Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • We propose two hypotheses to interpret our findings The

    2020-11-23

    We propose two hypotheses to interpret our findings. The first, ELR (+) CXC chemokines stimulate both CXCR-1 and CXCR-2 chemokine receptor while activating neutrophils; however CXCR-1 chemokine receptor seems to play more active role in the process of neutrophil migration as shown in previous studies [9], [18], [24], [25], [26]. CXCR-2 chemokine receptors might be mainly involved in the long lasting accumulation of neutrophils within the synovial fluid. Thus, relatively increased expression of CXCR-2 chemokine receptor on the SFN of patients with RA leads to a prolonged accumulation of neutrophils inside the synovial fluid as compared to BD and OA patients. It has been well known that various enzymes, cytokines (IL-1, IL-1Ra), and chemokines (IL-8, MIP-1) that are released by activated neutrophils have harmful effects on the joint structures. Moreover, it has been shown that prolonged accumulation of neutrophils at the site of inflammation leads to a phenotypic and functional changes in neutrophils that might be important in the course of chronic inflammation [23]. Consequently, detection of increased expression of CXCR-2 chemokine receptor on the SFN of patients with RA might explain the erosive character of arthritis in those patients. The second, ELR (+) CXC chemokines stimulate angiogenesis via increasing CXCR-2 chemokine receptor expression on endothelial Chromocarb [7]. ELR (+) CXC chemokines IL-8, GRO-α, ENA-78 and GCP-2 were much more abundantly secreted into synovial fluid of patients with RA than those with OA, BD and FMF [10]. In patients with RA, increased concentration of synovial ELR (+) CXC chemokines or, maybe, other some factors may cause an increased CXCR-2 chemokine receptor of the endothelial cells and SFN as well to promote neovascularization.
    Acknowledgments
    Introduction Currently, many studies have reported that bone marrow stromal cells (BMSCs) have beneficial effects for the recovery of the kidney in acute kidney injury (AKI) models (de Almeida et al., 2013, Oskowitz et al., 2011). Intravenous injection is preferred in most clinical and animal trials because it simplifies cell therapy administration procession and is easier for repeated dosing (Harting et al. 2009). In addition, it helps to ensure that the administrated stem cells remain in close contact with nutrition and oxygen in blood vessels. Despite all these benefits, only a small proportion of transplanted BMSCs enter the targeted kidney tissues, and they exhibit transient survival (Cheng et al., 2013, Lee et al., 2009). Many groups have shown that promoting BMSC migration could increase their therapeutic potential (Hoffmann et al., 2010, Liu et al., 2014a). Inability to target sufficient viable stem cells to AKI tissues is the most significant barrier to the effective implementation of cell therapies (Liu et al. 2013). Studies have proven that stromal cell-derived factor-1 (SDF-1) and its specific receptor, CXCR-4, play important roles in BMSCs' adhesion, migration and survival to targeted tissues (Liu et al., 2012, Ryu et al., 2010). Strategies to improve the homing ability of infused stem cells include modifying the cell CXCR-4 receptor or modifying SDF-1 levels in host tissues (Burks et al., 2013, Gul-Uludag et al., 2012). The expression of SDF-1 is up-regulated immediately after acute injury and ischemia, especially in AKI kidney tissues (Won et al. 2014). However, the expression of functional CXCR-4 chemokine receptor, which is highly expressed on the surface of BMSCs, declines with increased number of passages in culture (positive rate < 1% for CXCR-4), leading to the impaired effect of BMSC homing and repairing potential (Wang et al., 2008, Zhu et al., 2012). Although the freshly isolated BMSCs have better homing abilities, only a limited number of stem cells can be isolated and applied for clinical treatment (Honczarenko et al. 2006). Therefore, approaches to expand BMSCs while retaining CXCR-4 receptor expression on BMSCs' membranes are regarded as a prerequisite for efficient homing and retention of stem cells to AKI kidney tissues and toward the SDF-1 gradient.