Differential Modulation of Normal and Scleroderma Fibroblast Proliferation Matrix Biosynthesis by Endothelins

1997 ◽  
Vol 92 (s36) ◽  
pp. 1P-2P
Author(s):  
X Shi-Wen ◽  
CP Denton ◽  
MR Dashwood ◽  
DJ Abraham ◽  
CM Black
Keyword(s):  
Fibroblast Proliferation ◽  
Differential Modulation ◽  
Scleroderma Fibroblast

Effect of Asbestos on Fibroblast Proliferation of Rat

1996 ◽  
Vol 8 (3) ◽  
pp. 392
Author(s):  
Kyoung Ah Kim ◽  
Dong Won Lee ◽  
Young Lim ◽  
Im Goung Yun
Keyword(s):  
Fibroblast Proliferation

Apigenin Alleviates Renal Fibroblast Activation through AMPK and ERK Signaling Pathways In Vitro

2020 ◽  
Vol 21 (11) ◽  
pp. 1107-1118
Author(s):  
Ningning Li ◽  
Zhan Wang ◽  
Tao Sun ◽  
Yanfei Lei ◽  
Xianghua Liu ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Therapeutic Potential ◽  
Protective Role ◽  
Fibroblast Proliferation ◽  
Fibroblast Activation ◽  
And Function ◽  
Activated Fibroblasts ◽  
Tgf Β1

Objective: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. Materials and Methods: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 μM), followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts was assessed. As a consequence, apigenin alleviated fibroblast proliferation and fibroblastmyofibroblast differentiation induced by TGF-β1. Result: Notably, apigenin significantly inhibited the fibrosis-associated genes expression in renal fibroblasts. Moreover, apigenin treatment significantly increased the phosphorylation of AMP-activated protein kinase (AMPK). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation of ERK1/2 but not Smad2/3, p38 and JNK MAPK in renal fibroblasts. Conclusion: In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation, differentiation and function by AMPK activation and reduced ERK1/2 phosphorylation, suggesting it could be an attractive therapeutic potential for the treatment of renal fibrosis.

Overexpression of miR-340-5p Inhibits Skin Fibroblast Proliferation by Targeting Kruppel-like Factor 2

2019 ◽  
Vol 20 (13) ◽  
pp. 1147-1154 ◽  
Author(s):  
Ling Chen ◽  
Qian Li ◽  
Xun Lu ◽  
Xiaohua Dong ◽  
Jingyun Li
Keyword(s):  
Gene Ontology ◽  
Skin Fibroblast ◽  
Kegg Pathway ◽  
Normal Skin ◽  
Skin Fibroblasts ◽  
Differentially Expressed ◽  
Luciferase Reporter ◽  
Fibroblast Proliferation ◽  
Pathway Analyses ◽  
Normal Skin Fibroblast

<P>Objective: MicroRNA (miR)-340-5p has been identified to play a key role in several cancers. However, the function of miR-340-5p in skin fibroblasts remains largely unknown. </P><P> Methods: Gain of function experiments were performed by infecting normal skin fibroblast cells with a lentivirus carrying 22-bp miR-340-5p. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. To uncover the mechanisms, mRNA-seq was used. Differentially expressed mRNAs were further determined by Gene Ontology and KEGG pathway analyses. The protein levels were analysed by Western blotting. A dual-luciferase reporter assay was used to detect the direct binding of miR-340-5p with the 3&#039;UTR of Kruppel-like factor 2 (KLF2). </P><P> Results: MiR-340-5p lentivirus infection suppressed normal skin fibroblast proliferation. The mRNAseq data revealed that 41 mRNAs were differentially expressed, including 22 upregulated and 19 downregulated transcripts in the miR-340-5p overexpression group compared with those in the control group. Gene Ontology and KEGG pathway analyses revealed that miR-340-5p overexpression correlated with the macromolecule biosynthetic process, cellular macromolecule biosynthetic process, membrane, and MAPK signalling pathway. Bioinformatics analysis and luciferase reporter assays showed that miR-340-5p binds to the 3&#039;UTR of KLF2. Forced expression of miR-340-5p decreased the expression of KLF2 in normal skin fibroblasts. Overexpression of KLF2 restored skin fibroblast proliferation in the miR-340-5p overexpression group. </P><P> Conclusion: This study demonstrates that miR-340-5p may suppress skin fibroblast proliferation, possibly through targeting KLF2. These findings could help us understand the function of miR-340-5p in skin fibroblasts. miR-340-5p could be a therapeutic target for preventing scarring.</P>

scholarly journals The effect of platelet-rich fibrin on normal dermal fibroblast proliferation after mitomycin-c treatment: An in vitro study

2021 ◽  
Vol 62 ◽  
pp. 473-476
Author(s):  
Ishandono Dachlan ◽  
Hendy Satrya Kurniawan ◽  
Aditya Wicaksana ◽  
Aditya Rifqi Fauzi ◽  
Firdian Makrufardi ◽  
...  
Keyword(s):  
Mitomycin C ◽  
Dermal Fibroblast ◽  
In Vitro Study ◽  
Vitro Study ◽  
Fibroblast Proliferation ◽  
Platelet Rich Fibrin
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