Temat: ROCK1 - Katalog OPAC zbiorów

Skocz do pozycji: 1.

Tytuł:: Dexamethasone inhibits U937 cell adhesion via the down-regulation of ROCK1 activity
Autorzy:: Liu, Dong
Chen, Xing
Xiong, Ren
Ning, Ya
Li, Ping
Peng, Yan
Liu, Ping
Zhao, Yan
Yang, Nan
Zhou, Yuan
Powiązania:: https://bibliotekanauki.pl/articles/1039650.pdf
Data publikacji:: 2012
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: dexamethasone
ROCK1
fasudil
non-genomic effects
Opis:: Objective. To explore the effect of dexamethasone (DEX) on monocyte adhesion function and its underlying mechanism. Methods. The effects of DEX and fasudil on adhesion of cultured U937 monocytes to human umbilical vein endothelial cells (HUVEC) following stimulation with phorbol myristate acetate (PMA) were studied; Changes in the Rho-associated coiled-coil protein kinase 1 (ROCK1) protein content and activity were evaluated. Results. DEX and fasudil significantly inhibited U937 cell adhesion rates under PMA stimulation and inhibited ROCK1 activity. Mifepristone (RU-486) and cycloheximide (CHX) did not alter these effects of DEX. Conclusions. DEX interferes with the adhesion function of U937 cells through the inhibition of ROCK1 activity.
Źródło:: Acta Biochimica Polonica; 2012, 59, 4; 557-560
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 2.

Tytuł:: Crosstalk between the TGF-β and WNT signalling pathways during cardiac fibrogenesis
Autorzy:: Działo, Edyta
Tkacz, Karolina
Błyszczuk, Przemysław
Powiązania:: https://bibliotekanauki.pl/articles/1038355.pdf
Data publikacji:: 2018
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: TGF-beta
Smad
WNT
beta-catenin
RhoA-ROCK
p38
JNK
Erk1/2
MAPK
cardiac fibrosis
tissue remodelling
cardiac fibroblasts
heart
Opis:: Cardiac fibrosis is referred to as an excessive accumulation of stromal cells and extracellular matrix proteins in the myocardium. Progressive fibrosis causes stiffening of the cardiac tissue and affects conduction of electrical impulses, leading to heart failures in a broad range of cardiac conditions. At the cellular level, activation of the cardiac stromal cells and myofibroblast formation are considered as hallmarks of fibrogenesis. At the molecular level, transforming growth factor β (TGF-β) is traditionally considered as a master regulator of the profibrotic processes. More recently, the WNT signalling pathway has also been found to be implicated in the development of myocardial fibrosis. In this review, we summarize current knowledge on the involvement of TGF-β and WNT downstream molecular pathways to cardiac fibrogenesis and describe a crosstalk between these two profibrotic pathways. TGF-β and WNT ligands bind to different receptors and trigger various outputs. However, a growing body of evidence points to cross-regulation between these two pathways. It has been recognized that in cardiac pathologies TGF-β activates WNT/β-catenin signalling, which in turn stabilizes the TGF-β/Smad response. Furthermore both, the non-canonical TGF-β and non-canonical WNT signalling pathways, activate the same mitogen-activated protein kinases (MAPKs): the extracellular signal-regulated kinase (Erk), the c-Jun N-terminal kinases (JNKs) and p38. The crosstalk between TGF-β and WNT pathways seems to play an essential role in switching on the genetic machinery initiating profibrotic changes in the heart. Better understanding of these mechanisms will open new opportunities for development of targeted therapeutic approaches against cardiac fibrosis in the future.
Źródło:: Acta Biochimica Polonica; 2018, 65, 3; 341-349
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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