MiR-34a/miR-93 target c-Ski to modulate the proliferaton of rat cardiac fibroblasts and extracellular matrix deposition in vivo and in vitro

2018 ◽  
Vol 46 ◽  
pp. 145-153 ◽  
Author(s):  
Chengliang Zhang ◽  
Yanfeng Zhang ◽  
Hong Zhu ◽  
Jiajia Hu ◽  
Zhongshang Xie
Keyword(s):  
Extracellular Matrix ◽  
Cardiac Fibroblasts ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

scholarly journals GSK-3 Inhibition Modulates Metalloproteases in a Model of Lung Inflammation and Fibrosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Francesco Cinetto ◽  
Jessica Ceccato ◽  
Ilaria Caputo ◽  
Daniela Cangiano ◽  
Barbara Montini ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Lung Inflammation ◽  
Therapeutic Strategy ◽  
Glycogen Synthase ◽  
Alveolar Cells ◽  
Human Lung Fibroblast ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

Idiopathic pulmonary fibrosis (IPF) is mainly characterized by aberrant extracellular matrix deposition, consequent to epithelial lung injury and myofibroblast activation, and inflammatory response. Glycogen synthase kinase 3 (GSK-3) is a serine–threonine kinase involved in several pathways, and its inhibition has been already suggested as a therapeutic strategy for IPF patients. There is evidence that GSK-3 is able to induce matrix metalloproteinase (MMP) expression and that its inhibition modulates MMP expression in the tissues. The aim of our study was to investigate the role of GSK-3 and its inhibition in the modulation of MMP-9 and -2 in an in vivo mouse model of lung fibrosis and in vitro using different cell lines exposed to pro-inflammatory or pro-fibrotic stimuli. We found that GSK-3 inhibition down-modulates gene expression and protein levels of MMP-9, MMP-2, and their inhibitors TIMP-1 and TIMP-2 in inflammatory cells harvested from bronchoalveolar lavage fluid (BALF) of mice treated with bleomycin as well as in interstitial alveolar macrophages and cuboidalized epithelial alveolar cells. To the same extent, GSK-3 inhibition blunted the increased MMP-9 and MMP-2 activity induced by pro-fibrotic stimuli in a human lung fibroblast cell line. Moreover, the αSMA protein level, a marker of fibroblast-to-myofibroblast transition involved in fibrosis, was decreased in primary fibroblasts treated with TGFβ following GSK-3 inhibition. Our results confirm the implication of GSK-3 in lung inflammation and fibrosis, suggesting that it might play its role by modulating MMP expression and activity but also pushing fibroblasts toward a myofibroblast phenotype and therefore enhancing extracellular matrix deposition. Thus, its inhibition could represent a possible therapeutic strategy.

Schwann Cell Differentiation in vitro: Extracellular Matrix Deposition and Interaction

1986 ◽  
Vol 8 (3) ◽  
pp. 182-196 ◽  
Author(s):  
A. Baron-Van Evercooren ◽  
A. Gansmüller ◽  
M. Gumpel ◽  
N. Baumann ◽  
H.K. Kleinman
Keyword(s):  
Extracellular Matrix ◽  
Cell Differentiation ◽  
Schwann Cell ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Schwann Cell Differentiation

scholarly journals CircSMAD4 alleviates high glucose-induced inflammation, extracellular matrix deposition and apoptosis in mouse glomerulus mesangial cells by relieving miR-377-3p-mediated BMP7 inhibition

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Rina Wu ◽  
Zheli Niu ◽  
Guangwei Ren ◽  
Lin Ruan ◽  
Lijun Sun
Keyword(s):  
Extracellular Matrix ◽  
High Glucose ◽  
Mesangial Cells ◽  
Circular Rna ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Protein Levels ◽  
Matrix Deposition

Abstract Background Diabetic nephropathy (DN) is a common complication of diabetes mellitus. Accumulating studies suggest that the deregulation of circular RNA (circRNA) is involved in DN pathogenesis. This study aimed to investigate the role of circSMAD4 in DN models. Methods Mice were treated with streptozotocin to establish DN models in vivo. Mouse glomerulus mesangial cells (SV40-MES13) were treated with high glucose to establish DN models in vitro. The expression of circSMAD4, miR-377-3p and bone morphogenetic protein 7 (BMP7) mRNA was measured by quantitative real-time PCR (qPCR). The releases of inflammatory factors were examined by ELISA. The protein levels of fibrosis-related markers, apoptosis-related markers and BMP7 were checked by western blot. Cell apoptosis was monitored by flow cytometry assay. The predicted relationship between miR-377-3p and circSMAD4 or BMP7 was validated by dual-luciferase reporter assay or pull-down assay. Results CircSMAD4 was poorly expressed in DN mice and HG-treated SV40-MES13 cells. HG induced SV40-MES13 cell inflammation, extracellular matrix (ECM) deposition and apoptosis. CircSMAD4 overexpression alleviated, while circSMAD4 knockdown aggravated HG-induced SV40-MES13 cell injuries. MiR-377-3p was targeted by circSMAD4, and miR-377-3p enrichment partly reversed the effects of circSMAD4 overexpression. BMP7 was a target of miR-377-3p, and circSMAD4 regulated BMP7 expression by targeting miR-377-3p. MiR-377-3p overexpression aggravated HG-induced injuries by suppressing BMP7. Conclusion CircSMAD4 alleviates HG-induced SV40-MES13 cell inflammation, ECM deposition and apoptosis by relieving miR-377-3p-mediated inhibition on BMP7 in DN progression.

scholarly journals Mechanism underlying increased cardiac extracellular matrix deposition in perinatal nicotine-exposed offspring

2020 ◽  
Vol 319 (3) ◽  
pp. H651-H660
Author(s):  
Tsai-Der Chuang ◽  
Aamir Ansari ◽  
Celia Yu ◽  
Reiko Sakurai ◽  
Amir Harb ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Rat Model ◽  
Cardiac Dysfunction ◽  
Cardiac Fibroblasts ◽  
Underlying Mechanism ◽  
Nicotine Exposure ◽  
Collagen Deposition ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Mechanistic Basis

Using an established rat model and cultured primary neonatal cardiac fibroblasts, we show that nicotine mediated MIAT induction as the underlying mechanism for the excessive cardiac collagen deposition. These observations provide mechanistic basis for the increased predisposition to cardiac dysfunction following perinatal cigarette/nicotine exposure and offer novel potential therapeutic targets.

scholarly journals Contribution of Fibroblasts to the Mechanical Stability of In Vitro Engineered Dermal-Like Tissue Through Extracellular Matrix Deposition

2014 ◽  
Vol 3 (5) ◽  
pp. 217-225 ◽  
Author(s):  
Renjith P. Nair ◽  
Jasmin Joseph ◽  
V.S. Harikrishnan ◽  
V.K. Krishnan ◽  
Lissy Krishnan
Keyword(s):  
Extracellular Matrix ◽  
Mechanical Stability ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

scholarly journals pVHL Function Is Essential for Endothelial Extracellular Matrix Deposition

2006 ◽  
Vol 26 (7) ◽  
pp. 2519-2530 ◽  
Author(s):  
Nan Tang ◽  
Fiona Mack ◽  
Volker H. Haase ◽  
M. Celeste Simon ◽  
Randall S. Johnson
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Critical Role ◽  
Matrix Assembly ◽  
Developmental Defects ◽  
Vhl Gene ◽  
Matrix Deposition ◽  
Fibronectin Deposition

ABSTRACT The tumor suppressor von Hippel-Lindau protein (pVHL) is critical for cellular molecular oxygen sensing, acting to target degradation of the hypoxia-inducible factor alpha transcription factor subunits under normoxic conditions. We have found that independent of its function in regulating hypoxic response, the VHL gene plays a critical role in embryonic endothelium development through regulation of vascular extracellular matrix assembly. We created mice lacking the VHL gene in endothelial cells; these conditional null mice died at the same stage as homozygous VHL-null mice, with similar vascular developmental defects. These included defective vasculogenesis in the placental labyrinth, a collapsed endocardium, and impaired vessel network patterning. The defects in embryonic vascularization were correlated with a diminished vascular fibronectin deposition in vivo and defective endothelial extracellular fibronectin assembly in vitro. We found that the impaired migration and adhesion of VHL-null endothelial cells can be partially rescued by the addition of back exogenous fibronectin, which indicates that pVHL regulation of fibronectin deposition plays an important functional role in vascular patterning and maintenance of vascular integrity.

scholarly journals A three-dimensional in vitro dynamic micro-tissue model of cardiac scar formation

2018 ◽  
Vol 10 (3) ◽  
pp. 174-183 ◽  
Author(s):  
Paola Occhetta ◽  
Giuseppe Isu ◽  
Marta Lemme ◽  
Chiara Conficconi ◽  
Philipp Oertle ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Three Dimensional ◽  
Scar Formation ◽  
Fibroblast Proliferation ◽  
Tissue Model ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Mechanical Stretching

Our 3D-scar-on-a-chip model resembles fibroblast proliferation and activation, extracellular matrix deposition and stiffening upon application of only cyclic mechanical stretching.

scholarly journals The Need for Basic, Translational, and Clinical Research in the Field of Hypertrophic Scars

2021 ◽  
Author(s):  
Bonnie C. Carney ◽  
Jeffrey W. Shupp ◽  
Taryn E. Travis
Keyword(s):  
Clinical Research ◽  
Treatment Effectiveness ◽  
Science Research ◽  
Future Research ◽  
Traumatic Injuries ◽  
Matrix Deposition ◽  
Organ Systems ◽  
Extracellular Matrix Deposition

Hypertrophic scar (HTS) is a fibrotic skin disorder that is marked by excessive inflammation and extracellular matrix deposition in response to cutaneous traumatic injuries such as burns, lacerations, incisions, and abrasions. HTS has various risk factors, available treatments, and treatment effectiveness. Research at the basic, translational, and clinical levels are in their infancy compared to fibrotic diseases in other organ systems. This chapter will review current in vitro and in vivo modeling, and highlight research needs to address gaps in the study of HTS. The following topics will be discussed in the chapter: a. Basic Science Research i. Seminal findings ii. Limitations to these models iii. Suggestions for topics of future research b. Translational Science Research i. Seminal findings ii. Limitations to these models iii. Suggestions for topics of future research c. Clinical Research i. Seminal findings ii. Limitations to these models iii. Suggestions for topics of future research.

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