Sorting out noncanonical, paracrine functions of vitamin D. Focus on “Vitamin D receptor activation and downregulation of renin-angiotensin system attenuate morphine-induced T cell apoptosis”

2012 ◽  
Vol 303 (6) ◽  
pp. C592-C594 ◽  
Author(s):  
Ulrich Hopfer
2014 ◽  
Vol 20 (22) ◽  
pp. 5848-5859 ◽  
Author(s):  
Urszula Dougherty ◽  
Reba Mustafi ◽  
Farhana Sadiq ◽  
Anas Almoghrabi ◽  
Devkumar Mustafi ◽  
...  

2017 ◽  
Vol 102 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Nirupama Chandel ◽  
Kamesh Ayasolla ◽  
Hongxiu Wen ◽  
Xiqian Lan ◽  
Shabirul Haque ◽  
...  

2010 ◽  
Vol 21 (6) ◽  
pp. 966-973 ◽  
Author(s):  
Yan Zhang ◽  
Juan Kong ◽  
Dilip K. Deb ◽  
Anthony Chang ◽  
Yan Chun Li

2012 ◽  
Vol 303 (6) ◽  
pp. C607-C615 ◽  
Author(s):  
Nirupama Chandel ◽  
Bipin Sharma ◽  
Divya Salhan ◽  
Mohammad Husain ◽  
Ashwani Malhotra ◽  
...  

Opiates have been reported to induce T cell loss. We evaluated the role of vitamin D receptor (VDR) and the activation of the renin-angiotensin system (RAS) in morphine-induced T cell loss. Morphine-treated human T cells displayed downregulation of VDR and the activation of the RAS. On the other hand, a VDR agonist (EB1089) enhanced T cell VDR expression both under basal and morphine-stimulated states. Since T cells with silenced VDR displayed the activation of the RAS, whereas activation of the VDR was associated with downregulation of the RAS, it appears that morphine-induced T cell RAS activation was dependent on the VDR status. Morphine enhanced reactive oxygen species (ROS) generation in a dose-dependent manner. Naltrexone (an opiate receptor antagonist) inhibited morphine-induced ROS generation and thus, suggested the role of opiate receptors in T cell ROS generation. The activation of VDR as well as blockade of ANG II (by losartan, an AT1 receptor blocker) also inhibited morphine-induced T cell ROS generation. Morphine not only induced double-strand breaks (DSBs) in T cells but also attenuated DNA repair response, whereas activation of VDR not only inhibited morphine-induced DSBs but also enhanced DNA repair. Morphine promoted T cell apoptosis; however, this effect of morphine was inhibited by blockade of opiate receptors, activation of the VDR, and blockade of the RAS. These findings indicate that morphine-induced T cell apoptosis is mediated through ROS generation in response to morphine-induced downregulation of VDR and associated activation of the RAS.


2013 ◽  
Vol 144 (5) ◽  
pp. S-294 ◽  
Author(s):  
Reba Mustafi ◽  
Urszula Dougherty ◽  
Farhana Sadiq ◽  
Ajaypal Singh ◽  
Sharad Khare ◽  
...  

2012 ◽  
Vol 8 (1) ◽  
pp. 251-261 ◽  
Author(s):  
Shabina Rehman ◽  
Nirupama Chandel ◽  
Divya Salhan ◽  
Partab Rai ◽  
Bipin Sharma ◽  
...  

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