scholarly journals FGF-2– and TGF-β1–Induced Downregulation of Lumican and Keratocan in Activated Corneal Keratocytes by JNK Signaling Pathway

2011 ◽  
Vol 52 (12) ◽  
pp. 8957 ◽  
Author(s):  
Jian Chen ◽  
Julie Wong-Chong ◽  
Nirmala SundarRaj
Keyword(s):  
Signaling Pathway ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway ◽  
Corneal Keratocytes ◽  
Tgf Β1

scholarly journals Role of the ROS-JNK Signaling Pathway in Hypoxia-Induced Atrial Fibrotic Responses in HL-1 Cardiomyocytes

2021 ◽  
Vol 22 (6) ◽  
pp. 3249
Author(s):  
Chin-Feng Tsai ◽  
Shun-Fa Yang ◽  
Chien-Hsien Lo ◽  
Hsiao-Ju Chu ◽  
Kwo-Chang Ueng
Keyword(s):  
Atrial Fibrillation ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Nuclear Translocation ◽  
Dominant Negative ◽  
Jnk Signaling ◽  
Marker Proteins ◽  
Jnk Signaling Pathway ◽  
Pre Treatment ◽  
Tgf Β1

By promoting atrial structural remodeling, atrial hypoxia contributes to the development of the atrial fibrillation substrate. Our study aimed to investigate the modulatory effect of hypoxia on profibrotic activity in cultured HL-1 cardiomyocytes and explore the possible signaling transduction mechanisms of profibrotic activity in vitro. Hypoxia (1% O2) significantly and time-dependently increased the expression of hypoxia-inducible factor (HIF)-1α and fibrotic marker proteins collagen I and III (COL1A and COL3A), transforming growth factor (TGF)-β1 and α-smooth muscle actin (SMA). Western blot or immunohistochemistry analysis showed that hypoxia-induced increase in COL1A and COL3A was significantly attenuated by the addition of SP600125 (a specific c-Jun N-terminal kinase [JNK] inhibitor) or expression of dominant-negative JNK before hypoxia treatment. The inhibition of hypoxia-activated phosphorylation of JNK signal components (JNK, MKK4, nuclear c-Jun and ATF-2) by pre-treatment with SP600125 could suppress hypoxia-stimulated HIF-1α upregulation and fibrotic marker proteins expression. Hypoxia significantly increased reactive oxygen species (ROS) production in cultured HL-1 atrial cells. Pre-treatment with N-acetylcysteine significantly abrogated the expression of nuclear HIF-1α, JNK transduction components and fibrotic marker proteins. Taken together, these findings indicated that the hypoxia-induced atrial profibrotic response occurs mainly via the ROS/JNK pathway, its downstream upregulation of HIF-1α and c-Jun/ATF2 phosphorylation and nuclear translocation to up-regulate the expression of fibrosis-related proteins (COL1A, COL3A, TGF-β1 and α-SMA). Our result suggests that suppression of ROS/JNK signaling pathway is a critical mechanism for developing a novel therapeutic strategy against atrial fibrillation.

scholarly journals Transactivation of Naturally Occurring HIV-1 Long Terminal Repeats by the JNK Signaling Pathway

2000 ◽  
Vol 275 (27) ◽  
pp. 20382-20390 ◽  
Author(s):  
Peifeng Chen ◽  
Egbert Flory ◽  
Andris Avots ◽  
Bruce W. M. Jordan ◽  
Frank Kirchhoff ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Long Terminal Repeats ◽  
Jnk Signaling ◽  
Naturally Occurring ◽  
Jnk Signaling Pathway ◽  
Terminal Repeats ◽  
Hiv 1
Sign in / Sign up

Export Citation Format

Share Document