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  • 1
    Online Resource
    Online Resource
    Tokyo :Springer Japan,
    Keywords: Genomics. ; DNA-binding proteins. ; Transcription factors. ; Gene regulatory networks--Physiology. ; Medical genetics. ; Kruppel-Like Transcription Factors--physiology. ; Gene Regulatory Networks--physiology. ; Zinc Fingers--genetics. ; Gene regulatory networks. ; Electronic books.
    Description / Table of Contents: Synthesizing the latest research on Kruppel-like factors (KLFs), this volume covers the diverse roles they play in the physiological and pathological changes of cells and tissues. This reference is suitable for the biological science and medical communities.
    Type of Medium: Online Resource
    Pages: 1 online resource (267 pages)
    Edition: 1st ed.
    ISBN: 9784431877752
    DDC: 572.8845
    Language: English
    Note: Preliminary -- Kr ppel-like Factors: Ingenious Three Fingers Directing Biology and Pathobiology -- Molecular Structures of Kr ppel-like Factors -- Kr ppel-like Factor Proteins and Chromatin Dynamics -- Co-regulator Interactions in Kr ppel-like Factor Transcriptional Programs -- Developmental Expression of Kr ppel-like Factors -- Expanded Role for EKLF/KLF1 Within the Hematopoietic Lineage -- Roles of Kr ppel-like Factors in Lymphocytes -- Kr ppel-like Factors in Gastrointestinal Tract Development and Differentiation -- Gene Interactions Between Kr ppel-like Factors in Development -- Kr ppel-like Factors in Stem Cell Biology -- Kr ppel-like Factors and the Liver -- Role of Kr ppel-like Factor 15 in Adipocytes -- Kr ppel-like Factors in the Heart -- Kr ppel-like Factors in the Vascular Endothelium -- Kr ppel-like Factors KLF2, KLF4, and KLF5: Central Regulators of Smooth Muscle Function -- Kr ppel-like Factors in Cancers -- Kr ppel-like Factors KLF6 and KLF6-SV1 in the Diagnosis and Treatment of Cancer -- Drug Development and Kr ppel-like Factors -- Back matter.
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  • 2
    ISSN: 1573-7241
    Keywords: intimal hyperplasia ; antioxidant ; dedifferentiation ; PDGF ; platelet-derived growth factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We previously reported a clinical study in which probucol reduced the restenosis rate. The mechanism of this effect is unclear. Restenosis is characterized by neointimal hyperplasia caused by proliferation of smooth muscle cells (SMCs), which increases the expression of Platelet-derived growth factor (PDGF)-A and SMemb. SMemb, a non–muscle-type myosin heavy chain most predominantly expressed in embryonic smooth muscle, can be used as a good molecular marker for dedifferentiated SMC. The aim of this study was to analyze the effect of probucol on neointimal proliferation and the level of expression of PDGF-A and SMemb after balloon injury in rabbits. Probucol was given orally 1.3 g/d from 2 weeks prior to carotid balloon injury to the time of killing (2 or 4 weeks after balloon injury). Intimal area was determined histologically using a computerized morphometry program. For quantification of SMC proliferation, alpha-actin–positive cells and proliferating cell nuclear antigen (PCNA)-labeled cells were counted. The expression of PDGF-A and SMemb mRNA was analyzed by the RNase protection assay. SMemb expression was also examined by immunohistochemistry. Probucol remarkably decreased intimal area by 70% and the number of SMC and PCNA-labeled cells in the intima. The expression of PDGF-A mRNA was significantly increased after balloon injury in untreated rabbits, whereas it was markedly suppressed with probucol treatment. The expression of SMemb was significantly increased in injured arteries at mRNA and protein levels. However, probucol did not suppress SMemb expression. Probucol is effective in preventing SMC proliferation, which is possibly due to a decrease in the expression of PDGF.
    Type of Medium: Electronic Resource
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