Role of the long noncoding RNA H19 in TGF-β1-induced Tenon's capsule fibroblast proliferation and extracellular matrix deposition

2020 ◽  
Vol 387 (2) ◽  
pp. 111802
Author(s):  
Huirong Zhu ◽  
Li Dai ◽  
Xiabin Li ◽  
Zhilin Zhang ◽  
Yan Liu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Fibroblast Proliferation ◽  
Matrix Deposition ◽  
Tenon’S Capsule ◽  
Tenon's Capsule ◽  
Extracellular Matrix Deposition ◽  
Tgf Β1

Long Noncoding RNA MIAT Modulates the Extracellular Matrix Deposition in Leiomyomas by Sponging MiR-29 Family

Endocrinology ◽  
2021 ◽  
Vol 162 (11) ◽  
Author(s):  
Tsai-Der Chuang ◽  
Derek Quintanilla ◽  
Drake Boos ◽  
Omid Khorram
Keyword(s):  
Extracellular Matrix ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Collagen Type ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Luciferase Reporter ◽  
Cycle Phase ◽  
Type I ◽  
Matrix Deposition

Abstract The objective of this study was to determine the expression and functional role of a long noncoding RNA (lncRNA) MIAT (myocardial infarction–associated transcript) in leiomyoma pathogenesis. Leiomyoma compared with myometrium (n = 66) expressed significantly more MIAT that was independent of race/ethnicity and menstrual cycle phase but dependent on MED12 (mediator complex subunit 12) mutation status. Leiomyomas bearing the MED12 mutation expressed higher levels of MIAT and lower levels of microRNA 29 family (miR-29a, -b, and -c) compared with MED12 wild-type leiomyomas. Using luciferase reporter activity and RNA immunoprecipitation analysis, MIAT was shown to sponge the miR-29 family. In a 3-dimensional spheroid culture system, transient transfection of MIAT siRNA in leiomyoma smooth muscle cell (LSMC) spheroids resulted in upregulation of miR-29 family and downregulation of miR-29 targets, collagen type I (COL1A1), collagen type III (COL3A1), and TGF-β3 (transforming growth factor β-3). Treatment of LSMC spheroids with TGF-β3 induced COL1A1, COL3A1, and MIAT levels, but repressed miR-29 family expression. Knockdown of MIAT in LSMC spheroids blocked the effects of TGF-β3 on the induction of COL1A1 and COL3A1 expression. Collectively, these results underscore the physiological significance of MIAT in extracellular matrix accumulation in leiomyoma.

scholarly journals Role of Nampt-Sirt6 Axis in Renal Proximal Tubules in Extracellular Matrix Deposition in Diabetic Nephropathy

Cell Reports ◽  
2019 ◽  
Vol 27 (1) ◽  
pp. 199-212.e5 ◽  
Author(s):  
Hirokazu Muraoka ◽  
Kazuhiro Hasegawa ◽  
Yusuke Sakamaki ◽  
Hitoshi Minakuchi ◽  
Takahisa Kawaguchi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Diabetic Nephropathy ◽  
Proximal Tubules ◽  
Renal Proximal Tubules ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

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.

p75NTR silencing inhibits proliferation, migration and extracellular matrix deposition of hypertrophic scar fibroblasts by activating autophagy through inhibiting PI3K/Akt/mTOR pathway

2020 ◽  
Author(s):  
Wen Shi ◽  
Yan Wu ◽  
Donghui Bian
Keyword(s):  
Extracellular Matrix ◽  
Wound Healing ◽  
Hypertrophic Scar ◽  
Mtor Pathway ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Inhibitory Effects ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

Hypertrophic scar (HS) results from abnormal wound healing, accompanied by excessive hypercellularity, migration and extracellular matrix (ECM) deposition. Autophagy dysregulation plays crucial roles during HS formation. The overexpressed p75 neurotrophin receptor (p75NTR) in injured skin tissue after wound healing becomes a factor aggravating scar. The study was designed to investigate the role of p75NTR and p75NTR-mediated autophagy in the process of HS. The results revealed that p75NTR expression was significantly upregulated while that of autophagy proteins was downregulated in cicatrix at 3 and 6 months after burn, which was recovered at 12 months. p75NTR silencing inhibited proliferation, migration and ECM deposition of hypertrophic scar fibroblasts (HSF), whereas p75NTR overexpression presented the opposite results. Silencing of p75NTR reduced the expression of PI3K/Akt/mTOR signaling molecules while enhanced that of autophagy proteins. Importantly, PI3K agonist (IGF-1) intervention notably decreased the levels of LC3B II/I and Beclin-1, and restored the inhibitory effects of p75NTR silencing on proliferation, migration and ECM deposition of HSF. Concurrently, autophagy inhibitor 3-methyladenine (3-MA) treatment exhibited the same variation trends with IGF-1. Taken together, these findings demonstrated that p75NTR silencing inhibits proliferation, migration and ECM deposition of HSF by activating autophagy through inhibiting PI3K/Akt/mTOR pathway.

scholarly journals The Role of Hypoxia in Corneal Extracellular Matrix Deposition and Cell Motility

2019 ◽  
Vol 303 (6) ◽  
pp. 1703-1716 ◽  
Author(s):  
Obianamma E. Onochie ◽  
Anwuli J. Onyejose ◽  
Celeste B. Rich ◽  
Vickery Trinkaus‐Randall
Keyword(s):  
Extracellular Matrix ◽  
Cell Motility ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

Extracellular matrix deposition by primary human lung fibroblasts in response to TGF-β1 and TGF-β3

1999 ◽  
Vol 276 (5) ◽  
pp. L814-L824 ◽  
Author(s):  
Oliver Eickelberg ◽  
Eleonore Köhler ◽  
Frank Reichenberger ◽  
Sybille Bertschin ◽  
Thomas Woodtli ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Transforming Growth Factor ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblasts ◽  
Matrix Deposition ◽  
Proline Incorporation ◽  
Primary Fibroblasts ◽  
Extracellular Matrix Deposition ◽  
Tgf Β1

Increased collagen and extracellular matrix (ECM) deposition within the lung is a characteristic feature of lung fibrosis. Transforming growth factor (TGF)-β isoforms play a pivotal role in the production of collagen and ECM. In this study, we investigated the effects of TGF-β1 and TGF-β3 on the main processes controlling ECM deposition using primary human lung fibroblasts. We analyzed 1) collagen metabolism by [3H]proline incorporation, 2) matrix metalloproteinase (MMP) expression by substrate gel zymography, and 3) tissue inhibitor of metalloproteinases (TIMP) expression by Western blot analysis. TGF-β1 and TGF-β3 increased the percentage of secreted collagens in supernatants of primary fibroblasts from 8.0 ± 1.2 (control) to 23.6 ± 4.6 and 22.3 ± 1.3%, respectively. The collagen percentage in deposited ECM was increased from 5.8 ± 0.3 (control) to 9.0 ± 0.5 and 8.8 ± 0.5% by TGF-β1 and TGF-β3, respectively. Secretion of MMP-1 (interstitial collagenase) by fibroblasts was reduced by both TGF-β isoforms, whereas secretion of MMP-2 (gelatinase A) was unaffected by either of the two isoforms. Both TGF-β isoforms increased TIMP-1 protein expression, whereas TIMP-2 protein was decreased. We thus conclude that TGF-β1 and TGF-β3 are equally potent in increasing ECM deposition. Their fibrotic effect in lung fibroblasts results from 1) an increase in the secretion and deposition of total ECM and collagens, 2) a decrease in MMP-1 secretion, and 3) an increase of TIMP-1 expression.

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