Balance between bacterial extracellular matrix production and intramacrophage proliferation by a Salmonella ‐specific SPI‐2 encoded transcription factor

2021 ◽  
Author(s):  
María Laura Echarren ◽  
Nicolás R. Figueroa ◽  
Luisina Vitor‐Horen ◽  
M. Graciela Pucciarelli ◽  
Francisco García‐del Portillo ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Transcription Factor ◽  
Extracellular Matrix Production ◽  
Matrix Production

scholarly journals Balance between extracellular matrix production and macrophage survival by a Salmonella-specific SPI-2 encoded transcription factor

2021 ◽  
Author(s):  
María Laura Echarren ◽  
Nicolás R. Figueroa ◽  
Luisina Vitor-Horen ◽  
M. Graciela Pucciarelli ◽  
Francisco García-del Portillo ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Transcription Factor ◽  
Biofilm Formation ◽  
Cellulose Synthase ◽  
Host Cells ◽  
Wild Type ◽  
Master Regulator ◽  
Specific Transcription Factor ◽  
Extracellular Matrix Production ◽  
Matrix Production

AbstractCellulose is a major component of the Salmonella biofilm extracellular matrix and it is considered an antivirulence factor because it interferes with Salmonella survival inside macrophages and virulence in mice. Its synthesis is stimulated by CsgD, the master regulator of biofilm extracellular matrix formation in enterobacteria, which in turn is under the control of MlrA, a MerR-like transcription factor. In this work we identified a SPI-2 encoded Salmonella-specific transcription factor homolog to MlrA, MlrB, that represses transcription of its downstream gene, STM1389, also known as orf319, and of csgD inside host cells. MlrB is induced in laboratory media mimicking intracellular conditions and inside macrophages, and it is required for intramacrophage survival. An increased expression of csgD is observed in the absence of MlrB inside host cells. Interestingly, inactivation of the CsgD-controlled cellulose synthase coding-gene, bcsA, restored intramacrophage survival to rates comparable to wild type bacteria in the absence of MlrB. These data indicate that MlrB represses CsgD expression inside host cells and in consequence activation of the cellulose synthase. Our findings provide a novel link between biofilm formation and Salmonella virulence.

Dynamics of extracellular matrix production and turnover in tissue engineered cardiovascular structures

2001 ◽  
Vol 81 (2) ◽  
pp. 220-228 ◽  
Author(s):  
Ulrich A. Stock ◽  
Dmitri Wiederschain ◽  
Susan M. Kilroy ◽  
Dominique Shum-Tim ◽  
Philip N. Khalil ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Extracellular Matrix Production ◽  
Matrix Production

Glucosamine sulphate does not increase extracellular matrix production at low oxygen tension

2009 ◽  
Vol 337 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Cheng-Juan Qu ◽  
Teemu Pöytäkangas ◽  
Marjo Jauhiainen ◽  
Seppo Auriola ◽  
Mikko J. Lammi
Keyword(s):  
Extracellular Matrix ◽  
Oxygen Tension ◽  
Low Oxygen ◽  
Low Oxygen Tension ◽  
Extracellular Matrix Production ◽  
Glucosamine Sulphate ◽  
Matrix Production

scholarly journals Laminin-5 activates extracellular matrix production and osteogenic gene focusing in human mesenchymal stem cells

2007 ◽  
Vol 26 (2) ◽  
pp. 106-114 ◽  
Author(s):  
Robert F. Klees ◽  
Roman M. Salasznyk ◽  
Scott Vandenberg ◽  
Kristin Bennett ◽  
George E. Plopper
Keyword(s):  
Stem Cells ◽  
Extracellular Matrix ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells ◽  
Laminin 5 ◽  
Extracellular Matrix Production ◽  
Matrix Production ◽  
Osteogenic Gene

scholarly journals Differentiation of cardiomyocytes from human embryonic stem cells is accompanied by changes in the extracellular matrix production of versican and hyaluronan

2010 ◽  
Vol 111 (3) ◽  
pp. 585-596 ◽  
Author(s):  
Christina K. Chan ◽  
Marsha W. Rolle ◽  
Susan Potter-Perigo ◽  
Kathleen R. Braun ◽  
Benjamin P. Van Biber ◽  
...  
Keyword(s):  
Stem Cells ◽  
Extracellular Matrix ◽  
Embryonic Stem Cells ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Extracellular Matrix Production ◽  
Matrix Production

Targeting ER protein TXNDC5 in hepatic stellate cell mitigates liver fibrosis by repressing non-canonical TGFβ signalling

Gut ◽  
2021 ◽  
pp. gutjnl-2021-325065
Author(s):  
Chen-Ting Hung ◽  
Tung-Hung Su ◽  
Yen-Ting Chen ◽  
Yueh-Feng Wu ◽  
You-Tzung Chen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Transforming Growth Factor Β1 ◽  
Duct Ligation ◽  
Extracellular Matrix Production ◽  
Matrix Production

Background and objectivesLiver fibrosis (LF) occurs following chronic liver injuries. Currently, there is no effective therapy for LF. Recently, we identified thioredoxin domain containing 5 (TXNDC5), an ER protein disulfide isomerase (PDI), as a critical mediator of cardiac and lung fibrosis. We aimed to determine if TXNDC5 also contributes to LF and its potential as a therapeutic target for LF.DesignHistological and transcriptome analyses on human cirrhotic livers were performed. Col1a1-GFPTg, Alb-Cre;Rosa26-tdTomato and Tie2-Cre/ERT2;Rosa26-tdTomato mice were used to determine the cell type(s) where TXNDC5 was induced following liver injury. In vitro investigations were conducted in human hepatic stellate cells (HSCs). Col1a2-Cre/ERT2;Txndc5fl/fl (Txndc5cKO) and Alb-Cre;Txndc5fl/fl (Txndc5Hep-cKO) mice were generated to delete TXNDC5 in HSCs and hepatocytes, respectively. Carbon tetrachloride treatment and bile duct ligation surgery were employed to induce liver injury/fibrosis in mice. The extent of LF was quantified using histological, imaging and biochemical analyses.ResultsTXNDC5 was upregulated markedly in human and mouse fibrotic livers, particularly in activated HSC at the fibrotic foci. TXNDC5 was induced by transforming growth factor β1 (TGFβ1) in HSCs and it was both required and sufficient for the activation, proliferation, survival and extracellular matrix production of HSC. Mechanistically, TGFβ1 induces TXNDC5 expression through increased ER stress and ATF6-mediated transcriptional regulation. In addition, TXNDC5 promotes LF by redox-dependent JNK and signal transducer and activator of transcription 3 activation in HSCs through its PDI activity, activating HSCs and making them resistant to apoptosis. HSC-specific deletion of Txndc5 reverted established LF in mice.ConclusionsER protein TXNDC5 promotes LF through redox-dependent HSC activation, proliferation and excessive extracellular matrix production. Targeting TXNDC5, therefore, could be a potential novel therapeutic strategy to ameliorate LF.

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