Inhibition of Four- and-a-Half-Lim Domain Protein-2 Decreases Atherosclerosis in APOE -/- Mice Model: Role of Immune T-Cells

2013 ◽  
Vol 29 (10) ◽  
pp. S229-S230
Author(s):  
T. Ebrahimian ◽  
M. Heidari ◽  
C.A. Lemarie ◽  
S. Simeone ◽  
D. Simon ◽  
...  
2014 ◽  
Vol 30 (10) ◽  
pp. S320
Author(s):  
T. Ebrahimian ◽  
D. Simon ◽  
C.A. Lemarié ◽  
S. Simeone ◽  
M. Heidari ◽  
...  

2018 ◽  
Author(s):  
Zihao Liu ◽  
Shunshun Han ◽  
Yan Wang ◽  
Can Cui ◽  
Qing Zhu ◽  
...  

AbstractFour and a half LIM domain protein 2 (FHL2) is a LIM domain protein expressed in muscle tissue whose deletion is causative of myopathies. Although FHL2 has a confirmed important role in muscle development, its autophagy-related function in muscle differentiation has not been fully determined. To explore the role of FHL2 in autophagy-related muscle regulation, FHL2-silenced and -overexpressing C2C12 mouse cells were examined. Immunofluorescence and co-immunoprecipitation assay findings showed that FHL2 silencing reduced LC3-Ⅱ protein expression and the amount of LC3 that co-immunoprecipitated with FHL2, indicating that FHL2 interacts with LC3-Ⅱ in the formation of autophagosomes. Moreover, the expression of muscle development marker genes such as MyoD1 and MyoG was lower in FHL2-silenced C2C12 cells but not in FHL2-overexpressing C2C12 cells. Electron microscopy analysis revealed large empty autophagosomes in FHL2-silenced myoblasts, while flow cytometry suggested that FHL2 silencing made cells more vulnerable to staurosporine-induced cell death. In conclusion, we propose that FHL2 interacts with LC3-Ⅱ in autophagosome formation to regulate the development of muscle cells.


2020 ◽  
Vol 528 (11) ◽  
pp. 1820-1832 ◽  
Author(s):  
Hugo Ríos ◽  
Alejandra R. Paganelli ◽  
Nicolás S. Fosser

2009 ◽  
Vol 40 (01) ◽  
Author(s):  
J Schessl ◽  
Y Zou ◽  
MJ McGrath ◽  
BS Cowling ◽  
B Maiti ◽  
...  

Metabolism ◽  
2021 ◽  
pp. 154815
Author(s):  
Maria P. Clemente-Olivo ◽  
Jayron J. Habibe ◽  
Mariska Vos ◽  
Roelof Ottenhoff ◽  
Aldo Jongejan ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tannaz Norizadeh Abbariki ◽  
Zita Gonda ◽  
Denise Kemler ◽  
Pavel Urbanek ◽  
Tabea Wagner ◽  
...  

AbstractThe process of myogenesis which operates during skeletal muscle regeneration involves the activation of muscle stem cells, the so-called satellite cells. These then give rise to proliferating progenitors, the myoblasts which subsequently exit the cell cycle and differentiate into committed precursors, the myocytes. Ultimately, the fusion of myocytes leads to myofiber formation. Here we reveal a role for the transcriptional co-regulator nTRIP6, the nuclear isoform of the LIM-domain protein TRIP6, in the temporal control of myogenesis. In an in vitro model of myogenesis, the expression of nTRIP6 is transiently up-regulated at the transition between proliferation and differentiation, whereas that of the cytosolic isoform TRIP6 is not altered. Selectively blocking nTRIP6 function results in accelerated early differentiation followed by deregulated late differentiation and fusion. Thus, the transient increase in nTRIP6 expression appears to prevent premature differentiation. Accordingly, knocking out the Trip6 gene in satellite cells leads to deregulated skeletal muscle regeneration dynamics in the mouse. Thus, dynamic changes in nTRIP6 expression contributes to the temporal control of myogenesis.


Gene ◽  
1998 ◽  
Vol 216 (1) ◽  
pp. 163-170 ◽  
Author(s):  
Simon Ming Yuen Lee ◽  
Stephen Kwok Wing Tsui ◽  
Kwok Keung Chan ◽  
Merce Garcia-Barcelo ◽  
Mary Miu Yee Waye ◽  
...  

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