HIF-1α Was a Key Regulator to Improve hBMSCs to Secrete Vascular Endothelial Cytokine with Astragaloside in Hypoxia
Ji Hong Hu,
Jin Hua,
Jia Jia,
Lu Juan,
Jing Miao Zhao,
Shu Xia Wang,
Yun Wang,
Li Mei Jin,
Jin Juan Li
Issue:
Volume 7, Issue 4, July 2019
Pages:
75-82
Received:
1 August 2019
Accepted:
6 September 2019
Published:
23 September 2019
Abstract: This study aimed to assess the combined therapeutic efficacies with gene therapy and stem cell treatment and herb on the differentiation of hBMSCs into vascular endothelial cells under hypoxia condition. The third passage of hBMSCs were randomly divided into four groups, including control group (hBMSCs transfected with empty vectors), VEGF group (VEGF gene transfected to hBMSCs), AST group (cultured with AST), and VEGF + AST group (the intervention of VEGF group plus AST group). Each group was cultured at 37°C and 5% O2 for 2 weeks. Cell morphology was observed by inverted phase and were crowded and arranged irregularly in the control group and AST group, showing a fiber-like growth, while those in the VEGF group and VEGF plus AST group were mostly triangular or polygonal, exhibiting a colony-like growth, contrast microscope. CD31 was negative in the control group and AST group, while CD105 was positive in both groups, tested by flow cytometry assay. The positive rate of CD31 was significantly higher in the VEGF group than it in the VEGP + AST, and the positive rate of CD105 was lower in the VEGF group than it in the VEGF + AST group. The levels of VEGF and endothelial nitric oxide synthase (eNOS) by ELISA and the expression of endothelin and prostacyclin by west blot (WB) and RT-PCR were significantly higher in VEGF group and AST group and VEGF plus AST group, compared with control group. Further, the expression of endothelin and vWF and VEGFR-2 was highest in the VEGP + AST group and the expression of prostacyclin was lowest in VEGF group. AST can promote the secretion of VEGF from the differentiation of hBMSCs induced by VEGF gene transfected to hBMSCs by HIF-1α under hypoxia.
Abstract: This study aimed to assess the combined therapeutic efficacies with gene therapy and stem cell treatment and herb on the differentiation of hBMSCs into vascular endothelial cells under hypoxia condition. The third passage of hBMSCs were randomly divided into four groups, including control group (hBMSCs transfected with empty vectors), VEGF group (V...
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Research Progress of Th17/Treg Cells and Their Transcription Factors in Autoimmune Diseases
Zhenjiang Hou,
Zhaoxin Mu,
Cuicui Wang
Issue:
Volume 7, Issue 4, July 2019
Pages:
83-92
Received:
9 July 2019
Published:
27 September 2019
Abstract: Helper T cell 17 (Th17) being a new cell subset of CD4+T in the body, which is different from Th1 and Th2 cells, have independent mechanisms of differentiation and developmental regulation. Th17 cells mainly secrete various cytokines such as IL-17, IL-6 and TNF-α, which induce inflammation. Treg cells are T cells with high expression of CD25 differentiated by T cells under the action of certain cytokines, namely CD4+CD25+(hi) Foxp3+T cells, which can regulate the immune response mediated by effector cells and are an important line of defense for human autoimmune. Therefore, Treg cells play an important role in maintaining immune tolerance of the body. As an important subset of T cells, Treg cells have an inhibitory effect on inflammation. Its working principle is to selectively inhibit autoreactive T cells and effector T cells so as to maintain the body's immune balance, and normal quantity and function help the immune system to its antigen stimulation, establishing a good state of tolerance. The expression of Treg cells increased, can avoid the occurrence of autoimmune diseases. Treg cells inhibit the differentiation of Th17 cells by down-regulating the expression of IL-23 and IL-17 or by its specific transcription factor Foxp3; similarly, inhibition of Th17 cell production can promote the development of Treg cells. Both Th17 and Treg cells are functionally inhibited. Th17 cells promote inflammatory reaction, and Treg cells suppress immune reaction. Numerous cytokines are involved in regulation. For example, IL-6 and IL-21 can inhibit Foxp3 and promote the expression of RORγt, thereby inhibiting Treg cells and inducing the differentiation of Th17 cells. In the absence of IL-6 and other pro-inflammatory factors, TGF-β enhances the inhibitory effect of Foxp3 on RORγt and promotes the growth and development of Treg cells. The anti-inflammatory factor IL-10 also induces Treg cells to inhibit the reaction of Th17 cells. The effects of Treg and Th17 cells are normally in a dynamic equilibrium. Once the balance is imbalanced, autoimmune diseases will occur. This article reviews the differentiation, function and research progress of Th17/Treg cells in autoimmune diseases.
Abstract: Helper T cell 17 (Th17) being a new cell subset of CD4+T in the body, which is different from Th1 and Th2 cells, have independent mechanisms of differentiation and developmental regulation. Th17 cells mainly secrete various cytokines such as IL-17, IL-6 and TNF-α, which induce inflammation. Treg cells are T cells with high expression of CD25 differ...
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Relationship Between No/Slow Reflow Phenomenon in Acute Myocardial Infarction Patients After Percutaneous Coronary Intervention and Inflammatory Response
Binbin Wang,
Zhi Xiao,
Nana Peng
Issue:
Volume 7, Issue 4, July 2019
Pages:
93-96
Received:
26 August 2019
Published:
27 September 2019
Abstract: Background: To explore the relationship between the occurrence of no/slow reflow phenomenon in acute myocardial infarction patients after undergoing percutaneous coronary intervention (PCI) and inflammatory response. Objective: Prospective study was conducted on 519 acute myocardial infarction patients undergoing PCI, in which 509 patients were followed up for one year. Method: The 76 cases with no/slow reflow phenomenon after PCI was the adverse reflow group. One hundred patients were randomly selected from the remaining 443 patients with the Excel random function table as the control group to avoid statistical deviation. Result: The inflammatory indicators, such as the total numbers of white blood cells and neutrophils, high-sensitivity C-reactive protein, mortality, adverse cardiac event. Conclusion: Inflammatory response is related to the occurrence of no/slow reflow phenomenon in acute myocardial infarction patients after PCI, and seriously affects their prognosis.
Abstract: Background: To explore the relationship between the occurrence of no/slow reflow phenomenon in acute myocardial infarction patients after undergoing percutaneous coronary intervention (PCI) and inflammatory response. Objective: Prospective study was conducted on 519 acute myocardial infarction patients undergoing PCI, in which 509 patients were fol...
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