scholarly journals Receptor-specific increase in extracellular matrix production in mouse mesangial cells by advanced glycosylation end products is mediated via platelet-derived growth factor.

1992 ◽  
Vol 89 (7) ◽  
pp. 2873-2877 ◽  
Author(s):  
T. Doi ◽  
H. Vlassara ◽  
M. Kirstein ◽  
Y. Yamada ◽  
G. E. Striker ◽  
...  
2016 ◽  
Vol 242 (2) ◽  
pp. 160-168 ◽  
Author(s):  
Xue Zhao ◽  
Jun Hao ◽  
Huijun Duan ◽  
Zanhua Rong ◽  
Fan Li

In the present study, the effect and mechanism of periostin on renal proliferation and extracellular matrix accumulation of lupus mice were investigated. MRL /lpr mice, known as lupus mice, were revealed to show enhanced periostin, proliferating cell nuclear antigen (PCNA), and extracellular matrix accumulation in the kidney accompanied by increased serum platelet-derived growth factor (PDGF). Again, cultured mouse mesangial cells (MMCs) were treated with PDGF, then periostin, and PCNA and secreted fibronectin were detected. The results showed that intracellular periostin and PCNA were respectively enhanced by 2.691 and 2.308 times in PDGF-treated MMC cells at 6 h after stimulation. In addition, secreted fibronectin was increased by 1.442 times. Next, the transfection of periostin shRNA vector in PDGF-stimulated MMC cells effectively suppressed periostin, PCNA and secreted fibronectin by 45.27%, 47.75%, and 39.95%, compared with PDGF-stimulated cells transfected with control vector. Furthermore, it was found that PDGF increased the expression of phospho-Akt (Ser 473) from 30 min to 6 h in MMCs. LY294002 effectively inhibited phospho-Akt (Ser 473) expression caused by PDGF stimulation. Then, periostin, PCNA, and fibronectin were respectively decreased by 69.61%, 46.00%, and 46.20%. In the end, phosphoinositide 3-kinase/protein kinase B/periostin was suggested to mediate PDGF-induced cell proliferation and extracellular matrix production in lupus nephritis.


1995 ◽  
Vol 48 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Douglas C. Throckmorton ◽  
Anne P. Brogden ◽  
Brian Min ◽  
Howard Rasmussen ◽  
Michael Kashgarian

2016 ◽  
Vol 49 (2) ◽  
pp. 1501941 ◽  
Author(s):  
Zaneta Sibinska ◽  
Xia Tian ◽  
Martina Korfei ◽  
Baktybek Kojonazarov ◽  
Janina Susanne Kolb ◽  
...  

Interstitial lung fibroblast activation coupled with extracellular matrix production is a pathological signature of idiopathic pulmonary fibrosis (IPF), and is governed by transforming growth factor (TGF)-β/Smad signalling. We sought to define the role of heat shock protein (HSP)90 in profibrotic responses in IPF and to determine the therapeutic effects of HSP90 inhibition in a murine model of pulmonary fibrosis.We investigated the effects of HSP90 inhibition in vitro by applying 17-AAG (17-allylamino-17-demethoxygeldanamycin) to lung fibroblasts and A549 cells and in vivo by administering 17-DMAG (17-dimethylaminoethylamino-17-demethoxygeldanamycin) to mice with bleomycin-induced pulmonary fibrosis.HSP90 expression was increased in (myo)fibroblasts from fibrotic human and mouse lungs compared with controls. 17-AAG inhibited TGF-β1-induced extracellular matrix production and transdifferentiation of lung fibroblasts and epithelial–mesenchymal transition of A549 cells. The antifibrotic effects were associated with TGF-β receptor disruption and inhibition of Smad2/3 activation. Co-immunoprecipitation revealed that HSP90β interacted with TGF-β receptor II and stabilised TGF-β receptors. Furthermore, 17-DMAG improved lung function and decreased fibrosis and matrix metalloproteinase activity in the lungs of bleomycin-challenged mice.In conclusion, this is the first study to demonstrate that HSP90 inhibition blocks pulmonary fibroblast activation and ameliorates bleomycin-induced pulmonary fibrosis in mice.


Nephron ◽  
1996 ◽  
Vol 72 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Soon Bae Kim ◽  
Shin Ae Kang ◽  
Jung Sik Park ◽  
Jung Sang Lee ◽  
Changgi D. Hong

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Na Zhao ◽  
Bo Liu ◽  
Si-Wen Liu ◽  
Wei Zhang ◽  
Hua-Nan Li ◽  
...  

Complementary therapies, such as acupuncture and massage, had been previously reported to have therapeutic effects on skeletal muscle contusions. However, the recovery mechanisms on skeletal muscles after blunt trauma via the combination of electroacupuncture (EA) and massage therapy remain unclear. In the present study, a rat model of the skeletal muscle fibrosis following blunt trauma to rat skeletal muscle was established, and the potential molecular mechanisms of EA + massage therapy on the skeletal muscle fibrosis were investigated. The results suggested that EA + massage therapy could significantly decrease inflammatory cells infiltration and collagenous fiber content and ameliorate the disarrangement of sarcomeres within myofibrils compared to the model group. Further analysis revealed that EA + massage therapy could reduce the degree of fibrosis and increase the degree of myofibroblast apoptosis by downregulating the mRNA and protein expression of transforming growth factor- (TGF-) β1 and connective tissue growth factor (CTGF). Furthermore, the fibrosis of injured skeletal muscle was inhibited after treatment through the normalization of balance between matrix metalloproteinase- (MMP-) 1 and tissue inhibitor of matrix metalloproteinase (TIMP). These findings suggested that the combination of electroacupuncture and massage therapy could alleviate the fibrotic process by regulating TGF β1-CTGF-induced myofibroblast transdifferentiation and MMP-1/TIMP-1 balance for extracellular matrix production.


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