cDNA exist on human chromosomes. HN forms homodimers and multimers and this action seems to be essential for peptide function. HN acts as a ligand for formyl peptide receptor-like 1 (FPRL1) and 2 (FPRL2). It has been demonstrated that HN plays a protective role through its antiapoptotic activity that interferes with Bax activation, which suppresses Bax-dependent apoptosis. HN has also been shown to suppress the c-Jun N-terminal kinase (JNK) and ASK/JNK-mediated neuronal cell death. Several studies have also confirmed that HN could be important in the prevention of angiopathy-associated Alzheimer's disease dementia, diseases related to mitochondrial dysfunction (MELAS), and other types of β-amyloid accumulation-associated neurodegeneration. Avery recent study demonstrated a pluripotent cytoprotective effect and mechanisms of HNs in cells not from the CNS, such as germ cells or pancreatic β-cells, and the potent physiological consequences that result from HN interaction with IGFBP3 and STAT3. In vivo studies suggest that HN may also protect against cognitive impairment due to ischemia/reperfusion injury.
    MeSH term(s) Alzheimer Disease/metabolism ; Alzheimer Disease/prevention & control ; Amino Acid Sequence ; Animals ; Anti-Inflammatory Agents/chemistry ; Anti-Inflammatory Agents/pharmacology ; Apoptosis/drug effects ; Cytoprotection ; Humans ; Intracellular Signaling Peptides and Proteins/chemistry ; Intracellular Signaling Peptides and Proteins/pharmacology ; Intracellular Signaling Peptides and Proteins/physiology ; JNK Mitogen-Activated Protein Kinases/metabolism ; MELAS Syndrome/metabolism ; MELAS Syndrome/prevention & control ; Molecular Sequence Data ; Neuroprotective Agents/chemistry ; Neuroprotective Agents/pharmacology ; bcl-2-Associated X Protein/metabolism
    Chemical Substances Anti-Inflammatory Agents ; Intracellular Signaling Peptides and Proteins ; Neuroprotective Agents ; bcl-2-Associated X Protein ; humanin ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2010-11-11
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2186248-5
    ISSN 1734-1140
    ISSN 1734-1140
    DOI 10.1016/s1734-1140(10)70337-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Role of microRNAs in endothelial cell pathophysiology.

    Staszel, Teresa / Zapała, Barbara / Polus, Anna / Sadakierska-Chudy, Anna / Kieć-Wilk, Beata / Stępień, Ewa / Wybrańska, Iwona / Chojnacka, Monika / Dembińska-Kieć, Aldona

    Polskie Archiwum Medycyny Wewnetrznej

    2011  Volume 121, Issue 10, Page(s) 361–366

    Abstract: MicroRNAs (miRNAs) are a family of small, noncoding RNAs that repress gene expression at the post-transcriptional level. Over 700 miRNAs have been identified in the human genome, of which 20% to 30% regulate human protein-coding genes. Functional in ... ...

    Abstract MicroRNAs (miRNAs) are a family of small, noncoding RNAs that repress gene expression at the post-transcriptional level. Over 700 miRNAs have been identified in the human genome, of which 20% to 30% regulate human protein-coding genes. Functional in vitro studies have shown that miRNAs are critical for endothelial cell gene expression and function. miRNAs were found in atherosclerosis, cardiac hypertrophy, arterial hypertension, coronary artery disease, diabetes, and inflammatory diseases. We review the current knowledge about the role of miRNAs in endothelial cells with emphasis on the regulation of cellular senescence, angiogenesis, and vascular inflammation. It has been shown that miR-34a, miR-217, miR-200, miR-146c, and miR-181a are responsible for the regulation of cell stress and proliferation processes. Proangiogenic factors include miR-130a, miR-210, miR-424, miR-17-92, miR-27-b, let-7f, and miR-217, while miR-221 and miR-222 have antiangiogenic properties. Other known miRNAs, including miR-31, miR17-3p, miR-155, miR-221, miR-222, and miR-126, are important factors in the regulation of vascular inflammation. Studies show that miRNA expression analysis can be used in the diagnosis and treatment of various diseases; however, additional research is needed before it is used in routine clinical setting.
    MeSH term(s) Animals ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Cardiomegaly/metabolism ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Coronary Artery Disease/genetics ; Coronary Artery Disease/metabolism ; Endothelium, Vascular/metabolism ; Humans ; Hypertension/genetics ; Hypertension/metabolism ; Inflammation/genetics ; Inflammation/metabolism ; MicroRNAs/metabolism
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2011-10
    Publishing country Poland
    Document type Journal Article ; Review
    ZDB-ID 123500-x
    ISSN 1897-9483 ; 0032-3772
    ISSN (online) 1897-9483
    ISSN 0032-3772
    Database MEDical Literature Analysis and Retrieval System OnLINE

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