scholarly journals A Matrix Metalloproteinase Mediates Tracheal Development in Bombyx mori

2021 ◽  
Vol 22 (11) ◽  
pp. 5618
Author(s):  
Yi Wei ◽  
Xiao-Lin Zhou ◽  
Tai-Hang Liu ◽  
Peng Chen ◽  
Xia Jiang ◽  
...  
Keyword(s):  
Bombyx Mori ◽  
Underlying Mechanism ◽  
Tube Formation ◽  
Regulation Mechanism ◽  
Integrin Β1 ◽  
Branch Number ◽  
Tracheal Cell ◽  
Molecular Events ◽  
And Migration ◽  
Almost All

The trachea of insects is a tubular epithelia tissue that transports oxygen and other gases. It serves as a useful model for the studying of the cellular and molecular events involved in epithelial tube formation. Almost all of the extracellular matrix can be degraded by Matrix metalloproteinases (MMPs), which is closely related to the processes of development and regeneration. The regulation of trachea by MMPs is roughly known in previous studies, but the detailed regulation mechanism and involved gene function are not fully explored. In this article, we found MMP1 expressed highly during tracheal remodeling, and knocked out it makes the tracheal branch number reduced in Bombyx mori. In trachea of transgenic BmMMP1-KO silkworm, the space expanding of taenidium and epidermal cells and the structure of apical membrane were abnormal. To explore the underlying mechanism, we detected that DE-cadherin and Integrin β1 were accumulated in trachea of transgenic BmMMP1-KO silkworm by immunohistochemistry. Moreover, 5-Bromo-2′-Deoxyuridine (BrdU) labeling showed that knockout of BmMMP1 in silkworm inhibited tracheal cell proliferation, and BmMMP1 also regulated the proliferation and migration of BmNS cells. All of the results demonstrated that BmMMP1 regulates the development of the tracheal tissue by expanding the space of tracheal cuticles and increases the number of tracheal branches by degrading DE-cadherin and Integrin β1.

Stratigraphic Intervals for Oil and Tar Sand Deposits in the Uinta Basin, Utah

2017 ◽  
Vol 54 (4) ◽  
pp. 227-264
Author(s):  
Ronald Johnson ◽  
Justin Birdwell ◽  
Paul Lillis
Keyword(s):  
Brackish Water ◽  
Source Rocks ◽  
Uinta Basin ◽  
Green River ◽  
Reservoir Rocks ◽  
Stratigraphic Framework ◽  
Two Samples ◽  
The Rich ◽  
And Migration ◽  
Almost All

To better understand oil and bitumen generation and migration in the Paleogene lacustrine source rocks of the Uinta Basin, Utah, analyses of 182 oil samples and tar-impregnated intervals from 82 core holes were incorporated into a well-established stratigraphic framework for the basin. The oil samples are from the U.S. Geological Survey Energy Resources Program Geochemistry Laboratory Database; the tar-impregnated intervals are from core holes drilled at the Sunnyside and P.R. Spring-Hill Creek tar sands deposits. The stratigraphic framework includes transgressive and regressive phases of the early freshwater to near freshwater lacustrine interval of Lake Uinta and the rich and lean zone architecture developed for the later brackish-to-hypersaline stages of the lake. Two types of lacustrine-sourced oil are currently recognized in the Uinta Basin: (1) Green River A oils, with high wax and low β-carotane contents thought to be generated by source rocks in the fresh-to-brackish water lacustrine interval, and (2) much less common Green River B oils, an immature asphaltic oil with high β-carotane content thought to be generated by marginally mature to mature source rocks in the hypersaline lacustrine interval. Almost all oil samples from reservoir rocks in the fresh-to-brackish water interval are Green River A oils; however four samples of Green River A oils were present in the hypersaline interval, which likely indicates vertical migration. In addition, two samples of Green River B oil are from intervals that were assumed to contain only Green River A oil. Tar sand at the P.R. Spring-Hill Creek deposit are restricted to marginal lacustrine and fluvial sandstones deposited during the hypersaline phase of Lake Uinta, suggesting a genetic relationship to Green River B oils. Tar sand at the Sunnyside deposit, in contrast, occur in marginal lacustrine and alluvial sandstones deposited from the early fresh to nearly freshwater phase of Lake Uinta through the hypersaline phase. The Sunnyside deposit occurs in an area with structural dips that range from 7 to 14 degrees, and it is possible that some tar migrated stratigraphically down section.

scholarly journals PTPRD-inactivation-induced CXCL8 promotes angiogenesis and metastasis in gastric cancer and is inhibited by metformin

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Won Jung Bae ◽  
Ji Mi Ahn ◽  
Hye Eun Byeon ◽  
Seokwhi Kim ◽  
Dakeun Lee
Keyword(s):  
Microarray Analysis ◽  
Protein Tyrosine Phosphatase ◽  
Cancer Metastasis ◽  
Tyrosine Phosphatase ◽  
Underlying Mechanism ◽  
Tube Formation ◽  
Potential Therapeutic Target ◽  
Efficient Treatment ◽  
Stat3 Signaling

Abstract Background Protein tyrosine phosphatase receptor delta (PTPRD) is frequently inactivated in various types of cancers. Here, we explored the underlying mechanism of PTPRD-loss-induced cancer metastasis and investigated an efficient treatment option for PTPRD-inactivated gastric cancers (GCs). Methods PTPRD expression was evaluated by immunohistochemistry. Microarray analysis was used to identify differentially expressed genes in PTPRD-inactivated cancer cells. Quantitative reverse transcription (qRT-PCR), western blotting, and/or enzyme-linked immunosorbent assays were used to investigate the PTPRD-CXCL8 axis and the expression of other related genes. An in vitro tube formation assay was performed using HUVECs. The efficacy of metformin was assessed by MTS assay. Results PTPRD was frequently downregulated in GCs and the loss of PTPRD expression was associated with advanced stage, worse overall survival, and a higher risk of distant metastasis. Microarray analysis revealed a significant increase in CXCL8 expression upon loss of PTPRD. This was validated in various GC cell lines using transient and stable PTPRD knockdown. PTPRD-loss-induced angiogenesis was mediated by CXCL8, and the increase in CXCL8 expression was mediated by both ERK and STAT3 signaling. Thus, specific inhibitors targeting ERK or STAT3 abrogated the corresponding signaling nodes and inhibited PTPRD-loss-induced angiogenesis. Additionally, metformin was found to efficiently inhibit PTPRD-loss-induced angiogenesis, decrease cell viability in PTPRD-inactivated cancers, and reverse the decrease in PTPRD expression. Conclusions Thus, the PTPRD-CXCL8 axis may serve as a potential therapeutic target, particularly for the suppression of metastasis in PTPRD-inactivated GCs. Hence, we propose that the therapeutic efficacy of metformin in PTPRD-inactivated cancers should be further investigated.

scholarly journals TRPM4 in Cancer—A New Potential Drug Target

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 229
Author(s):  
Anna Borgström ◽  
Christine Peinelt ◽  
Paulina Stokłosa
Keyword(s):  
Anticancer Drug ◽  
Drug Target ◽  
Transient Receptor Potential ◽  
Human Cancer ◽  
Receptor Potential ◽  
B Cell Lymphoma ◽  
Underlying Mechanism ◽  
Monovalent Cation ◽  
Transient Receptor Potential Melastatin ◽  
And Migration

Transient receptor potential melastatin 4 (TRPM4) is widely expressed in various organs and associated with cardiovascular and immune diseases. Lately, the interest in studies on TRPM4 in cancer has increased. Thus far, TRPM4 has been investigated in diffuse large B-cell lymphoma, prostate, colorectal, liver, breast, urinary bladder, cervical, and endometrial cancer. In several types of cancer TRPM4 is overexpressed and contributes to cancer hallmark functions such as increased proliferation and migration and cell cycle shift. Hence, TRPM4 is a potential prognostic cancer marker and a promising anticancer drug target candidate. Currently, the underlying mechanism by which TRPM4 contributes to cancer hallmark functions is under investigation. TRPM4 is a Ca2+-activated monovalent cation channel, and its ion conductivity can decrease intracellular Ca2+ signaling. Furthermore, TRPM4 can interact with different partner proteins. However, the lack of potent and specific TRPM4 inhibitors has delayed the investigations of TRPM4. In this review, we summarize the potential mechanisms of action and discuss new small molecule TRPM4 inhibitors, as well as the TRPM4 antibody, M4P. Additionally, we provide an overview of TRPM4 in human cancer and discuss TRPM4 as a diagnostic marker and anticancer drug target.

scholarly journals Panax notoginseng saponins promote endothelial progenitor cell angiogenesis via the Wnt/β-catenin pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Peiqi Zhu ◽  
Weidong Jiang ◽  
Shixi He ◽  
Tao Zhang ◽  
Fengchun Liao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Panax Notoginseng ◽  
Tube Formation ◽  
Optimal Concentration ◽  
Mrna Levels ◽  
Panax Notoginseng Saponins ◽  
Endothelial Progenitor ◽  
Angiogenic Potential ◽  
Craniomaxillofacial Surgery ◽  
And Migration

Abstract Background Distraction osteogenesis (DO) is an effective treatment in craniomaxillofacial surgery. However, the issue of sufficient blood supply at the regeneration tissue has limited its wide application. Panax notoginseng saponins (PNS) is a Traditional Chinese Medicine that is commonly used to treat a range of angiogenic diseases. However, the mechanisms whereby PNS alters angiogenesis in endothelial progenitor cells (EPCs) have yet to be clarified. Methods EPCs were identified by immunofluorescence, confirmed by their uptake of fluorescently labeled Dil-ac-LDL and FITC-UEA-1. EPCs were treated with different concentrations of PNS, and the effects of PNS on cell proliferation were measured on the optimal concentration of PNS determined. The effects of PNS on angiogenesis and migration, angiogenic cytokines mRNA expression and the proteins of the Wnt pathway were investigated. Then knocked down β-catenin in EPCs and treated with the optimum concentrational PNS, their angiogenic potential was evaluated in tube formation and migration assays. In addition, the expression of cytokines associated with angiogenesis and Wnt/β-catenin was then assessed via WB and RT-qPCR. Results We were able to determine the optimal concentration of PNS in the promotion of cell proliferation, tube formation, and migration to be 6.25 mg/L. PNS treatment increased the mRNA levels of VEGF, bFGF, VE-Cadherin, WNT3a, LRP5, β-catenin, and TCF4. After knocked down β-catenin expression, we found that PNS could sufficient to partially reverse the suppression of EPC angiogenesis. Conclusions Overall, 6.25 mg/L PNS can promote EPC angiogenesis via Wnt/β-catenin signaling pathway activation.

scholarly journals Improved response of human gingival fibroblasts to titanium coated with micro-/nano-structured tantalum

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Chu-nan Zhang ◽  
Lin-yi Zhou ◽  
Shu-jiao Qian ◽  
Ying-xin Gu ◽  
Jun-yu Shi ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Underlying Mechanism ◽  
Cell Number ◽  
Human Gingival Fibroblasts ◽  
Superior Performance ◽  
Control Group ◽  
Human Gingival Fibroblast ◽  
Gingival Fibroblast ◽  
Gingival Fibroblasts ◽  
Integrin Β1

Abstract Objectives This study aims to evaluate the ability of tantalum-coated titanium to improve human gingival fibroblasts’ adhesion, viability, proliferation, migration performance, and the potential molecular mechanisms. Materials and methods Titanium plates were divided into two groups: (1) no coating (Ti, control), (2) Tantalum-coated titanium (Ta-coated Ti). All samples were characterized by scanning electronic microscopy, surface roughness, and hydrophilicity. Fibroblasts’ performance were analyzed by attached cell number at 1 h, 4 h, and 24 h, morphology at 1 h and 4 h, viability at 1 day, 3 days, 5 days, and 7 days, recovery after wounding at 6 h, 12 h, and 24 h. RT-PCR, western blot were applied to detect attachment-related genes’ expression and protein synthesis at 4 h and 24 h. Student’s t test was used for statistical analysis. Results Tantalum-coated titanium demonstrates a layer of homogeneously distributed nano-grains with mean diameter of 25.98 (± 14.75) nm. It was found that after tantalum deposition, human gingival fibroblasts (HGFs) adhesion, viability, proliferation, and migration were promoted in comparison to the control group. An upregulated level of Integrin β1 and FAK signaling was also detected, which might be the underlying mechanism. Conclusion In the present study, adhesion, viability, proliferation, migration of human gingival fibroblasts are promoted on tantalum-coated titanium, upregulated integrin β1 and FAK might contribute to its superior performance, indicating tantalum coating can be applied in transmucosal part of dental implant. Clinical significance Tantalum deposition on titanium surfaces can promote human gingival fibroblast adhesion, accordingly forming a well-organized soft tissue sealing and may contribute to a successful osseointegration.

Polymeric Delivery of siRNA against Integrin-β1 (CD29) to Reduce Attachment and Migration of Breast Cancer Cells

2017 ◽  
Vol 17 (6) ◽  
pp. 1600430 ◽  
Author(s):  
Daniel Nisakar Meenakshi Sundaram ◽  
Cezary Kucharski ◽  
Manoj B. Parmar ◽  
Remant Bahadur KC ◽  
Hasan Uludağ
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Integrin Β1 ◽  
Polymeric Delivery ◽  
And Migration

scholarly journals Total body irradiation induced mouse small intestine senescence as a late effect

2019 ◽  
Vol 60 (4) ◽  
pp. 442-450 ◽  
Author(s):  
Yu Zhao ◽  
Junling Zhang ◽  
Xiaodan Han ◽  
Saijun Fan
Keyword(s):  
Small Intestine ◽  
Total Body Irradiation ◽  
Profile Analysis ◽  
Bacterial Flora ◽  
Body Weight Loss ◽  
Underlying Mechanism ◽  
The Body ◽  
Mouse Small Intestine ◽  
Total Body ◽  
Almost All

Abstract Radiation can induce senescence in many organs and tissues; however, it is still unclear how radiation stimulates senescence in mouse small intestine. In this study, we use the bone marrow transplantation mouse model to explore the late effects of total body irradiation on small intestine. Our results showed that almost all of the body hairs of the irradiated mice were white (which is an indication of aging) 10 months after the exposure to radiation. Furthermore, compared with the age-matched control mice, there were more SA-β-galactosidase (SA-β-gal)–positive cells and an upregulation of p16 and p21 in 8 Gy–irradiated mice intestinal crypts, indicating that radiation induced senescence in the small intestine. Intestinal bacterial flora profile analysis showed that the diversity of the intestinal bacterial flora decreased in irradiated mice; in addition it showed that the principal components of the irradiated and control mice differed: there was increased abundance of Bacteroidia and a decreased abundance of Clostridia in irradiated mice. To explore the underlying mechanism, an RNA-sequence was executed; the results suggested that pancreatic secretion, and the digestion and absorption of proteins, carbohydrates, fats and vitamins were damaged in irradiated mice, which may be responsible for the body weight loss observed in irradiated mice. In summary, our study suggested that total body irradiation may induce senescence in the small intestine and damage the health status of the irradiated mice.

scholarly journals Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

2017 ◽  
Vol 44 (6) ◽  
pp. 2357-2367 ◽  
Author(s):  
Yiquan Wang ◽  
Chencheng Dai ◽  
Cheng Zhou ◽  
Wenqu Li ◽  
Yujia Qian ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Expression Patterns ◽  
Underlying Mechanism ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Female Reproductive Health ◽  
Gene Microarray Analysis ◽  
And Migration

Background/Aims: Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism. Methods: The CCK-8 assay was performed to detect cell viability; transwell-filter assay was used to assess cell invasion; gene microarray analysis was employed to determine gene expression patterns in response to BTR treatment; western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were carried out to detect the expression levels of BTR-related genes. Results: Our data showed that BTR could induce the invasion and migration of endometrial carcinoma cells (Ishikawa and HEC-1-B). In addition, BTR increased the expression level of CTBP1, which could enhance the epithelial-mesenchymal transition (EMT) in cancer cells. Moreover, CTBP1 silencing reversed the effect of BTR on EMT progression in endometrial carcinoma cells. Conclusion: This study indicates that BTR could act as a carcinogen to promote the development of endometrial carcinoma mainly through CTBP1-mediated EMT, which deserves more attention.

scholarly journals bFGF Activates Integrin β1 and Subsequently Upregulates Collagens via the p-MEK1/2/p-ERK1/2 Signaling Pathway in L929 Cells

2021 ◽  
Author(s):  
Lian Yang ◽  
Shasha Hong ◽  
Yang Li ◽  
Tingting Wang ◽  
Li Hong
Keyword(s):  
Pelvic Organ Prolapse ◽  
Pelvic Floor ◽  
Signaling Pathway ◽  
Pelvic Floor Dysfunction ◽  
Underlying Mechanism ◽  
Pelvic Organ ◽  
Integrin Β1 ◽  
L929 Cells ◽  
Signal Transduction Protein ◽  
Special Project

Abstract The substantial loss of collagen in the supporting tissues of the pelvic floor is characteristic of pelvic organ prolapse (POP). A bFGF-induced collagen increase has been widely recognized by scholars, but the role of bFGF in pelvic floor dysfunction and the mechanism by which bFGF promotes collagen have not been reported. Here, we elucidated this mechanism. After bFGF stimulation, L929 cells showed significantly increased expression of collagen, integrin β1, and MEK1/2 signaling proteins. Our previous studies showed that integrin β1 plays an important role in electric stimulation-induced collagen expression, which suggests an underlying mechanism. By overexpressing and silencing integrin β1, we proved that integrin β1 is also an important signal transduction protein of bFGF that promotes collagen through the MEK1/2 pathway, which is a classic collagen-promoting pathway. In summary, these findings suggest that bFGF can stimulate the expression of collagen through the integrin β1/p-MEK1/2/p-ERK/1/2 signaling pathway in L929 cells. Keyword Pelvic organ prolapse; bFGF; integrinβ1; ERK1/2; Collagen Special project for Chinese women's pelvic floor dysfunction prevention and treatment (no. 201817092) and the Natural Science Foundation of Hubei Province（no.2019CFB149）.

scholarly journals SHED Aggregate Derived Exosomes-shuttled miR-222 Promotes the Regenerative Properties of Periodontal Ligament Stem Cells

2021 ◽  
Author(s):  
Feng Zhou ◽  
Jia Guo ◽  
Fang Wang ◽  
Wanmin Zhao ◽  
Xiaoning He ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Defect ◽  
Periodontal Ligament ◽  
Underlying Mechanism ◽  
Tube Formation ◽  
Deciduous Teeth ◽  
Aggregate Formation ◽  
Periodontal Ligament Stem Cells ◽  
Mirna Sequencing

Abstract Background: Periodontal ligament stem cells (PDLSCs) aggregate is still limited in clinical application for lack of angiogenesis. This study aimed to investigate the effects and underlying mechanism of exosomes derived from stem cells from human exfoliated deciduous teeth (SHED) aggregate (SA-Exo) on the aggregate formation and angiogenic properties of PDLSCs.Methods: SA-Exo were isolated by ultracentrifugation. The effect of SA-Exo on the aggregate formation and angiogenic differentiation of PDLSCs were evaluated by investigating extracellular matrix (ECM) deposition and tube formation assay. MicroRNA (miRNA) sequencing was employed to screen different miRNA expression. The effect of targeting miRNA on ECM deposition and angiogenesis of PDLSCs aggregate was investigated after overexpression and inhibition of miRNA. Periodontal bone defect rat models were established to evaluate the effect of the PDLSCs aggregate and SA-Exo combination on periodontal bone regeneration. Results: SA-Exo could significantly enhance the ECM deposition and angiogenic ability of PDLSCs. The expression of ECM-associated proteins (COL-I, integrinβ1, and fibronectin), angiogenesis-related proteins (PDGF, ANG, TGFβRII), and related pathway (p-SMAD1/5 and p-SMAD2/3) were upregulated in PDLSCs aggregate with SA-Exo. Mechanistically, miR-222 was found relatively abundant in SA-Exo, which promoted ECM deposition and angiogenesis of PDLSCs. In vivo experiment further validated that combinational use of PDLSCs aggregate and SA-Exo promote more bone formation and neovascularization in rat’s periodontal bone defect.Conclusions: SA-Exo-shuttled miR-222 contributes to PDLSCs aggregate engineering by promoting aggregate formation and angiogenesis, which might through activate the TGF-β/SMAD signaling pathway.

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