Coronavirus (COVID-19) updates for UC San Diego Health patients and visitors. Learn More

Menu
Search

UCSD Researchers Identify Critical Receptor in Liver Regeneration

 

March 29, 2007  |  

In studies in mouse models, researchers at the University of California, San Diego (UCSD) School of Medicine have found that a cellular receptor involved in triggering cell death is also a necessary component of tissue repair and regeneration immediately following liver injury.  This discovery couuld have implications for early intervention or therapy in liver disease such as cirrhosis or hepatitis.

A hepatic stellate cell activated by the p75 Neurotrophin Receptor promotes repair in the liver

In a report to be published in the March 30 issue of the journal Science, Katerina Akassoglou, Ph.D. assistant professor in UCSD’s Department of Pharmacology, and colleagues describe the mechanism by which cells associated with liver damage, called hepatic stellate cells (HSCs), are activated by a cell surface molecule called the p75 neurotrophin receptor (p75NTR) to promote repair in the liver.

“Many therapeutics for liver disease target HSCs in order to kill them, but our study in animal models found that their initial activity could actually be protective,” said Akassoglou.

When chronic liver injury occurs, cells in the liver begin producing collagen and other proteins that lead to the formation of fibrous tissue and scarring.  Akassoglou’s team looked at the molecular-cellular interface to discover how tissues respond to deposition of the fibrous protein, fibrin.  In studies of a mouse model with excessive fibrin deposition in the liver, the researchers found that p75NTR signaling promotes the initial activation of HSC, which stimulates the proliferation of new hepatic cells to replace those that have been damaged. The effects of p75NTR at late stages of HSC activation and liver disease remain to be determined.

“We were intrigued by the increase of p75NTR expression after liver injury and hypothesized that p75NTR might regulate the progression of liver disease,” said Akassoglou.  “By identifying p75NTR as the specific molecular link between HSCs and liver regeneration, p75NTR could provide a new therapeutic target for promoting cell regeneration and repair during chronic liver disease or injury.”

This discovery suggests the importance of sustaining p75 and early HSC activation – for example, in the case of liver transplantation when regeneration of liver cells is critical.

Additional contributors to the paper are first author Melissa A. Passino, Ryan A. Adams and Shoana L. Sikorski of the UCSD Department of Pharmacology.  The research was supported by a grant from the National Institutes of Health/National Institute of Neurological Disorders and Stroke.

# # #

Media Contact:  Debra Kain, 619-543-6163, ddkain@ucsd.edu

 

 


Related Specialties

Liver Center


Media Contact

Share This Article


Related News

7/2/2020
By mapping molecular changes in the genome over time, UC San Diego researchers developed a formula to more accurately compare dog age to human age — a tool that could also help them evaluate how well ...
6/30/2020
UC San Diego School of Medicine researchers report that stool microbiomes of NAFLD patients are distinct enough to potentially be used to accurately predict which persons with NAFLD are at greatest ri ...
6/24/2020
UC San Diego researchers have discovered that a single treatment to inhibit a gene called PTB in mice converts native astrocytes, brain support cells, into neurons that produce the neurotransmitter do ...
6/22/2020
UC San Diego researchers uncovered in mice how IRE1α, a molecule involved in cells’ response to stress, determines whether macrophages promote inflammation in the tumor microenvironment. Inflammation ...



Follow Us