Melatonin attenuates growth factor receptor signaling required for SARS-CoV-2 replication

2020 ◽  
Vol 3 (4) ◽  
pp. 534-537
Author(s):  
Jan Tesarik

Melatonin has recently been suggested as a non-specific agent to prevent early (asymptomatic or moderate) infections with SARS-CoV-2 virus, the agent responsible for COVID-19, from developing to severe conditions requiring hospitalization. This recommendation was based on the ability of melatonin to suppress excessive inflammatory reactions and to modulate the immune system by attenuating the innate (blind and potentially harmful) response and potentiating the adaptive (selective and helpful) one. Recent data on the molecular mechanism of COVID-19 infection show that growth factor signaling is required for SARS-CoV-2 replication in the infected cells. When confronted with previously published data on the effects of melatonin on epidermal growth factor signaling, these data strongly suggest that melatonin can also act against the virus itself. Taken together, these data represent an additional argument in favor of using melatonin treatment as both a preventive and curative measure against COVID-19.

2005 ◽  
Vol 170 (4) ◽  
pp. 559-570 ◽  
Author(s):  
Laura Alonso ◽  
Hitoshi Okada ◽  
Hilda Amalia Pasolli ◽  
Andrew Wakeham ◽  
Annick Itie You-Ten ◽  
...  

Tyrosine kinase growth factor receptor signaling influences proliferation, survival, and apoptosis. Hair follicles undergo cycles of proliferation and apoptotic regression, offering an excellent paradigm to study how this transition is governed. Several factors are known to affect the hair cycle, but it remains a mystery whether Akt kinases that are downstream of growth factor signaling impact this equilibrium. We now show that an Akt relative, Sgk (serum and glucocorticoid responsive kinase) 3, plays a critical role in this process. Hair follicles of mice lacking Sgk3 fail to mature normally. Proliferation is reduced, apoptosis is increased, and follicles prematurely regress. Maintenance of the pool of transiently amplifying matrix cells is impaired. Intriguingly, loss of Sgk3 resembles the gain of function of epidermal growth factor signaling. Using cultured primary keratinocytes, we find that Sgk3 functions by negatively regulating phosphatidylinositol 3 kinase signaling. Our results reveal a novel and important function for Sgk3 in controlling life and death in the hair follicle.


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