Sentence examples for transition of fibroblasts from inspiring English sources

Validation of the developed model showed similarity to etiology and pathophysiology of in vivo hypertrophic scar with respect to several features: 1) transition of fibroblasts to myofibroblasts with convincing expression of α-SMA stress fibers; 2) contraction; 3) excessive collagen and fibronectin secretion; 4) expression of fibrotic ECM proteins (SPARC and Tenascin); 5) low MMP secretion.

HIMF has been shown to play a key role in the transition of fibroblasts to myofibroblasts in experimentally-induced pulmonary fibrosis [8].

TGF-β induces HGF expression by fibroblasts [47] but also induces the transition of fibroblasts to myofibroblasts by increasing α-SMA and Tn-C expression [48].

Liu et al. [8] has shown that HIMF plays a key role in the transition of fibroblasts to myofibroblasts, which is essential to bleomycin-induced fibrosis and may play a role in vascular remodeling associated with PH.

Other studies demonstrate that PGE2 inhibits transition of fibroblasts to myofibroblasts by an EP2 receptor-activated pathway [ 21].

It has been reported that PGE2 inhibits TGFβ1-induced transition of fibroblasts to myofibroblasts by increasing cAMP levels via EP2 receptor [ 21].

This report demonstrates two novel aspects of the TGFβ1 signalling cascade, namely the generation of ROS due to a biphasic NAD(P H oxidase activity and a ROS-dependent downstream activation of p38 leading to a transition of dermal fibroblasts to MFs that can be inhibited by the selective NAD(P H oxidase inhibitor apocynin.

RA synovial fluid stimulated this so-called epithelial-mesenchymal transition of normal fibroblast-like synoviocytes, an effect that could be inhibited in vitro by BMP7.

Similar findings were described in the transition of human lung fibroblasts to myofibroblasts [ 12].

To evaluate the transition of PTECs to fibroblasts, we used HK-2 cells cultured in supplement-free fresh media in the presence or absence of various treatments.

Abdul-Hafez et al. demonstrated that the transition of normal lung fibroblasts to myofibroblasts by TGF-β1 in vitro is accompanied by robust expression of angiotensin mRNA, protein, and AngII peptide [ 56].