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Article ; Online: Extracellular matrix derived from Wharton's Jelly-derived mesenchymal stem cells promotes angiogenesis via integrin αVβ3/c-Myc/P300/VEGF.

Ma, Beilei / Wang, Tengkai / Li, Juan / Wang, Qian

2022 Volume 13, Issue 1, Page(s) 327

Abstract: Background: Angiogenesis is required in many physiological conditions, including bone regeneration, wound healing, and tissue regeneration. Mesenchymal stem cells-derived extracellular matrix (MSCs-ECM) could guide intricate cellular and tissue ... ...

Abstract	Background: Angiogenesis is required in many physiological conditions, including bone regeneration, wound healing, and tissue regeneration. Mesenchymal stem cells-derived extracellular matrix (MSCs-ECM) could guide intricate cellular and tissue processes such as homeostasis, healing and regeneration. Methods: The purpose of this study is to explore the effect and mechanism of ECM derived from decellularized Wharton's Jelly-derived mesenchymal stem cells (WJ-MSCs) on endothelial cell viability and angiogenesis. The human umbilical vein endothelial cells (HUVECs) were pretreated with WJ-MSCs ECM for 2d/7d/14d, respectively. After pretreatment, the angiogenesis ability of HUVECs was detected. Results: In this study, we found for the first time that WJ-MSCs ECM could improve the angiogenesis ability of HUVECs with a time-dependent manner in vitro. Mechanically, WJ-MSCs ECM activated the focal adhesion kinase (FAK)/P38 signaling pathway via integrin αVβ3, which further promoted the expression of the cellular (c)-Myc. Further, c-Myc increased histone acetylation levels of the vascular endothelial growth factor (VEGF) promoter by recruiting P300, which ultimately promoting VEGF expression. Conclusions: ECM derived from Wharton's Jelly-derived mesenchymal stem cells promotes angiogenesis via integrin αVβ3/c-Myc/P300/VEGF. This study is expected to provide a new approach to promote angiogenesis in bone and tissue regeneration.
MeSH term(s)	Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; E1A-Associated p300 Protein/metabolism ; Extracellular Matrix/metabolism ; Human Umbilical Vein Endothelial Cells/cytology ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Integrin alphaVbeta3/metabolism ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; Neovascularization, Physiologic ; Proto-Oncogene Proteins c-myc/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Wharton Jelly/cytology ; Wharton Jelly/metabolism
Chemical Substances	Integrin alphaVbeta3 ; MYC protein, human ; Proto-Oncogene Proteins c-myc ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; E1A-Associated p300 Protein (EC 2.3.1.48) ; EP300 protein, human (EC 2.3.1.48)
Language	English
Publishing date	2022-07-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2548671-8
ISSN	1757-6512 ; 1757-6512
ISSN (online)	1757-6512
ISSN	1757-6512
DOI	10.1186/s13287-022-03009-5
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Article ; Online: Bisphenol A exposure prenatally delays bone development and bone mass accumulation in female rat offspring via the ERβ/HDAC5/TGFβ signaling pathway.

Wang, Tengkai / Xu, Fen / Song, Lijun / Li, Juan / Wang, Qian

Toxicology

2021 Volume 458, Page(s) 152830

Abstract: Previous studies have suggested that bisphenol A (BPA) has a toxic effect on bone development; however, its pathological mechanism has not been fully elucidated. In the present study, pregnant Wistar rats were intragastrically administered BPA (10 μg/kg ... ...

Abstract	Previous studies have suggested that bisphenol A (BPA) has a toxic effect on bone development; however, its pathological mechanism has not been fully elucidated. In the present study, pregnant Wistar rats were intragastrically administered BPA (10 μg/kg per day) during gestational days 14-21. Then, bone tissues were obtained from neonatal rats on postnatal day 1 for histological analysis, and the bone mass of adult rat offspring was analyzed by micro-CT at postnatal week 10. Furthermore, osteoprogenitors from neonatal rats were obtained and treated with various concentrations of BPA in vitro to clarify the associated mechanism. In vivo, we found that prenatal BPA exposure reduced body weight and body length in female neonatal rats but not in male neonatal rats. Meanwhile, BPA exposure during pregnancy delayed bone development and reduced bone mass only in female rat offspring. Moreover, BPA exposure during pregnancy inhibited osteogenic function and downregulated the transforming growth factor β (TGF β) signaling pathway in the bone tissue of female neonatal rats. Our in vitro findings further indicated that various concentrations of BPA suppressed the osteogenic function of osteoprogenitors by downregulating the TGFβ signaling pathway. Meanwhile, BPA downregulated H3K9ac and expression levels of TGFβ via the ERβ/HDAC5 signaling pathway. Collectively, this research revealed that prenatal BPA exposure impairs bone development and bone mass accumulation in female rat offspring, which was attributed to inhibitory osteogenic function via the ERβ/HDAC5/TGFβ signaling pathway.
MeSH term(s)	Animals ; Animals, Newborn ; Benzhydryl Compounds/toxicity ; Bone Development/drug effects ; Bone and Bones/anatomy & histology ; Bone and Bones/diagnostic imaging ; Bone and Bones/drug effects ; Down-Regulation/drug effects ; Endocrine Disruptors/toxicity ; Estrogen Receptor beta/drug effects ; Female ; Histone Deacetylases/drug effects ; Male ; Phenols/toxicity ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rats ; Rats, Wistar ; Signal Transduction/drug effects ; Stem Cells/drug effects ; Transforming Growth Factor beta/drug effects ; X-Ray Microtomography
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Estrogen Receptor beta ; Phenols ; Transforming Growth Factor beta ; Hdac5 protein, rat (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98) ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2021-06-07
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/j.tox.2021.152830
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Article ; Online: Dual PI3K/mTOR inhibitor PF-04979064 regulates tumor growth in gastric cancer and enhances drug sensitivity of gastric cancer cells to 5-FU.

Zhong, Ziyuan / Wang, Tengkai / Zang, Ruochen / Zang, Yufei / Feng, Yaoyao / Yan, Shujun / Geng, Congcong / Zhu, Na / Wang, Qian

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 170, Page(s) 116086

Abstract: Gastric cancer (GC) is characterized by high tumor heterogeneity, increased surgical difficulty, and limited chemotherapy efficacy, and it is associated with a poor prognosis. The abnormal proliferation of cells involves abnormal activation of the PI3K/ ... ...

Abstract	Gastric cancer (GC) is characterized by high tumor heterogeneity, increased surgical difficulty, and limited chemotherapy efficacy, and it is associated with a poor prognosis. The abnormal proliferation of cells involves abnormal activation of the PI3K/AKT/mTOR signaling pathway. Inhibition of this signaling pathway can inhibit tumor cell proliferation and induce cell apoptosis. This study evaluated the effect of PF-04979064, a dual inhibitor of PI3K and mTOR, on human GC cells. PF-04979064 significantly inhibited the proliferation of human gastric adenocarcinoma AGS cells and the undifferentiated GC cell line HGC-27, promoting cell apoptosis. Combination treatment with PF-04979064 and the GC first-line clinical drug 5-FU showed synergistic effects, and PF-04979064 markedly increased the sensitivity of GC cells to chemotherapy drugs. Western blot results showed that PF-04979064 significantly inhibited the PI3K/AKT/mTOR signaling pathway in GC cells, whereas RNA seq results demonstrated substantial alterations in gene expression profiles upon treatment with PF-04979064. This study provides insight into the effects of PF-04979064, thereby establishing a solid foundation for its potential clinical application in the treatment of GC.
MeSH term(s)	Humans ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/genetics ; Stomach Neoplasms/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors/pharmacology ; Cell Proliferation ; Apoptosis ; Fluorouracil/pharmacology ; Fluorouracil/therapeutic use ; Cell Line, Tumor
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Phosphoinositide-3 Kinase Inhibitors ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2023-12-29
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.116086
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Article: Bisphenol A exposure prenatally delays bone development and bone mass accumulation in female rat offspring via the ERβ/HDAC5/TGFβ signaling pathway

Wang, Tengkai / Xu, Fen / Song, Lijun / Li, Juan / Wang, Qian

Toxicology. 2021 June 30, v. 458

2021

Abstract	Previous studies have suggested that bisphenol A (BPA) has a toxic effect on bone development; however, its pathological mechanism has not been fully elucidated. In the present study, pregnant Wistar rats were intragastrically administered BPA (10 μg/kg per day) during gestational days 14–21. Then, bone tissues were obtained from neonatal rats on postnatal day 1 for histological analysis, and the bone mass of adult rat offspring was analyzed by micro-CT at postnatal week 10. Furthermore, osteoprogenitors from neonatal rats were obtained and treated with various concentrations of BPA in vitro to clarify the associated mechanism. In vivo, we found that prenatal BPA exposure reduced body weight and body length in female neonatal rats but not in male neonatal rats. Meanwhile, BPA exposure during pregnancy delayed bone development and reduced bone mass only in female rat offspring. Moreover, BPA exposure during pregnancy inhibited osteogenic function and downregulated the transforming growth factor β (TGF β) signaling pathway in the bone tissue of female neonatal rats. Our in vitro findings further indicated that various concentrations of BPA suppressed the osteogenic function of osteoprogenitors by downregulating the TGFβ signaling pathway. Meanwhile, BPA downregulated H3K9ac and expression levels of TGFβ via the ERβ/HDAC5 signaling pathway. Collectively, this research revealed that prenatal BPA exposure impairs bone development and bone mass accumulation in female rat offspring, which was attributed to inhibitory osteogenic function via the ERβ/HDAC5/TGFβ signaling pathway.
Keywords	adults ; bisphenol A ; body length ; body weight ; bone density ; bone formation ; females ; histology ; males ; micro-computed tomography ; pregnancy ; progeny ; rats ; skeletal development ; toxicity ; toxicology
Language	English
Dates of publication	2021-0630
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/j.tox.2021.152830
Database	NAL-Catalogue (AGRICOLA)

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Article: Lactate induces aberration in the miR-30a-DBF4 axis to promote the development of gastric cancer and weakens the sensitivity to 5-Fu.

Wang, Tengkai / Ji, Rui / Liu, Guanqun / Ma, Beilei / Wang, Zehua / Wang, Qian

Cancer cell international

2021 Volume 21, Issue 1, Page(s) 602

Abstract: Background: Gastric cancer (GC) is one of the most common malignancies, molecular mechanism of which is still not clear. Aberrant expression of tumor-associated genes is the major cause of tumorigenesis. DBF4 is an important factor in cancers, although ... ...

Abstract	Background: Gastric cancer (GC) is one of the most common malignancies, molecular mechanism of which is still not clear. Aberrant expression of tumor-associated genes is the major cause of tumorigenesis. DBF4 is an important factor in cancers, although there is yet no report on its function and molecular mechanism in GC. Methods: The expression of DBF4 in tumor tissues or cells of GC was detected by qRT-PCR and western blotting. Gastric cancer cell line MGC-803 and AGS were transfected with DBF4 siRNA or overexpression vector to detect the function of DBF4 in proliferation, migration and the sensitivity to 5-Fu with CCK-8 assay, colony formation assay, transwell assay, and wound healing assay. miR-30a was found to be the regulator of DBF4 by online bioinformatics software and confirmed with qRT-PCR, western blot and dual-luciferase reporter assays. Results: In our study, increased expression of DBF4 in GC tissues was first identified through The Cancer Genome Atlas (TCGA) and later confirmed using specimens from GC patients. Furthermore, functional experiments were applied to demonstrate that DBF4 promotes cell proliferation and migration in GC cell lines, moreover weakens the sensitivity of MGC803 and AGS cells to 5-Fu. We further demonstrated that miR-30a showed significantly lower expression in GC cells and inhibited the expression of DBF4 through 3'-UTR suppression. Furthermore, rescue experiments revealed that the miR-30a-DBF4 axis regulated the GC cell proliferation, migration and the sensitivity to 5-Fu. The important composition in tumor microenvironment, lactate, may be the primary factor that suppressed miR-30a to strengthen the expression of DBF4. Conclusions: Taken together, our study was the first to identify DBF4 as a regulator of cell proliferation and migration in GC. Furthermore, our study identified the lactate-miR-30a-DBF4 axis as a crucial regulator of tumor progression and the tumor sensitivity to 5-Fu, which maybe serve useful for the development of novel therapeutic targets.
Language	English
Publishing date	2021-11-10
Publishing country	England
Document type	Journal Article
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-021-02291-2
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Article ; Online: Expression and existence forms of mast cell activating molecules and their antibodies in systemic lupus erythematosus.

Wang, Yuping / Wang, Tengkai / Cai, Meijuan / Zhu, Shuzhen / Song, Lijun / Wang, Qian

Immunity, inflammation and disease

2021 Volume 10, Issue 2, Page(s) 235–240

Abstract: Introduction: Mast cells are regarded as a kind of classical anaphylaxis cells. However autoimmune diseases and allergic reactions have many similarities or overlaps. A large number of papers have proved that mast cells play a significant role in the ... ...

Abstract	Introduction: Mast cells are regarded as a kind of classical anaphylaxis cells. However autoimmune diseases and allergic reactions have many similarities or overlaps. A large number of papers have proved that mast cells play a significant role in the pathogenesis of systemic lupus erythematosus (SLE). It is speculated that IgE, anti-IgE antibodies, FcεRI, and anti-FcεRI antibodies activate mast cells through autoimmune pathways and participate in the disease process of SLE. Naturally occurring protein molecules not only exist in monomer form, but also in polymer of protein molecules. Therefore, whether IgE, FcεRIα, anti-IgE antibodies, and anti-FcεRI antibodies also exist in polymeric forms in the natural state is worthy of further investigation. Methods: The serum samples and clinical data of 131 patients with SLE were collected from Qilu Hospital (Qingdao). Sixty healthy individuals were collected as the control group. Serum FcεRIα, anti-IgE, and anti-FcεRI were detected by enzyme-linked immunosorbent assay. Serum IgE was detected by rate scatter nephelometry. A Chinese hamster ovarian cancer cell line CHO3D10 transfected with human FcεRIα was cultured and the cell protein extract was prepared. The existence forms of FcεRIα in the cell protein extract were detected by the native-page method. Results: The serum FcεRIα in SLE patients was significantly higher than that in control group (3.52 [2.18, 4.71] µg/ml and 1.87 [1.52, 2.33] µg/ml, respectively; p < .05). Anti-IgE was significantly lower than that in the control group (0.85 [0.55, 1.21] µg/ml and 1.23 [0.95, 1.58] µg/ml, respectively; p < .05). The CHO3D10 cell line expressed the FcεRIα, which had one kind of monomer (mFcεRIα) and two kinds of polymers (pFcεRIα) in the degeneration conditions. Conclusion: In patients with SLE, the expression of FcεRIα was increased and the level of anti-IgE was decreased. FcεRIα had one kind of monomer and two kinds of polymers. Mast cell-associated FcεRIα involved in the inflammatory lesion of SLE.
MeSH term(s)	Anaphylaxis ; Basophils ; Humans ; Immunoglobulin E ; Lupus Erythematosus, Systemic ; Mast Cells
Chemical Substances	Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2021-11-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2740382-8
ISSN	2050-4527 ; 2050-4527
ISSN (online)	2050-4527
ISSN	2050-4527
DOI	10.1002/iid3.567
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Article ; Online: Indirubin regulates MPL and TNF expression in peripheral blood mononuclear cells from patients with primary immune thrombocytopenia.

Shao, Kai / Wang, Tengkai / Li, Tiantian / Zhang, Aijun / Cai, Meijuan / Zhao, Guanghui / Fu, Qingsong / Wang, Qian / Liu, Xinguang / Hou, Ming

Experimental hematology

2019 Volume 73, Page(s) 18–24

Abstract: Indirubin, a traditional Chinese medicine, is currently used to treat certain autoimmune diseases such as primary immune thrombocytopenia (ITP) in clinics. However, the effects of indirubin on expression of related genes in peripheral blood mononuclear ... ...

Abstract	Indirubin, a traditional Chinese medicine, is currently used to treat certain autoimmune diseases such as primary immune thrombocytopenia (ITP) in clinics. However, the effects of indirubin on expression of related genes in peripheral blood mononuclear cells (PBMCs) from ITP patients have not been investigated. In the present study, PBMCs were isolated from 19 adult patients with well-characterized active ITP and 20 healthy controls (HCs) and then treated with increasing concentrations of indirubin. The mRNA expression levels of thrombopoietin receptor (MPL), GATA binding protein 3 (GATA3), DNA methyltransferase 3B (DNMT3B), interleukin-6 (IL6), tumor necrosis factor (TNF), and interferon gamma (IFN-γ) were determined by quantitative real-time polymerase chain reaction (PCR). We found that indirubin had no cytotoxic effect on PBMC viability. Significantly lower MPL (p < 0.05) and GATA3 (p < 0.05) expression together with markedly higher IL6 (p < 0.05), TNF (p < 0.0001), and IFN-γ (p < 0.001) mRNA levels were observed in ITP patients compared with HCs. Notably, indirubin significantly enhanced MPL expression and inhibited TNF expression in PBMCs from ITP patients (p < 0.05). In summary, indirubin may play a direct role in thrombopoiesis by activating cellular MPL and normalizing TNF expression to suppress inflammation in ITP. This study may thus improve our understanding of indirubin and provide important information for optimizing therapeutic strategies for ITP patients.
MeSH term(s)	Adult ; Aged ; DNA (Cytosine-5-)-Methyltransferases/blood ; Female ; GATA3 Transcription Factor/blood ; Gene Expression Regulation/drug effects ; Humans ; Indoles/administration & dosage ; Interferon-gamma/blood ; Interleukin-6/blood ; Leukocytes, Mononuclear/metabolism ; Leukocytes, Mononuclear/pathology ; Male ; Middle Aged ; Purpura, Thrombocytopenic, Idiopathic/blood ; Purpura, Thrombocytopenic, Idiopathic/drug therapy ; Purpura, Thrombocytopenic, Idiopathic/pathology ; Receptors, Thrombopoietin/blood ; Tumor Necrosis Factor-alpha/blood ; DNA Methyltransferase 3B
Chemical Substances	GATA3 Transcription Factor ; GATA3 protein, human ; IFNG protein, human ; IL6 protein, human ; Indoles ; Interleukin-6 ; Receptors, Thrombopoietin ; Tumor Necrosis Factor-alpha ; MPL protein, human (143641-95-6) ; Interferon-gamma (82115-62-6) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; indirubin (V86L8P74GI)
Language	English
Publishing date	2019-04-20
Publishing country	Netherlands
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2019.04.002
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Article: Diagnostic value of the combined measurement of serum hcy, serum cys C, and urinary microalbumin in type 2 diabetes mellitus with early complicating diabetic nephropathy.

Wang, Tengkai / Wang, Qian / Wang, Zhimei / Xiao, Zuomin / Liu, Lunqin

ISRN endocrinology

2013 Volume 2013, Page(s) 407452

Abstract: Diabetic nephropathy (DN) is a major cause of end-stage kidney disease, and therefore early diagnosis and intervention may help reverse renal damage. One hundred and sixty-eight patients with T2DM and 56 healthy volunteers (control group) were enrolled ... ...

Abstract	Diabetic nephropathy (DN) is a major cause of end-stage kidney disease, and therefore early diagnosis and intervention may help reverse renal damage. One hundred and sixty-eight patients with T2DM and 56 healthy volunteers (control group) were enrolled at Shandong University Qilu Hospital between April 2010 and October 2012. All subjects underwent blood sampling for sera homocysteine (Hcy) and cystatin C (Cys C) assays and a urine microalbumin test. The patients were divided into three groups according to the urine microalbumin excretion rate (UMAER): the simple DM group (SDM group, n = 51), the early-stage DN group (EDN group, n = 60), and the clinical DN and renal failure group (CDN group, n = 57). Correlation analysis was performed to examine the association between sera Hcy and Cys C levels with UMAER. Our findings showed that sera Hcy level, Cys C level, and UMAER increased significantly in the SDM group (P < 0.05, P < 0.01), the EDN group (P < 0.01), and the CDN group (P < 0.01) as compared with the control group. These three biochemical markers also increased significantly with DN progression (P < 0.01). Correlation analysis showed that sera Hcy and Cys C levels were positively correlated with UMAER (r = 0.702, P < 0.01; r = 0.873, P < 0.01). In conclusion, our results showed that sera Hcy and Cys C levels increased consistently with the development and progression of DN as indicated by UMAER. Sera Hcy and Cys C are sensitive biomarkers for the detection of early-stage DN and monitoring its progression.
Language	English
Publishing date	2013-09-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2623566-3
ISSN	2090-4649 ; 2090-4630
ISSN (online)	2090-4649
ISSN	2090-4630
DOI	10.1155/2013/407452
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