Le knockdown de Fus inhibe l’effet profibrogène

Le knockdown de Fus inhibe l’effet profibrogène

| Coryne

Le knockdown de Fus inhibe l’effet profibrogène des fibroblastes cardiaques induits par l’angiotensine II en ciblant Pax3, régulant ainsi la voie TGF- / 1 / Smad

 The Angiotensin II/transforming growth factor-β1 (AngII/TGF-β1) signal axis is an important regulatory pathway for atrial fibrosis, which can contribute to atrial fibrillation (AF). Fused in sarcoma (FUS) was recently found to regulate cardiac diseases. This study aimed to investigate whether FUS could regulate AngII induced fibrosis and uncover the possible mechanisms. The expression of FUS in AF patients and AngII-induced cardiac fibroblasts was measured by RT-qPCR and western blot assays. Fus was silenced in cells using short hairpin RNA (shRNA), then cell proliferation, migration, collagen synthesis and TGF-β1/Smad signaling were detected by CCK-8, wound healing and western blot assays, respectively. The possible target for Fus was predicted by searching Starbase database and verified by RNA-binding protein immunoprecipitation (RIP) and RNA pull down.

Cells were overexpressed with Pax3 in the presence of Fus silence and AngII stimulation, then the above cellular processes were further evaluated. Results showed that FUS was upregulated in AF patients and AngII-induced cardiac fibroblasts. Fus knockdown inhibited AngII-enhanced cell proliferation, migration, collagen synthesis and TGF-β1/Smad signaling activation. Furthermore, Fus functions as an RNA-binding protein to bind to Pax3 mRNA and positively regulate its expression. Further studies demonstrated that Pax3 overexpression canceled the above effects of Fus knockdown on cell proliferation, migration, collagen synthesis, and TGF-β1/Smad signaling activation in AngII-induced cells. In conclusion, Fus could target Pax3 to increase the pro-fibrotic effect of AngII in cardiac fibroblasts via activating TGF-β1/Smad signaling. Knockdown of Fus/Pax3 axis may provide a potential therapy for relieving AF.

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Immortalized Human Uterine Fibroblasts
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ASAP1 antibody Antibody
DF8746 200ul
EUR 420

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A1360-500 each Ask for price

Ly1 Antibody Reactive (LYAR) Antibody
20-abx123734
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Anti-Glycolipid Antibody (AGA) Antibody
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Ly1 Antibody Reactive (LYAR) Antibody
20-abx014333
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L’acide salvianolique B inhibe la différenciation des myofibroblastes et l’accumulation de matrice extracellulaire dans les fibroblastes polypes nasaux via la voie de signalisation TGF-sign1 

In the process of nasal tissue remodeling, nasal fibroblasts serve an important role via myofibroblast differentiation and the production of extracellular matrix (ECM). Nasal fibroblast abnormalities can lead to conditions such as chronic rhinosinusitis. Salvianolic acid B (Sal B), a water-soluble active pharmaceutical compound extract from the root of the traditional Chinese medicine Salvia miltiorrhiza, displays antioxidative, antiproliferative and antifibrosis properties. The present study aimed to investigate the mechanism underlying the effects of Sal B on nasal polyp fibroblast (NPF) myofibroblast differentiation and ECM accumulation. Primary NPFs were obtained from nasal polyps of patients with chronic sinusitis. The proliferative and cytotoxic effects of Sal B on NPFs were evaluated by performing the Cell Counting Kit-8 assay.

The Transwell assay was conducted to assess cell migration. α-smooth muscle actin (α-SMA), TGF-β1 receptor (TβR)-I, TβR-II, Smad2/3 mRNA and protein expression levels and (p)-Smad2/3 phosphorylation levels were measured via reverse transcription-quantitative PCR and western blotting, respectively. Type III collagen and fibronectin levels were analyzed by ELISA. The results indicated that Sal B significantly downregulated TGF-β1-induced α-SMA, fibronectin and collagen III expression levels in NPFs. Similarly, Sal B significantly decreased TGF-β1-induced TβR-I, TβR-II, p-Smad2/3, MMP-2 and MMP-9 mRNA and protein expression levels in NPFs. Furthermore, Sal B significantly decreased TGF-β1-induced NPF migration. Therefore, the present study indicated that Sal B inhibited myofibroblast differentiation and ECM accumulation in nasal fibroblasts, suggesting that Sal B may inhibit nasal polyp formation via certain mechanisms.

E2F2 stimule l’expression de CCR4 et active les cellules de type fibroblaste synovial dans la polyarthrite rhumatoïde 

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Material and methods: Cultured RASF were transfected with anti-E2F2 siRNA, and the expression profile was analyzed with an inflammatory response and autoimmunity PCR array loaded with 84-relative genes to explore the pathogenic pathway of E2F2. Apoptosis, migration and tube-like structure formation in the RASF with transfection of anti-E2F2 siRNA or E2F2-expressing plasmids were examined using flow cytometry, transwell assays and Matrigel assays, respectively.

Results: Significantly decreased expression of chemokine receptor 4 (CCR4) was detected in RASF with inhibited E2F2 expression, and the CCR4 expression was increased in RASF with transfection of E2F2-expressing plasmids. Silencing E2F2 expression stimulated apoptosis, but retarded migration and tube-like structure formation in RASF. The opposite observation was obtained in RASF with E2F2 overexpression.

Conclusions: High E2F2 expression decreases apoptosis and increases migration and tube-like structure ability in RASF and might perform this role by up-regulating CCR4 expression, which ultimately contributes to the disease progression of RA synovial tissues.

Taux de sécrétion et composition protéique des vésicules extracellulaires libérées par les fibroblastes associés au cancer après irradiation 

Reciprocal communication between the malignant and non-malignant cellular elements in tumors is essential for cancer sustainability and plays an important role in the response of cancers to treatments. Some of this cellular crosstalk takes place via secretion of vesicles that are actively released into the extracellular space by most cell types in tumors. Recent studies have demonstrated radiation-induced changes in the secretion rate and composition of extracellular vesicles (EVs), with impact on radiation-related cellular communication.

However, little is known about the effects of different radiation regimens on the release of EVs by cells of the tumor microenvironment. In this study, we provide a comprehensive molecular characterization of EVs released by cultured primary lung tumor fibroblasts. We explore the quantitative and morphological changes triggered by ionizing radiation (IR), delivered as a single dose of 18 Gy or three consecutive daily medium-doses of 6 Gy. Cancer-associated fibroblasts (CAFs) secrete EVs with sizes ranging from 80 to 200 nm, expressing some of the classical exosome markers. Exposing CAFs to a single-high radiation dose (1 × 18 Gy) or fractionated medium-dose did not alter the release of CAF-EVs.

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Human Eye PrimaCell3: Normal Corneal Fibroblasts
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Human Heart PrimaCell3: Normal Heart Fibroblasts
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Human Lung PrimaCell1: Normal Lung Fibroblasts
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Human Lymph PrimaCell3: Normal Lymphatic Fibroblasts
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4-29295 ea Ask for price

Rat Bladder PrimaCell2: Normal Bladder Fibroblasts Growth Medium
9-25007 5 x 100 ml Ask for price

Rat Brain PrimaCell1: Normal Brain Fibroblasts Growth Medium
9-25011 5 x 100 ml Ask for price

Rat Cervix PrimaCell2: Normal Cervical Fibroblasts Growth Medium
9-25025 5 x 100 ml Ask for price

Rat Eye PrimaCell3: Normal Corneal Fibroblasts Growth Medium
9-25040 5 x 100 ml Ask for price

Rat Heart PrimaCell3: Normal Heart Fibroblasts Growth Medium
9-25048 5 x 100 ml Ask for price

Rat Lung PrimaCell1: Normal Lung Fibroblasts Growth Medium
9-25064 5 x 100 ml Ask for price

Rat Lymph PrimaCell3: Normal Lymphatic Fibroblasts Growth Medium
9-25072 5 x 100 ml Ask for price

Mouse Bladder PrimaCell2: Normal Bladder Fibroblasts Growth Medium
9-32007 5 x 100 ml Ask for price

Mouse Brain PrimaCell1: Normal Brain Fibroblasts Growth Medium
9-32010 5 x 100 ml Ask for price

Mouse Cervix PrimaCell2: Normal Cervical Fibroblasts Growth Medium
9-32024 5 x 100 ml Ask for price

Mouse Eye PrimaCell3: Normal Corneal Fibroblasts Growth Medium
9-32039 5 x 100 ml Ask for price

Mouse Heart PrimaCell3: Normal Heart Fibroblasts Growth Medium
9-32047 5 x 100 ml Ask for price

Mouse Lung PrimaCell2: Normal Lung Fibroblasts Growth Medium
9-32065 5 x 100 ml Ask for price

Mouse Lymph PrimaCell3: Normal Lymphatic Fibroblasts Growth Medium
9-32073 5 x 100 ml Ask for price

Human Bladder PrimaCell2: Normal Bladder Fibroblasts Growth Medium
9-46008 5 x 100 ml Ask for price

Human Brain PrimaCell1: Normal Brain Fibroblasts Growth Medium
9-46013 5 x 100 ml Ask for price

Human Cervix PrimaCell2: Normal Cervical Fibroblasts Growth Medium
9-46045 5 x 100 ml Ask for price

Human Eye PrimaCell3: Normal Corneal Fibroblasts Growth Medium
9-46059 5 x 100 ml Ask for price

Human Heart PrimaCell3: Normal Heart Fibroblasts Growth Medium
9-46068 5 x 100 ml Ask for price

Human Lung PrimaCell1: Normal Lung Fibroblasts Growth Medium
9-46081 5 x 100 ml Ask for price

Human Lymph PrimaCell3: Normal Lymphatic Fibroblasts Growth Medium
9-46089 5 x 100 ml Ask for price

Human Mouth PrimaCell: Normal Periodontal Fibroblasts Growth Medium
9-46090 5 x 100 ml Ask for price

Human Skin PrimaCell: Normal Skin Fibroblasts Growth Medium
9-46103 5 x 100 ml Ask for price

Human Cancer Tissue Preparation Buffer 7: Esophageal Fibroblasts
9-80030 1 x 100 ml Ask for price

Human Mouth Tissue Preparation Buffer: Normal Periodontal Fibroblasts
9-80090 1 x 100 ml Ask for price

Heart Dissociation System 11 (Cardiomycytes,Fibroblasts), Mouse and Rat
4-20281 ea Ask for price

Mouse Ariway PrimaCell3: Normal Bronchial and and Tracheal Fibroblasts
2-82003 1 Kit Ask for price

Rat Ariway PrimaCell3: Normal Bronchial and and Tracheal Fibroblasts
2-82503 1 Kit Ask for price

Human Airway PrimaCell4: Normal Bronchial and and Tracheal Fibroblasts
2-96004 1 Kit Ask for price

Rat Embryo PrimaCell2: Normal Fetal Dermal Fibroblasts Growth Medium
9-25032 5 x 100 ml Ask for price

Rat Lung PrimaCell3: Normal Pulmonary Artery Fibroblasts Growth Medium
9-25066 5 x 100 ml Ask for price

Mouse Embryo PrimaCell2: Normal Fetal Dermal Fibroblasts Growth Medium
9-32031 5 x 100 ml Ask for price

Mouse Lung PrimaCell4: Normal Pulmonary Artery Fibroblasts Growth Medium
9-32067 5 x 100 ml Ask for price

Human Embryo PrimaCell2: Normal Fetal Dermal Fibroblasts Growth Medium
9-46051 5 x 100 ml Ask for price

Human Lung PrimaCell3: Normal Pulmonary Artery Fibroblasts Growth Medium
9-46083 5 x 100 ml Ask for price

Human Bladder Tissue Preparation Buffer 2: Normal Bladder Fibroblasts
9-80008 1 x 100 ml Ask for price

Human Brain Tissue Preparation Buffer 1: Normal Brain Fibroblasts
9-80013 1 x 100 ml Ask for price

Human Cervix Tissue Preparation Buffer 2: Normal Cervical Fibroblasts
9-80045 1 x 100 ml Ask for price

Human Eye Tissue Preparation Buffer 3: Normal Corneal Fibroblasts
9-80059 1 x 100 ml Ask for price

Human Heart Tissue Preparation Buffer 3: Normal Heart Fibroblasts
9-80068 1 x 100 ml Ask for price

Human Lung Tissue Preparation Buffer 1: Normal Lung Fibroblasts
9-80081 1 x 100 ml Ask for price

Human Lymph Tissue Preparation Buffer 3: Normal Lymphatic Fibroblasts
9-80089 1 x 100 ml Ask for price

Human Skin Tissue Preparation Buffer 3: Normal Skin Fibroblasts
9-80103 1 x 100 ml Ask for price

Mouse Bladder Tissue Preparation Buffer 2: Normal Bladder Fibroblasts
9-80121 1 x 100 ml Ask for price

Mouse Brain Tissue Preparation Buffer 1: Normal Brain Fibroblasts
9-80124 1 x 100 ml Ask for price
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