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  • 1
    Online Resource
    Online Resource
    Granulocyte colony-stimulating factor protects cardiac mitochondria in the early phase of cardiac injury
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 296, No. 3 ( 2009-03), p. H823-H832
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 296, No. 3 ( 2009-03), p. H823-H832
    Abstract: Although granulocyte colony-stimulating factor (G-CSF) reportedly plays a cardioprotective role in several models of cardiac injury, clinical use of this drug in cardiac patients has been controversial. Here, we tested, in vivo and in vitro, the effect of G-CSF on cardiac mitochondria, which play a key role in determining cardiac cellular fate and function. Mild stimulation of C57/BL6 mice with doxorubicin (Dox) did not induce cardiac apoptosis or fibrosis but did induce damage to mitochondrial organization of the myocardium as observed through an electron microscope. Cardiac catheterization and echocardiography revealed that Dox did not alter cardiac systolic function or left ventricular size but did reduce diastolic function, an early sign of cardiac damage. Treatment with G-CSF attenuated significantly the damage to mitochondrial organization and rescued diastolic function. In an in vitro model for rat neonatal cardiomyocytes, a subapoptotic dose of Dox induced severe mitochondrial damage, including marked swelling of the cardiac mitochondria and/or decreased mitochondrial membrane potential. These mitochondrial changes were completely blocked by pretreatment with G-CSF. In addition, G-CSF dramatically improved ATP generation, which rescued Dox-impaired mitochondrial electron transport and oxygen consumption mainly through complex IV. These findings clearly indicate that G-CSF protects cardiac mitochondria, which are key organelles in the determination of cardiac cellular fate, in the early phase of cardiac injury.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00774.2008
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Binding of synthetic β‐human atrial natriuretic peptide to cultured rat vascular smooth muscle cells
    Wiley ; 1987
    In:  FEBS Letters Vol. 219, No. 2 ( 1987-07-27), p. 369-374
    Details
    In: FEBS Letters, Wiley, Vol. 219, No. 2 ( 1987-07-27), p. 369-374
    Abstract: We have studied the effects of synthetic β‐human atrial natriuretic peptide (β‐hANP), an antiparallel dimer of α‐hANP, on receptor binding and cGMP generation in cultured rat vascular smooth muscle cells and compared the effects with those of α‐hANP. Characteristics of temperature‐dependent binding and degradation of 125 I‐β‐hANP were similar to those 125 I‐α‐hANP. Scatchard analysis indicated a single class of binding sites for β‐hANP with a maximal binding capacity one‐half that of α‐hANP. Parallel and antiparallel dimers were equipotent in inhibiting the binding and stimulating intracellular cGMP formation, of which the maximal effect was about one‐half that of α‐hANP. Reverse‐phase high performance liquid chromatography revealed that most of β‐hANP added to cells was converted to a small molecular mass component corresponding to α‐hANP after incubation. These data suggest that the less potent effect of β‐hANP in receptor binding and cGMP generation may be partly accounted for by the possible conversion of β‐HANP to α‐hANP at the site of target cells.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Article
    DOI: 10.1016/0014-5793(87)80255-7
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 1987
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Regulation of atrial natriuretic hormone production by triiodothyronine in cultured rat atrial myocytes
    Oxford University Press (OUP) ; 1991
    In:  Acta Endocrinologica Vol. 125, No. 6 ( 1991-12), p. 694-699
    Details
    In: Acta Endocrinologica, Oxford University Press (OUP), Vol. 125, No. 6 ( 1991-12), p. 694-699
    Abstract: Since thyroid hormones have been reported to increase the synthesis of rat atrial natriuretic hormone and its mRNA accumulation, we further investigated the mechanism of stimulation of rANH synthesis by T 3 using cultured rat atrial myocytes. T 3 (10 −9 -10 −7 mol/l) increased cellular content and secretion into the medium of immunoreactive rANH in a dose-dependent manner. However, the ratio of secreted/cellular rANH was not altered by the addition of T 3 . Furthermore, in both cellular and secreted rANH, the larger molecular form (γ-rANH) apparently predominated over the smaller one (α-rANH), and this profile was not influenced by T 3 (10 −7 mol/l). Although T 3 (10 −9 -10 −7 mol/l) also increased cellular rANH mRNA accumulation, the ratio of cellular rANH/rANH mRNA was not changed. Moreover, using actinomycin D, we found that T 3 (10 −7 mol/l) did not affect the degradation of rANH mRNA. From these findings, we suggest that T 3 has no specific effects on the translational and posttranslational processes and the release of rANH, but that T 3 stimulates rANH synthesis in the pretranslational levels, probably in the transcriptional level of rANH gene.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    URL: Article
    DOI: 10.1530/acta.0.1250694
    RVK:
    WA 15000
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 1991
    detail.hit.zdb_id: 1485160-X
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  • 4
    Online Resource
    Online Resource
    Matrix Metalloproteinase-2 Inhibitors from Clinopodium chinense var. parviflorum
    American Chemical Society (ACS) ; 2009
    In:  Journal of Natural Products Vol. 72, No. 8 ( 2009-08-28), p. 1379-1384
    Details
    In: Journal of Natural Products, American Chemical Society (ACS), Vol. 72, No. 8 ( 2009-08-28), p. 1379-1384
    Type of Medium: Online Resource
    ISSN: 0163-3864 , 1520-6025
    URL: Article
    DOI: 10.1021/np800781t
    RVK:
    WA 15000
    Language: English
    Publisher: American Chemical Society (ACS)
    Publication Date: 2009
    detail.hit.zdb_id: 1491522-4
    SSG: 12
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Mammalian 5-Formyluracil−DNA Glycosylase. 1. Identification and Characterization of a Novel Activity That Releases 5-Formyluracil from DNA
    American Chemical Society (ACS) ; 2003
    In:  Biochemistry Vol. 42, No. 17 ( 2003-05-01), p. 4993-5002
    Details
    In: Biochemistry, American Chemical Society (ACS), Vol. 42, No. 17 ( 2003-05-01), p. 4993-5002
    Type of Medium: Online Resource
    ISSN: 0006-2960 , 1520-4995
    URL: Article
    DOI: 10.1021/bi027322v
    RVK:
    WA 15000
    Language: English
    Publisher: American Chemical Society (ACS)
    Publication Date: 2003
    detail.hit.zdb_id: 1472258-6
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    NHE and ICAM-1 expression in hypoxic/reoxygenated coronary microvascular endothelial cells
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 280, No. 6 ( 2001-06-01), p. H2796-H2803
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 280, No. 6 ( 2001-06-01), p. H2796-H2803
    Abstract: Although Na + /H + exchange (NHE) has been implicated in myocardial reperfusion injury, participation of coronary microvascular endothelial cells (CMECs) in this pathogenesis has been poorly understood. NHE-induced intracellular Ca 2+ concentration ([Ca 2+ ] i ) overload in CMECs may increase the synthesis of intercellular adhesion molecules (ICAM), which is potentially involved in myocardial reperfusion injury. The present study tested the hypothesis that NHE plays a crucial role in [Ca 2+ ] i overload and ICAM-1 synthesis in CMECs. Primary cultures of CMECs isolated from adult rat hearts were subjected to acidic hypoxia for 30 min followed by reoxygenation. Two structurally distinct NHE inhibitors, cariporide and 5-( N- N-dimethyl)-amiloride (DMA), had no significant effect on the acidic hypoxia-induced decrease in intracellular pH (pH i ) of CMECs but significantly retarded pH i recovery after reoxygenation. These NHE inhibitors abolished the hypoxia- and reoxygenation-induced increase in [Ca 2+ ] i . Expression of ICAM-1 mRNA was markedly increased in the vehicle-treated CMECs 3 h after reoxygenation, and this was significantly inhibited by treatment with cariporide, DMA, or Ca 2+ -free buffer. In addition, enhanced ICAM-I protein expression on the cell surface of CMECs 8 h after reoxygenation was attenuated by treatment with cariporide, DMA, or Ca 2+ -free buffer. These results suggest that NHE plays a crucial role in the rise of [Ca 2+ ] i and ICAM-1 expression during acidic hypoxia/reoxygenation in CMECs. We propose that inhibition of ICAM-1 expression in CMECs may represent a novel mechanism of action of NHE inhibitors against ischemia-reperfusion injury.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2001.280.6.H2796
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Apoptotic myocytes generate monocyte chemoattractant protein-1 and mediate macrophage recruitment
    American Physiological Society ; 2008
    In:  Journal of Applied Physiology Vol. 104, No. 3 ( 2008-03), p. 601-609
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 104, No. 3 ( 2008-03), p. 601-609
    Abstract: The mechanisms by which apoptotic myocytes are removed by macrophages have not been fully elucidated. This study examined whether apoptotic myocytes actively recruit macrophages by generating monocyte chemoattractant protein-1 (MCP-1) in experiments in vitro and in vivo. Neonatal rat cardiac myocytes were incubated for 4 h in the presence or absence of staurosporine (STS, 0.2–1 μmol/l), an apoptosis inducer. Nuclear staining with DAPI showed that STS induced apoptosis in a dose-dependent fashion. STS (1 μmol/l) caused extensive DNA fragmentation and increased caspase-3 activity compared with a serum-deprived control. MCP-1 mRNA and protein levels in myocytes increased twofold and fourfold, respectively, on STS treatment, and immunochemical staining revealed that apoptotic myocytes expressed MCP-1. To elucidate the role of MCP-1 expressed in apoptotic myocytes to recruit macrophages/monocytes, rat monocytes were incubated in the supernatant of STS-treated myocytes using a trans-well system. The culture medium of STS-treated myocytes recruited monocytes in a MCP-1-dependent fashion. In addition, experiments were performed in vivo using ischemia-reperfused rat hearts. Rats were subjected to 30 min of ligation of the left coronary artery followed by 24 h of reperfusion. After the reperfusion, in the ischemic border myocardium, 17.1 ± 1.1% of myocytes were terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) positive. Moreover, double staining using the TUNEL technique and immunohistochemistry with MCP-1 antibody showed that 69.8 ± 3.9% of TUNEL-positive myocytes expressed MCP-1 protein. Concomitantly, activated macrophages infiltrated the areas of apoptosis remarkably. These results suggest that apoptotic myocytes produce MCP-1, which have a critical role in the active recruitment of macrophages.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00254.2007
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 8
    Online Resource
    Online Resource
    Interaction between AT 1 and AT 2 receptors during postinfarction left ventricular remodeling
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 290, No. 3 ( 2006-03), p. H1004-H1010
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 290, No. 3 ( 2006-03), p. H1004-H1010
    Abstract: The relative contribution of the angiotensin II type 1 and 2 receptors (AT 1 -R and AT 2 -R) in postmyocardial infarction (MI) remodeling remains incompletely understood. We studied five groups of C57Bl/6 mice after 1 h of left anterior descending artery occlusion-reperfusion: 1) wild type, untreated ( n = 12); 2) wild type, treated with the AT 1 -R blocker losartan (10–20 mg·kg −1 ·day −1 in drinking water) from day 1 to day 28 post-MI ( n = 10); 3) cardiac overexpression of the AT 2 -R [AT 2 -transgenic (TG); n = 14]; 4) AT 2 -TG treated with losartan ( n = 13); and 5) AT 2 -TG and null for the AT 1a -R [AT 2 -TG/AT 1 knockout (KO); n = 10]. Cardiac magnetic resonance imaging (CMR) measured ejection fraction and left ventricular end-diastolic and end-systolic volume (EDVI and ESVI) and mass indexed to weight on days 0, 1, 7, and 28 post-MI. Infarct size was measured on day 1 by late gadolinium-enhanced CMR. Regional myocyte hypertrophy and collagen content were measured on day 28 post-MI. Infarct size was similar among groups. Systolic blood pressure was lowest in AT 2 -TG/AT 1 KO. By day 28 post-MI, when corrected for baseline differences, EDVI and ESVI were higher and ejection fraction was lower in wild type than other groups. Ejection fraction was highest and EDVI and mass index were lowest in AT 2 -TG/AT 1 KO at day 28. The AT 2 -TG/AT 1 KO demonstrated less fibrosis in adjacent regions. Regional myocyte hypertrophy was similar in all groups. The AT 1 -R and AT 2 -R are intricately intertwined in post-MI remodeling. Pharmacological blockade of AT 1 -R is equivalent to AT 2 -R overexpression in attenuating post-MI remodeling. Genetic knockout of the AT 1a -R is additive to AT 2 -R overexpression, due, at least in part, to blood pressure lowering.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00886.2005
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Downregulation of Dicer expression by serum withdrawal sensitizes human endothelial cells to apoptosis
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 295, No. 6 ( 2008-12), p. H2512-H2521
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 295, No. 6 ( 2008-12), p. H2512-H2521
    Abstract: Although the modulated expression of Dicer is documented upon neoplastic transformation, little is known of the regulation of Dicer expression by environmental stimuli and its roles in the regulation of cellular functions in primary cells. In this study, we found that Dicer expression was downregulated upon serum withdrawal in human umbilical vein endothelial cells (HUVECs). Serum withdrawal induced a time-dependent repression of Dicer expression, which was specifically rescued by vascular endothelial cell growth factor or sphingosine-1-phosphate. When Dicer expression was silenced by short-hairpin RNA against Dicer, the cells were more prone to apoptosis under serum withdrawal, whereas the rate of apoptosis was comparable with control cells in the serum-containing condition. Real-time PCR-based gene expression profiling identified several genes, the expression of which was modulated by Dicer silencing, including adhesion and matrix-related molecules, caspase-3, and nitric oxide synthase 3 (NOS3). Dicer silencing markedly impaired migratory functions without affecting cell adhesion and repressed phosphorylation of focal adhesion kinase and proline-rich tyrosine kinase 2 in adherent HUVECs. Dicer knockdown upregulated caspase-3 and downregulated NOS3 expression, and serum withdrawal indeed increased caspase-3 and decreased NOS3 expression. Furthermore, the overexpression of Dicer in HUVECs resulted in a marked reduction in apoptosis upon serum withdrawal and a decreased caspase-3 and increased NOS3 expression. The inhibition of NOS activity by N ω -nitro-l-arginine methyl ester abrogated the effect of Dicer overexpression to rescue the cells from serum withdrawal-induced apoptosis. These results indicated that serum withdrawal decreases Dicer expression, leading to an increased susceptibility to apoptosis through the regulation of caspase-3 and NOS3 expression.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00233.2008
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Replicative senescence of vascular smooth muscle cells enhances the calcification through initiating the osteoblastic transition
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 297, No. 5 ( 2009-11), p. H1673-H1684
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 297, No. 5 ( 2009-11), p. H1673-H1684
    Abstract: Medial artery calcification, which does not accompany lipid or cholesterol deposit, preferentially occurs in elderly population, but its underlying mechanisms remain unclear. In the present study, we investigated the potential role of senescent vascular smooth muscle cells (VSMCs) in the formation of senescence-associated medial calcification. Replicative senescence was induced by the extended passages (until passages 11–13) in human primary VSMCs, and cells in early passage ( passage 6) were used as control young cells. VSMC calcification was markedly enhanced in the senescent cells compared with that in the control young cells. We identified that genes highly expressed in osteoblasts, such as alkaline phosphatase (ALP) and type I collagen, were significantly upregulated in the senescent VSMCs, suggesting their osteoblastic transition during the senescence. Knockdown of either ALP or type I collagen significantly reduced the calcification in the senescent VSMCs. Of note, runt-related transcription factor-2 (RUNX-2), a core transcriptional factor that initiates the osteoblastic differentiation, was also upregulated in the senescent VSMCs. Knockdown of RUNX-2 significantly reduced the ALP expression and calcification in the senescent VSMCs, suggesting that RUNX-2 is involved in the senescence-mediated osteoblastic transition. Furthermore, immunohistochemistry of aorta from the klotho −/− aging mouse model demonstrated in vivo emergence of osteoblast-like cells expressing RUNX-2 exclusively in the calcified media. We also found that statin and Rho-kinase inhibitor effectively reduced the VSMC calcification by inhibiting P i -induced apoptosis and potentially enhancing matrix Gla protein expression in the senescent VSMCs. These findings strongly suggest an important role of senescent VSMCs in the pathophysiology of senescence-associated medial calcification, and the inhibition of osteoblastic transition could be a new therapeutic approach for the prevention of senescence-associated medial calcification.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00455.2009
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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