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  • Hao, Hong  (7)
  • Xiao, Yichao  (7)
  • 1
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 37, No. suppl_1 ( 2017-05)
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. suppl_1 ( 2017-05)
    Abstract: Bone marrow mesenchymal stem cells are one of the important sources for cell replacement therapies. The outcome of the cell-based therapies is determined by a variety of factors including the source of the cells and their functional status. The functional status is usually measured by the expression of stem cell specific marker Oct-4 (stemness), differentiation potential (multipotency), and production of paracrine factors. It could be beneficial to keep the stem cells in a multipotent state for their optimal therapeutic outcome. The present study was to investigate the effect of basic fibroblast growth factor (bFGF) on the stemness of bone marrow stem cells and related mechanism. Rat multipotent adult progenitor cells (MAPCs) were used as the source of bone marrow stem cells, and induced to differentiate in vitro with (bFGF:5ng/ml and 20ng/ml) and without bFGF for up to 7 days. The expression of Oct4 and endothelial markers including Flk1, VWF and CD31, and smooth muscle cell markers including α-SMA, SM22 and CNN1 were determined with real-time (RT) PCR and western blot. We observed that both transcriptional (as reflected by RT-PCR) and protein expression (by western blot) of Oct4 was maintained at relatively stable levels in the cells treated with bFGF during the early phase of differentition. On the other hand, the expression of Flk1, VWF, CD31 and α-SMA, SM22, CNN1 were significantly decreased in the cells with the presence of bFGF. Treatment with bFGF significantly increased the phosphorylation of Erk1/2, not Akt nor STAT3, in the cells. Inhibition of Erk1/2 phosphorylation with PD98059 partially but significantly attenuated the effect of bFGF on Oct4 expression in the cells. These data suggest that bFGF could be able to maintain the bone marrow stem cells in their undifferentiated state in vitro partially through Erk1/2 signaling-mediated mechanism.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1494427-3
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  • 2
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 121, No. suppl_1 ( 2017-07-21)
    Abstract: Oxidative stress and inflammation are considered an important mechanism for the development of cardiovascular diseases. Cytokines including interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) play an important role in oxidative stress and inflammation. It is known that ambient fine particulate matter ( PM ) exposure is closely associated with cardiovascular diseases and oxidative stress. Caspase-recruitment domain 9 ( Card9 ) signaling is critically involvement in the function of macrophages, neutrophils and monocytes that are important for oxidative stress and inflammation. The present study was designed to evaluate the role of CARD9-mediated signaling in cytokines production in mice with PM exposure. Both male wild-type (WT) C57BL/6 mice (8-10 weeks) and age-matched CARD9 knockout (KO) mice (with C57BL/6 background) were exposed to PM2.5 for 6 weeks via intranasal approach with PBS as the control. Serum concentrations of the cytokines including IL-6, IL-1β, and TNF-α were measured with ELISA in the mice before and after PM exposure. There was no difference in the serum levels of IL-6, IL-1β, or TNF-α between WT mice and CARD9 KO mice exposed to PBS. As expected, PM exposure substantially increased the serum levels of IL-6, IL-1β, and TNF-α in the WT mice (by up to 6 times). However, no significant increase in the serum concentrations for IL-6, IL-1β, and TNF-α was observed in CARD9 KO mice exposed to PM. Increased inflammatory infiltrations in the lungs were observed in the WT mice as compared to the CARD9 KO mice with PM exposure. In conclusion, the present study demonstrated that increased cytokines were produced in WT mice, but not in CARD9 KO mice with PM exposure. The data suggested that CARD9 signaling played a critical role in the production of inflammatory cytokines in the mice in response to PM exposure, and might contribute to the development of cardiovascular diseases related to PM exposure.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1467838-X
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 37, No. suppl_1 ( 2017-05)
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. suppl_1 ( 2017-05)
    Abstract: Gender difference is present in a variety of diseases especially cardiovascular diseases like coronary artery diseases ( CAD ). It is well known that males tend to suffer from CAD earlier than females for largely unknown reasons. Oxidative stress and inflammation are considered an important mechanism for the development of cardiovascular diseases. Cytokines including interleukin (IL)-6 and tumor necrosis factor-α (TNF-α) play an important role in oxidative stress and inflammation. Ambient fine particulate matter ( PM ) exposure is closely associated with cardiovascular diseases and oxidative stress. The present study was designed to determine if there was a gender difference in the production of cytokines in the mice with PM exposure. Both male and female wild-type C57BL/6 mice (8-10 weeks) were exposed to PM2.5 for 6 weeks via intranasal approach with PBS as the control. Serum concentrations of the cytokines including IL-6, IL-1β, and TNF-α were measured with ELISA in the mice before and after PM exposure. There was no difference between male and female mice in the serum levels of IL-6, IL-1β, or TNF-α at the baseline. As expected, PM exposure substantially increased the serum levels of IL-6, IL-1β, and TNF-α both in male and female mice (by up to 6 times). However, their serum concentrations were significantly higher in male mice than in the females by 64.2%, 26.5%, and 30.7% for IL-6, IL-1β, and TNF-α, respectively (p 〈 0.05, n = 10). Similar changes in the inflammatory infiltrations in the lungs were observed in the male and female mice with PM exposure. The data from the present study demonstrated that more cytokines were produced in male mice than in the females with PM exposure. The clear gender difference in the serum levels of cytokines in response to PM exposure may partially contribute to the gender difference in the development of cardiovascular diseases. Further studies are needed to investigate the mechanisms related to the gender difference in the response to PM exposure.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1494427-3
    Location Call Number Limitation Availability
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  • 4
    In: Atherosclerosis, Elsevier BV, Vol. 357 ( 2022-09), p. 41-50
    Type of Medium: Online Resource
    ISSN: 0021-9150
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1499887-7
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  • 5
    In: Journal of Tissue Engineering and Regenerative Medicine, Hindawi Limited, Vol. 14, No. 6 ( 2020-06), p. 884-892
    Type of Medium: Online Resource
    ISSN: 1932-6254 , 1932-7005
    URL: Issue
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2316155-3
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  • 6
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 22, No. 13 ( 2021-07-04), p. 7200-
    Abstract: Males have a higher risk for cardiovascular diseases (CVDs) than females. Ambient fine particulate matter (PM) exposure increases CVD risk with increased reactive oxygen species (ROS) production and oxidative stress. Endothelial progenitor cells (EPCs) are important to vascular structure and function and can contribute to the development of CVDs. The aims of the present study were to determine if sex differences exist in the effect of PM exposure on circulating EPCs in mice and, if so, whether oxidative stress plays a role. Male and female C57BL/6 mice (8–10 weeks old) were exposed to PM or a vehicle control for six weeks. ELISA analysis showed that PM exposure substantially increased the serum levels of IL-6 and IL-1β in both males and females, but the concentrations were significantly higher in males. PM exposure only increased the serum levels of TNF-α in males. Flow cytometry analysis demonstrated that ROS production was significantly increased by PM treatment in males but not in females. Similarly, the level of circulating EPCs (CD34+/CD133+ and Sca-1+/Flk-1+) was significantly decreased by PM treatment in males but not in females. Antioxidants N-acetylcysteine (NAC) effectively prevented PM exposure-induced ROS and inflammatory cytokine production and restored circulating EPC levels in male mice. In sharp contrast, circulating EPC levels remained unchanged in female mice with PM exposure, an effect that was not altered by ovariectomy. In conclusion, PM exposure selectively decreased the circulating EPC population in male mice via increased oxidative stress without a significant impact on circulating EPCs in females independent of estrogen.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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  • 7
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 121, No. suppl_1 ( 2017-07-21)
    Abstract: Bone marrow-derived c-kit-positive (c-kit + ) cells are a potential source for cell-based therapy and tissue repair and regeneration. The ability of tissue repair and regeneration is significantly decreased in the aging population for various reasons. Western diet usually has increased level of fat. The present study was designed to evaluate the effect of long-term high fat diet on bone marrow c-Kit positive cells and the role of ROS in aging mice. Aging male wild-type (WT) C57BL/6 mice (40 weeks) were fed with high fat diet (HFD) for 3 months with regular diet as the control. To evaluate the role of reactive oxygen species (ROS) in mediating the effect of HFD on bone marrow cell population, a separate group of mice were treated with N-acetylcysteine (NAC) to reduce ROS production. Bone marrow (BM) and blood cells were harvested and prepared in the mice after 3 months of HFD treatment for flowcytometry analysis for Sca-1+, or c-Kit+, or CD133+ cells. The lineage negative (Lin-) and c-Kit positive (Lin-/c-Kit+) cell population was significantly decreased in the BM, not in blood, in the mice with HFD, while no significant change was observed in Sca-1+ or CD133+ cell populations in the BM or blood. The BM Lin-/c-Kit+ cells also exhibited increased intracellular ROS level, increased level of apoptosis, and deceased level of proliferation in HFD-treated mice. NAC treatment significantly decreased intracellular ROS level and normalized the BM Lin-/c-Kit+ cell population in HFD mice. In conclusion, the present study demonstrated that long-term HFD selectively decreased BM Lin-/c-Kit+ cell population in the aging mice through increased ROS production.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
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