scholarly journals Phycocyanin Protects Against UVB-induced Apoptosis Through the PKC α/βII-Nrf-2/HO-1 Dependent Pathway in Human Primary Skin Cells

Molecules ◽  
2018 ◽  
Vol 23 (2) ◽  
pp. 478 ◽  
Author(s):  
Ki Mo Kim ◽  
Joo Young Lee ◽  
A-Rang Im ◽  
Sungwook Chae
2019 ◽  
Vol 118 ◽  
pp. 109376
Author(s):  
Abdul Khalid Siraj ◽  
Rafia Begum ◽  
Roxanne Melosantos ◽  
Wafaa Albalawy ◽  
Jehan Abboud ◽  
...  

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masafumi Myoishi ◽  
Testuo Minamino ◽  
Masafumi Kitakaze

Background Endoplasmic reticulum (ER) responds to various stresses by up-regulation of ER chaperones, and prolonged ER stress eventually causes apoptosis. Although apoptosis is considered to be essential for the progression and rupture of atherosclerotic plaques, the influence of ER stress and apoptosis on rupture of unstable coronary plaques remains unclear. Methods and Results We obtained 152 coronary artery segments at autopsy and 40 atherectomy specimens from 71 and 40 patients, respectively . Smooth muscle cells (SMCs) and macrophages in the fibrous caps of thin cap atheroma and ruptured plaques, but not in the fibrous caps of thick cap atheroma and fibrous plaques, showed a marked increase in the expression of ER chaperone and numbers of apoptotic cells. ER chaperones also expressed higher in atherectomy specimens from patients with unstable angina pectoris than with stable angina. To explore the plausible molecular mechanism of activation of ER stress and the mechanistic link to apoptosis, we investigated plaque lipids such as oxysterols. Among oxysterols, expression of 7-ketocholesterol was increased in the fibrous caps of thin cap atheroma compared with thick cap atheroma. Treatment of either cultured coronary artery SMCs or THP-1 cells with 7-ketocholesterol induced upregulation of ER chaperones and apoptosis, while these changes were prevented by antioxidants. We also investigated possible signaling pathways for ER-initiated apoptosis and found that the CHOP (a transcription factor induced by ER stress)-dependent pathway was activated in unstable plaques. In addition, knockdown of CHOP expression by siRNA decreased ER stress-dependent death of cultured coronary artery SMCs and THP-1 cells. Conclusions Increased ER stress occurs in unstable plaques. Our findings suggest that ER stress-induced apoptosis of SMCs and macrophages may contribute to plaque vulnerability.


2019 ◽  
Vol Volume 14 ◽  
pp. 3283-3295 ◽  
Author(s):  
Wan-Li Liang ◽  
Lan Xiao ◽  
Hong-Wei Gu ◽  
Xiao-Jun Li ◽  
Yu-Sang Li ◽  
...  

2010 ◽  
Vol 20 (23) ◽  
pp. 4077-4090 ◽  
Author(s):  
Barbara Geusens ◽  
Mireille Van Gele ◽  
Sien Braat ◽  
Stefaan C. De Smedt ◽  
Marc C. A. Stuart ◽  
...  

Nature ◽  
1995 ◽  
Vol 376 (6541) ◽  
pp. 596-599 ◽  
Author(s):  
Tomohiko Tamura ◽  
Masahiko Ishihara ◽  
Marc S. Lamphier ◽  
Nobuyuki Tanaka ◽  
Isao Oishi ◽  
...  

2010 ◽  
Vol 54 (11) ◽  
pp. 1585-1595 ◽  
Author(s):  
Wen-Wen Huang ◽  
Yu-Jen Chiu ◽  
Ming-Jen Fan ◽  
Hsu-Feng Lu ◽  
Hsiu-Feng Yeh ◽  
...  

2007 ◽  
Vol 31 (9) ◽  
pp. 979-984 ◽  
Author(s):  
E. Ümit Bağrıaçık ◽  
Kadriye Uslu ◽  
Erkan Yurtçu ◽  
Milan Stefek ◽  
Çimen Karasu

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