The patent badge is an abbreviated version of the USPTO patent document. The patent badge does contain a link to the full patent document.

The patent badge is an abbreviated version of the USPTO patent document. The patent badge covers the following: Patent number, Date patent was issued, Date patent was filed, Title of the patent, Applicant, Inventor, Assignee, Attorney firm, Primary examiner, Assistant examiner, CPCs, and Abstract. The patent badge does contain a link to the full patent document (in Adobe Acrobat format, aka pdf). To download or print any patent click here.

Date of Patent:
Aug. 16, 2022

Filed:

Oct. 24, 2019
Applicant:

American University, Washington, DC (US);

Inventor:

John R. Bracht, Washington, DC (US);

Assignee:

American University, Washington, DC (US);

Attorney:
Primary Examiner:
Assistant Examiner:
Int. Cl.
CPC ...
A61K 38/17 (2006.01); A61K 38/18 (2006.01); C07K 14/475 (2006.01); C07K 14/47 (2006.01); C12N 5/077 (2010.01); A61K 38/00 (2006.01);
U.S. Cl.
CPC ...
C07K 14/473 (2013.01); C12N 5/0653 (2013.01); A61K 38/00 (2013.01); C12N 2501/13 (2013.01); C12N 2506/1384 (2013.01);
Abstract

Here we show that epigenetic control of Neuregulin-1 (NRG1) affects adipose differentiation of stem cells in vitro. Building on this finding, we established a model in which NRG1 is a white adipose tissue (WAT) specific regulator analogous to the role of NRG4 in black adipose tissue (BAT). In this light, NRG1 functions in a paracrine or autocrine manner to regulate formation of new adipocytes from stem populations, both in vitro and in vivo. In neurons, NRG1 has been shown already to play a similar role, promoting neuronal cell differentiation from progenitors in the vertebrate cortex and retina and even promoting neuronal differentiation in vitro. Similarly, in the heart, NRG1 promotes differentiation of cardiomyocytes from their stem cell progenitors both in vivo and in vitro and for this reason has been successfully tested in clinical trials for heart failure. Our model extends these findings to adipose biology and indicates that epigenetic control of NRG1 may constitute an intrinsic mechanism limiting the expansion of WAT depots, potentially elucidating important health implications for the comorbidities of obesity and providing treatment for obesity-related diseases.


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