scholarly journals Inhibition of collagen gel contraction in cardiac fibroblasts by imipramine

2005 ◽  
Vol 18 (5) ◽  
pp. A163-A164
Author(s):  
P LIJNEN ◽  
V PETROV ◽  
R FAGARD
Keyword(s):  
Cardiac Fibroblasts ◽  
Collagen Gel ◽  
Collagen Gel Contraction

scholarly journals Angiotensin II Promotes Integrin-Mediated Collagen Gel Contraction by Adult Rat Cardiac Fibroblasts.

1999 ◽  
Vol 40 (4) ◽  
pp. 461-469 ◽  
Author(s):  
Tatsuya NUNOHIRO ◽  
Naoto ASHIZAWA ◽  
Kristof GRAF ◽  
Willa HSUEH ◽  
Katsusuke YANO
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Fibroblasts ◽  
Collagen Gel ◽  
Adult Rat ◽  
Collagen Gel Contraction

Isotonic Biaxial Loading: An Economic, Versatile Method for the Study of Fibroblast-Populated Collagen Gels

1999 ◽  
Author(s):  
Jeffrey W. Holmes ◽  
Thomas K. Borg
Keyword(s):  
Biaxial Loading ◽  
Cardiac Fibroblasts ◽  
Collagen Gel ◽  
Simple System ◽  
Neonatal Rat ◽  
Collagen Gels ◽  
Maximal Contraction ◽  
Contraction Force ◽  
A Value ◽  
Collagen Gel Contraction

Abstract Studies of collagen gel contraction by embedded fibroblasts have characterized the response of free (unloaded) or isometric (maximally loaded) gels but not the response to intermediate loads. An inexpensive, simple system was devised to isotonically load fibroblast-populated collagen gels using freely hanging weights. This system provided excellent repeatability. Maximal contraction force was estimated at 1 mN per million cells in neonatal rat cardiac fibroblasts, a value that agreed well with reported isometric experiments in fibroblasts from other tissues. The ability to load uniaxially or biaxially and with variable loads will facilitate exploration of the regulation of fibroblast mechanics and biology by stress.

scholarly journals Stimulation of collagen gel contraction by angiotensin II and III in cardiac fibroblasts

2002 ◽  
Vol 3 (3) ◽  
pp. 160-166 ◽  
Author(s):  
Paul Lijnen ◽  
Victor Petrov ◽  
Kandelaria Rumilla ◽  
Robert Fagard
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Fibroblasts ◽  
Collagen Gel ◽  
Collagen Gel Contraction ◽  
Stimulation Of

Abstract 348: Phorbol 12-myristate 13-acetate Induces Dedifferentiation of Cardiac Myofibroblasts to Fibroblasts and Other Unidentified Type of Cells

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Vy Tran Luu ◽  
Sang Phan ◽  
Zhuqiu Jin
Keyword(s):  
Cardiac Fibrosis ◽  
De Novo ◽  
Cardiac Fibroblasts ◽  
Collagen Gel ◽  
Collagen Gel Contraction ◽  
Human Cardiac Fibroblasts ◽  
Multiple Cells ◽  
Tgf Β1 ◽  
Cardiac Myofibroblasts ◽  
Shape And Size

Cardiac fibrosis plays an essential role in cardiac pathogenic processes that occur as a result of myocardial infarction or hypertrophic cardiomyopathy. The differentiation of cardiac fibroblasts to myofibroblasts is considered to be a critical step in the activation and progression of cardiac fibrosis. TGFβ is one of the essential molecules that promote transition of fibroblasts to myofibroblasts. Reversal of formed myofibroblasts to fibroblasts remains incompletely understood. Phorbol 12-Myristate 13-Acetate (PMA) regulates metabolism and functions of multiple cells via PKC activation mostly. To study effects of PMA on differentiation of de novo formed cardiac myofibroblasts, human cardiac fibroblasts were utilized. Human cardiac fibroblasts (HCF) cultured in fibroblast medium (FM)-2 were converted into myofibroblasts in the presence of 2 ng/mL of TGF-β1 for 48 hours. Expression of α-SMA, the biomarker of myofibroblasts, and FSP1, the biomarker of fibroblasts, was detected using Western blot and immunofluorescence. Collagen gel contraction induced by fibroblasts was determined as well. TGF-β1 increased the expression of α-SMA and reduced the expression of FSP1. Distinct cellular morphology changes in the shape and size of HCF were observed after incubation with TGF-β1 for 48 hours. To investigate effect of PMA on dedifferentiation of formed myofibroblasts, these TGF-β1-pretreated cells were divided into four groups for additional 48 hours incubation: PMA groups (10, 50, and 100 ng/mL) or DMSO (vehicle control). Both 50 and 100 ng/mL of PMA reduced the expression of α-SMA but only 100 ng/mL of PMA increased the expression of FSP1. The shape and size of cells changed after treatment with PMA. PMA also reduced TGF-β1-induced collagen gel contraction (P<0.05, compared to DMSO group). These data indicated that PMA can reverse the differentiation of de novo formed human cardiac myofibroblasts induced by TGF-β1 to fibroblasts and other unidentified type of cells. Although the mechanism of dedifferentiation remains to be identified, the novel finding of this study shed light on future development of agents to treat fibrotic diseases.

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