Browsing by Subject "TGF-β"

Now showing 1 - 6 of 6
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    Expression of myostatin in early postnatal mouse masseter and rectus femoris muscles
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2015) Takada, Hiroshi; Miwa, Yoko; Sato, Iwao
    Aims: Myostatin (Mstn) is a member of the transforming growth factor-β (TGF-β) family that inhibits muscle differentiation. In this study, we aimed to identify the relationships between Mstn, thyroid hormone receptor alpha (TRα), and myosin heavy chain (MyHC) isoform expression during early postnatal development. Methods: We investigated the expression of Mstn, TRα, and MyHCs (embryonic, slow, IIa, IIb, and IIx) using quantitative real-time RT-PCR and ELISA (Mstn) in postnatal mouse muscles between day 0 and day 10. We also examined the correlations between Mstn, TR and MyHCs during the early development of mouse masseter muscle (MM) and rectus femoris muscle (RFM). Results: Distinct Mstn mRNA expression patterns were observed in the two muscles despite nearly non-significant changes in the Mstn protein abundance in MM. The expression pattern of the TRα mRNA in the MM differed from that observed in the RFM. The expression of MyHC IIa, IIb and IIx mRNAs increased in the MM and decreased in the RFM from day 0 to day 10, whereas embryonic fiber MyHC mRNA expression was similar in both muscle types. Principal component analysis showed the existence of a correlation between: (1) TRα and MyHC, (2) Mstn and MyHC, and (3) TRα and Mstn in MM. The correlations were different in RFM and MM. Cluster analyses identified the distinct clusters: cluster 1, days 0-4 for the MM and day 0 for the RFM;cluster 2, day 6 for the MM and day 2 for the RFM; and cluster 3, days 8-10 for the MM and days 4-10 for the RFM. Conclusions: These data suggest that TRα influences MyHC expression in both muscle types. In addition, Mstn has a limited effect in the MM related to the expression of individual MyHCs, as opposed to its role in the RFM, at early postnatal developmental stages. TRα could be involved in regulating both the temporal expression of MyHCs and Mstn at the early postnatal stages in the MM and RFM.
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    Hsa_circ_0072765 knockdown inhibits proliferation, activation and migration in transforming growth factor-beta (TGF-β)-induced hepatic stellate cells (HSCs) by the miR-197-3p/TRPV3 axis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Jin, Yan; Guo, Xueyan; Zhang, Rong; Yan, Chunying
    Background. Circular RNAs (circRNAs) participate in the progression of diverse human diseases. However, the effects of circRNAs on liver fibrosis are limited. In this study, we aimed to investigate the functions of hsa_circ_0072765 in liver fibrosis. Methods. Transforming growth factor-beta (TGF-β)treated hepatic stellate cells (HSCs) were used as the cell model of liver fibrosis. Quantitative real-time polymerase chain reaction (qRT-PCR) or western blot was performed to determine the expression of hsa_circ_0072765, microRNA-197-3p (miR-197-3p) and transient receptor potential cation channel subfamily V member 3 (TRPV3). 5’-ethynyl-2’-deoxyuridine (EdU) assay, flow cytometry analysis and woundhealing assay were conducted to evaluate cell proliferation, cell cycle and migration. HSC activation was assessed by determining the expression of alphasmooth muscle actin (α-SMA) and type I collagen alpha 1 (Col1A1). Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) were manipulated to analyze the relationship of hsa_circ_0072765, miR-197-3p and TRPV3. The exosome morphology was observed under transmission electron microscopy (TEM). Results. Hsa_circ_0072765 level was increased in TGF-β-induced HSCs. Hsa_circ_0072765 knockdown inhibited cell proliferation, cell cycle, activation and migration in TGF-β-induced HSCs. Hsa_circ_0072765 sponged miR-197-3p and negatively regulated miR-1973p expression. MiR-197-3p inhibition reversed the effects of hsa_circ_0072765 knockdown on TGF-βinduced HSC proliferation, cell cycle, activation and migration. In addition, TRPV3 was the target gene of miR-197-3p and miR-197-3p overexpression inhibited TGF-β-treated HSC proliferation, cell cycle, activation and migration by targeting TRPV3. Besides, we found that exosomal hsa_circ_0072765 was increased in TGFβ-treated HSCs. Conclusion. Hsa_circ_0072765 promoted the progression of TGF-β-treated HSCs by decoying miR197-3p and upregulating TRPV3
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    TGF-β links glycolysis and immunosuppression in glioblastoma
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Gong, Lingli; Ji, Li; Xu, Daxing; Wang, Jingjing; Zou, Jian
    Glioblastoma (GBM) is the most common and aggressive brain tumor in adults, characterized by diffuse infiltration, dysplasia, and resistance to therapy. Metabolic remodeling and immunosuppression are typical events which contribute to GBM progression, but the molecular link between these two events remains largely undetermined. Studies have shown that high levels of transforming growth factor-β (TGF-β) and its receptors are associated with glioma malignancy and a poor prognosis. TGF-β plays an important role in cell metabolism and immunity. During tumorigenesis, TGFβ induces a shift in cell metabolism from oxidative phosphorylation to aerobic glycolysis, providing a favorable environment for tumor growth. Locally, TGFβ creates an immunosuppressive microenvironment and promotes the malignant phenotype of GBM. In this review, we aim to link GBM aerobic glycolysis and immunosuppression through TGF-β to provide new ideas for the study of GBM.
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    The expression of Smad signaling pathway in myocardium and potential therapeutic effects
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Duan, Yongjian; Zhu, Wei; Liu, Min; Ashraf, Muhammad; Xu, Meifeng
    Myocardial infarction (MI) is a lifethreatening disease. The expression of Smad proteins in the ischemic myocardium changes significantly following myocardial infarction, suggesting a close relationship between Smad proteins and heart remodeling. Moreover, it is known that the expression of Smads is regulated by transforming growth factor-β (TGF-β) and bone morphogenetic proteins (BMP). Based on these findings, regulating the expression of Smad proteins by targeting TGF-β and BMP in the ischemic myocardium may be considered to be a possible therapeutic strategy for the treatment of myocardial infarction
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    The role of EpCAM in physiology and pathology of the epithelium
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Martowicz, Agnieszka; Seeber, Andreas; Untergasser, Gerold
    Epithelial Cell Adhesion Molecule (EpCAM) has been discovered as one of the first tumor-specific antigens overexpressed in epithelial cancer. The present review focuses on the role of EpCAM in physiology and homeostasis of epithelia. Recent research pointed to a close interaction of EpCAM with other cell-cell contact molecules like E-cadherin and claudins and an intimate crosstalk with Wnt and TGF-beta signaling in the regulation of cell growth. Moreover, EpCAM has been shown to modulate trans-epithelial migration processes of white blood cells. Mutations of the EpCAM gene lead to disturbances of epithelial homeostasis and cellular differentiation from the stem cell compartment. In the intestinal tract EpCAM mutations contribute to congenital tufting enteropathy. Regarding tumorigenesis EpCAM can act as an oncogene still depending on additional driver mutations and epithelial phenotype of tumor cells. Tumor cells display increased EpCAM expression that often correlates with the loss of strict basolateral localization. Many tumors show enhanced regulated intramembrane proteolysis (RIP) of EpCAM and loose EpCAM expression under conditions of epithelial to mesenchymal transition. The resulting extracellular EpEX and intracellular EpICD fragments mediate proliferative signals to the cell. Resulting fragments can be validated either by sensitive enzymelinked immune-sandwich assays (EpEX) or by immunohistochemistry (EpICD). The present review gives an overview on the detection of EpCAM fragments as predictive markers for disease progression and survival of cancer patients.
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    Tripartite motif-containing 35 (TRIM35) is up-regulated in UUO-induced renal fibrosis animal model
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Chen, Yu; Ding, Yue; Wang, Li-Ming
    Renal fibrosis has been recognized as a serious health threat in the world because of the high cost of treatment and poor prognosis. However, the molecular mechanism of renal fibrosis is still largely unknown. In this study, we aimed at illustrating the role of TRIM35 in the renal fibrosis process. A UUO mouse model and a TGF-β1-induced tubulointerstitial fibrosis model were constructed for the research of renal fibrosis at animal and cell level, respectively. Hematoxylin-eosin and Masson staining were used for visualizing the pathological change. qRT-PCR, Western blot analysis and immunohistochemical staining were used to detect the expression of fibrosis-associated proteins and TRIM35. The results showed that, after the modeling, the expressions of α-SMA, Collagen I, Collagen III, Fibronectin and Snail1 were up-regulated, while the expression of E-cadherin was down-regulated, indicating the successful construction of animal and cell models. More importantly, TRIM35 was proved to be upregulated in both animal and cell models. Therefore, this study demonstrates the potential promotional effect of TRIM35 in the renal fibrosis process, which may prove to be a new biomarker for the diagnosis and development of new treatments of renal fibrosis.