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  1. Article ; Online: Retraction Note

    Jianxiao Chen / Xiwen Zhang / Jianfeng Xie / Ming Xue / Ling Liu / Yi Yang / Haibo Qiu

    Stem Cell Research & Therapy, Vol 13, Iss 1, Pp 1-

    Overexpression of TGFβ1 in murine mesenchymal stem cells improves lung inflammation by impacting the Th17/Treg balance in LPS-induced ARDS mice

    2022  Volume 1

    Keywords Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Language English
    Publishing date 2022-03-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Retraction Note

    Xiwen Zhang / Jianxiao Chen / Ming Xue / Yuying Tang / Jingyuan Xu / Ling Liu / Yingzi Huang / Yi Yang / Haibo Qiu / Fengmei Guo

    Stem Cell Research & Therapy, Vol 13, Iss 1, Pp 1-

    Overexpressing p130/E2F4 in mesenchymal stem cells facilitates the repair of injured alveolar epithelial cells in LPS-induced ARDS mice

    2022  Volume 1

    Keywords Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Correction

    Feng Liu / Jianfeng Xie / Xiwen Zhang / Zongsheng Wu / Shi Zhang / Ming Xue / Jianxiao Chen / Yi Yang / Haibo Qiu

    Stem Cell Research & Therapy, Vol 13, Iss 1, Pp 1-

    Overexpressing TGF-β1 in mesenchymal stem cells attenuates organ dysfunction during CLP-induced septic mice by reducing macrophage-driven

    2022  Volume 2

    Keywords Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Language English
    Publishing date 2022-07-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Overexpression of TGFβ1 in murine mesenchymal stem cells improves lung inflammation by impacting the Th17/Treg balance in LPS-induced ARDS mice

    Jianxiao Chen / Xiwen Zhang / Jianfeng Xie / Ming Xue / Ling Liu / Yi Yang / Haibo Qiu

    Stem Cell Research & Therapy, Vol 11, Iss 1, Pp 1-

    2020  Volume 16

    Abstract: Abstract Background T helper 17 cells (Th17)/regulatory T cells (Treg), as subtypes of CD4+ T cells, play an important role in the inflammatory response of acute respiratory distress syndrome (ARDS). However, there is still a lack of effective methods to ...

    Abstract Abstract Background T helper 17 cells (Th17)/regulatory T cells (Treg), as subtypes of CD4+ T cells, play an important role in the inflammatory response of acute respiratory distress syndrome (ARDS). However, there is still a lack of effective methods to regulate the differentiation balance of Th17/Treg. It was proven that mesenchymal stem cells (MSCs) could regulate the differentiation of CD4+ T cells, but the mechanism is still unclear. TGFβ1, a paracrine cytokine of MSCs, could also regulate the differentiation of Th17/Treg but is lowly expressed in MSCs. Therefore, mouse MSCs (mMSCs) overexpressing TGFβ1 were constructed by lentivirus transduction and intratracheally transplanted into LPS-induced ARDS mice in our study. The aim of this study was to evaluate the therapeutic effects of mMSCs overexpressing TGFβ1 on inflammation and immunoregulation by impacting the Th17/Treg balance in LPS-induced ARDS mice. Methods mMSCs overexpressing TGFβ1 were constructed using lentiviral vectors. Then, mouse bone-marrow-derived MSCs (mBM-MSC) and mBM-MSC-TGFβ1 (mBM-MSC overexpressing TGFβ1) were transplanted intratracheally into ARDS mice induced by lipopolysaccharide. At 3 and 7 days after transplantation, the mice were sacrificed, and the homing of the mMSCs was assayed by ex vivo optical imaging. The relative numbers of Th17 and Treg in the lungs and spleens of mice were detected by FCM. IL-17A and IL-10 levels in the lungs of mice were analysed by western blot. Permeability and inflammatory cytokines were evaluated by analysing the protein concentration of BALF using ELISA. Histopathology of the lungs was assessed by haematoxylin and eosin staining and lung injury scoring. Alveolar lung fibrosis was assessed by Masson’s trichrome staining and Ashcroft scoring. The mortality of ARDS mice was followed until 7 days after transplantation. Results The transduction efficiencies mediated by the lentiviral vectors ranged from 82.3 to 88.6%. Overexpressing TGFβ1 inhibited the proliferation of mMSCs during days 5–7 (p < ...
    Keywords Acute respiratory distress syndrome ; Mesenchymal stem cells ; TGFβ1 ; Th17/Treg ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Subject code 630
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Overexpressing TGF-β1 in mesenchymal stem cells attenuates organ dysfunction during CLP-induced septic mice by reducing macrophage-driven inflammation

    Feng Liu / Jianfeng Xie / Xiwen Zhang / Zongsheng Wu / Shi Zhang / Ming Xue / Jianxiao Chen / Yi Yang / Haibo Qiu

    Stem Cell Research & Therapy, Vol 11, Iss 1, Pp 1-

    2020  Volume 13

    Abstract: Abstract Background Sepsis remains a leading cause of death in critically ill patients. It is well known that mesenchymal stem cells (MSCs) are a promising therapy partly due to their paracrine-mediated immunoregulatory function. Previous study ... ...

    Abstract Abstract Background Sepsis remains a leading cause of death in critically ill patients. It is well known that mesenchymal stem cells (MSCs) are a promising therapy partly due to their paracrine-mediated immunoregulatory function. Previous study demonstrated that transforming growth factor-beta1 (TGF-β1) is an important cytokine secreted by MSCs and that it participates in MSC-mediated macrophage phenotype switch from pro-inflammatory to pro-resolution. In addition, the transformation of macrophage phenotype may be a potential treatment for sepsis. However, the therapeutic effect of overexpressing TGF-β1 in MSCs (MSC-TGF-β1) on sepsis is not well understood. Therefore, this study aimed to evaluate the effects of TGF-β1 overexpressing MSCs on organ injury in cecal ligation and puncture (CLP)-induced septic mice and to detect the changes in macrophage phenotype during this process. Methods Mouse MSCs stably transfected with TGF-β1 were constructed and injected into CLP-induced septic mice via tail vein. After 24 h, the mice were sacrificed; then, the histopathology of the organ was evaluated by hematoxylin-eosin (H&E) staining. Inflammatory cytokines were detected by ELISA. Macrophage infiltration and phenotype transformation in the tissues were determined by immunohistochemistry and flow cytometry. In addition, we performed adoptive transfer of mouse peritoneal macrophage pretreated with TGF-β1 overexpressing MSCs in septic mice. Results We found that infusion of TGF-β1 overexpressing MSCs attenuated the histopathological impairment of the organ, decreased the pro-inflammatory cytokine levels and inhibited macrophage infiltration in tissues. TGF-β1 overexpressing MSCs induced macrophage phenotypes changed from pro-inflammatory to pro-resolution in inflammatory environment. The adoptive transfer of mouse peritoneal macrophages pretreated with TGF-β1 overexpressing MSCs also relieved organ damage in CLP-induced septic mice. Conclusion Under septic conditions, TGF-β1 overexpressing MSCs can enhance the ...
    Keywords Mesenchymal stem cells ; Sepsis ; Transforming growth factor-β1 ; Macrophage activation ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Subject code 630 ; 500
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Overexpressing p130/E2F4 in mesenchymal stem cells facilitates the repair of injured alveolar epithelial cells in LPS-induced ARDS mice

    Xiwen Zhang / Jianxiao Chen / Ming Xue / Yuying Tang / Jingyuan Xu / Ling Liu / Yingzi Huang / Yi Yang / Haibo Qiu / Fengmei Guo

    Stem Cell Research & Therapy, Vol 10, Iss 1, Pp 1-

    2019  Volume 11

    Abstract: Abstract Background Low differentiation rates of mesenchymal stem cells (MSCs) limit their therapeutic effects on patients in clinical studies. Our previous study demonstrated that overexpressing p130 or E2F4 affected the multipotential differentiation ... ...

    Abstract Abstract Background Low differentiation rates of mesenchymal stem cells (MSCs) limit their therapeutic effects on patients in clinical studies. Our previous study demonstrated that overexpressing p130 or E2F4 affected the multipotential differentiation of MSCs, and the underlying mechanism was attributed to the regulation of the G1 phase. Improving the efficiency of MSC differentiation into epithelial cells is considered to be a new method. Therefore, this study was conducted to evaluate the effects of overexpressing p130 or E2F4 in MSCs on improving re-epithelization in lipopolysaccharide (LPS)-induced ARDS animals. Methods Mouse MSCs (mMSCs) stably transfected with p130 and E2F4 were transplanted intratracheally into LPS-induced ARDS mice. After 7 and 14 days, the mice were sacrificed, and the histopathology of the lungs was assessed by haematoxylin-eosin staining and lung injury scoring. Homing and differentiation of mMSCs were analysed by labelling and tracking mMSCs with NIR815 dye and immunofluorescent staining. Surfactant proteins A and C and occludin in the lungs were assessed by western blot. Permeability was evaluated by analysing the protein concentration of BALF using ELISA. Alveolar fluid clearance was assessed by absorbance measurements of BALF. Lung fibrosis was assessed by Masson’s trichrome staining and Ashcroft scoring. Results The engraftment of mMSCs overexpressing p130 or E2F4 led to attenuated histopathological impairment of the lung tissue, and the lung injury scores of the LPS+mBM-MSC-p130 and LPS+mBM-MSC-E2F4 groups were also decreased (p < 0.05). Overexpression of p130 or E2F4 also increased the retention of mMSCs in the lung (p < 0.05), increased differentiation into type II alveolar epithelial cells (p < 0.05), and improved alveolar epithelial permeability (p < 0.05). Additionally, mMSCs overexpressing p130 or E2F4 inhibited lung fibrosis according to the deposition of collagen and the fibrosis score in the lungs (p < 0.05). Conclusion Overexpressing p130 or E2F4 in mMSCs could further improve the injured structure and function of epithelial cells in the lungs of ARDS mice as a result of improved differentiation of mMSCs into epithelial cells.
    Keywords Mesenchymal stem cells ; Acute respiratory distress syndrome ; p130 ; E2F4 ; Differentiation into type II alveolar epithelial cells ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Subject code 630
    Language English
    Publishing date 2019-03-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: MSC-secreted TGF-β regulates lipopolysaccharide-stimulated macrophage M2-like polarization via the Akt/FoxO1 pathway

    Feng Liu / Haibo Qiu / Ming Xue / Shi Zhang / Xiwen Zhang / Jingyuan Xu / Jianxiao Chen / Yi Yang / Jianfeng Xie

    Stem Cell Research & Therapy, Vol 10, Iss 1, Pp 1-

    2019  Volume 14

    Abstract: Abstract Background An uncontrolled inflammatory response is a critical pathophysiological feature of sepsis. Mesenchymal stem cells (MSCs) induce macrophage phenotype polarization and reduce inflammation in sepsis. MSC-secreted transforming growth ... ...

    Abstract Abstract Background An uncontrolled inflammatory response is a critical pathophysiological feature of sepsis. Mesenchymal stem cells (MSCs) induce macrophage phenotype polarization and reduce inflammation in sepsis. MSC-secreted transforming growth factor beta (TGF-β) participated in the immune modulatory function of MSCs. However, the underlying mechanism of MSC-secreted TGF-β was not fully elucidated in regulation macrophage M2-like polarization. Methods The paracrine effects of MSCs on macrophage polarization were studied using a co-culture protocol with LPS-stimulated RAW264.7 cells/mouse peritoneal macrophages and MSCs. The effect of TGF-β in the co-culture system was blocked by the TGF-β receptor inhibitor. To determine the role of MSC-secreted TGF-β, we used recombinant TGF-β to culture with LPS-stimulated RAW264.7 cells. In addition, we employed antibody microarray analysis to determine the mechanisms of MSC secreted TGF-β on LPS-stimulated RAW264.7 cell/mouse peritoneal macrophage M2-like polarization. Furthermore, we used an Akt inhibitor and a FoxO1 inhibitor to inhibit the Akt/FoxO1 pathway. The nuclear translocation of FoxO1 was detected by Western blot. Results MSCs induced LPS-stimulated RAW264.7 cell/mouse peritoneal macrophage polarization towards the M2-like phenotype and significantly reduced pro-inflammatory cytokine levels via paracrine, which was inhibited by TGF-β receptor inhibitor. Furthermore, we found that MSC-secreted TGF-β enhanced the macrophage phagocytic ability. The antibody microarray analysis and Western blot verified that TGF-β treatment activated the Akt/FoxO1 pathway in LPS-stimulated macrophages, TGF-β-induced FoxO1 nuclear translocation and obviously expressed in the cytoplasm, the effects of TGF-β regulatory effects on LPS-stimulated macrophage were inhibited by pre-treatment with Akt inhibitor and FoxO1 inhibitor. Conclusions TGF-β secreted by MSCs could skew LPS-stimulated macrophage polarization towards the M2-like phenotype, reduce inflammatory reactions, and improve ...
    Keywords Sepsis ; Transforming growth factor beta ; Mesenchymal stem cells ; Macrophages ; Akt/FoxO1 ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
    Subject code 630 ; 500
    Language English
    Publishing date 2019-11-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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