Fto-modulated lipid niche regulates adult neurogenesis through modulating adenosine metabolism

2020 ◽  
Vol 29 (16) ◽  
pp. 2775-2787
Author(s):  
Hui Gao ◽  
Xuejun Cheng ◽  
Junchen Chen ◽  
Chai Ji ◽  
Hongfeng Guo ◽  
...  

Abstract Adult neurogenesis is regulated by diverse factors including the local environment, i.e. the neurogenic niche. However, whether the lipid in the brain regulates adult neurogenesis and related mechanisms remains largely unknown. In the present study, we found that lipid accumulates in the brain during postnatal neuronal development. Conditional knockout of Fto (cKO) in lipid not only reduced the level of lipid in the brain but also impaired the learning and memory of mice. In addition, Fto deficiency in lipid did not affect the proliferation of adult neural stem cells (aNSCs), but it did inhibit adult neurogenesis by inducing cell apoptosis. Mechanistically, specific deleting Fto in lipid altered gene expression and increased adenosine secretion of adipocytes. The treatment of adenosine promoted the apoptosis of newborn neurons. As a whole, these results reveal the important function of the lipid niche and its associated mechanism in regulating adult neurogenesis.

2011 ◽  
Vol 13 (3) ◽  
pp. 215-223 ◽  
Author(s):  
Joonghoon Park ◽  
Liangxue Lai ◽  
Melissa Samuel ◽  
David Wax ◽  
Richard S. Bruno ◽  
...  

2008 ◽  
Vol 72 (9) ◽  
pp. 2281-2340 ◽  
Author(s):  
D. L. Villeneuve ◽  
I. Knoebl ◽  
P. Larkin ◽  
A. L. Miracle ◽  
B. J. Carter ◽  
...  

2010 ◽  
Vol 12 (5) ◽  
pp. 589-597 ◽  
Author(s):  
Joonghoon Park ◽  
Sadie L. Marjani ◽  
Liangxue Lai ◽  
Melissa Samuel ◽  
David Wax ◽  
...  

Author(s):  
W. K. Jones ◽  
J. Robbins

Two myosin heavy chains (MyHC) are expressed in the mammalian heart and are differentially regulated during development. In the mouse, the α-MyHC is expressed constitutively in the atrium. At birth, the β-MyHC is downregulated and replaced by the α-MyHC, which is the sole cardiac MyHC isoform in the adult heart. We have employed transgenic and gene-targeting methodologies to study the regulation of cardiac MyHC gene expression and the functional and developmental consequences of altered α-MyHC expression in the mouse.We previously characterized an α-MyHC promoter capable of driving tissue-specific and developmentally correct expression of a CAT (chloramphenicol acetyltransferase) marker in the mouse. Tissue surveys detected a small amount of CAT activity in the lung (Fig. 1a). The results of in situ hybridization analyses indicated that the pattern of CAT transcript in the adult heart (Fig. 1b, top panel) is the same as that of α-MyHC (Fig. 1b, lower panel). The α-MyHC gene is expressed in a layer of cardiac muscle (pulmonary myocardium) associated with the pulmonary veins (Fig. 1c). These studies extend our understanding of α-MyHC expression and delimit a third cardiac compartment.


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