University of Missouri School of Medicine MU Health School of Medicine
News Divider
Parrish
University of Missouri researchers led by Alan Parrish, PhD, have found a cellular signal that causes kidney cells to die, making the kidneys prone to injury. This finding could lead to improved kidney function in the elderly.


Age-related self-destruction of cells makes kidney prone to injury


Researchers identify how the kidney cells’ self-destruct messages are spread, a finding that may lead to improved kidney function in the elderly

As advances in medicine allow individuals to live longer, people are facing unique age-related health challenges. As they age, organs such as the kidneys become more susceptible to injury, and their ability to self-repair is decreased. Researchers from the University of Missouri have found a cellular signal that causes kidney cells to die, making the kidneys prone to injury. This finding could lead to improved kidney function in the elderly.

“The kidney is a remarkable organ,” said Alan Parrish, PhD, associate professor of medical pharmacology and physiology at the MU School of Medicine and co-author of the study. “If it is injured, it has a pronounced ability to repair itself. But as we age, many individuals have a reduced production of a protein known as alpha (E)-catenin. When this protein isn’t produced, cells inside the kidney undergo an abnormal type of cellular suicide known as apoptosis. This causes kidney cells to die in excess numbers, putting the organ at risk for acute kidney injuries.”

Catenin proteins serve a number of functions in the cell, such as maintaining the cell’s shape. The proteins also regulate how quickly cells multiply. When the protein is lost, cells grow more quickly, leading to an increased production of kidney cells. A signal in the cell is then activated for these extra cells to be destroyed, causing unregulated apoptosis. When too many of these cells self-destruct, kidney function can be compromised.

“Apoptosis is vital to the health of organs, because it kills cells that are no longer needed or that pose a threat to the organism,” Parrish said. “But when this self-destruct sequence is activated due to a lack of alpha (E)-catenin, healthy cells end up being destroyed. We don’t know why the aging body doesn’t produce enough of this protein. However, we’ve found how this self-destruct message is being communicated.”

By identifying how the self-destruct message is being received, the researchers are hopeful that they can find a way to interrupt this message and ultimately improve the health and function of the kidney.

“Now that we have identified this communication pathway, how do we manipulate this pathway to protect the kidney?” Parrish said. “We know that as we age we’re losing alpha (E)-catenin, so we hope to find out how we can either prevent that loss or substitute for its function. That’s what we will study next.”

In addition to Parrish, the research team includes Xinhui Wang, graduate student in the MU Department of Medical Pharmacology and Physiology. The study, “Loss of α(E)-catenin Promotes Fas Mediated Apoptosis in Tubular Epithelial Cells,” recently was published in Apoptosis, an international peer-reviewed journal devoted to the publication of innovative basic and clinically oriented investigations into programmed cell death. The research is funded by the National Institute of Aging of the National Institutes of Health (RO1AG034154).

Click here to download a high-resolution portrait of Parrish.

Posted July 7, 2015



News and Events

Parrish Age-related self-destruction of cells makes kidney prone to injury
Researchers identify how the kidney cells’ self-destruct messages are spread

Staveley-O'Carroll Staveley-O’Carroll Named Surgery Chair, Cancer Center Director
Staveley-O’Carroll is accomplished physician-scientist

Mini Med High School Students get Hands-On Medical School Experience
MU School of Medicine hosts High School Mini Medical School

Cristo Rey MU Health System Partnership Promotes Diversity
Annual summit encourages students to try on health care careers

Hwang Key Component in Protein that Causes Cystic Fibrosis Identified
Findings may lay foundation for the development of medications

SOM Graduation 2015 MU School of Medicine to Award 101 Medical Degrees at Commencement
Forty-five will remain in Missouri for specialty training in residency

George Kracke Potential New Painkiller Provides Longer Lasting Effects
Early studies show promise for alternative type of anesthetic

Durante Enzyme Responsible for Obesity-Related Hypertension Identified
Discovery may lead to new treatment options for arterial disease caused by obesity

Family Medicine AAFP Award MU Family Medicine Ranked Among Nation’s Best by AAFP
Medical school in top 10 for helping build family physician workforce

Legacy Teachers Medical Students Thank Legacy Teachers
MU’s unique program celebrates patients’ role in teaching future physicians




Media Relations
University of Missouri Health System
One Hospital Drive, DC028.00
Columbia, MO 65212
24/7 on-call pager: (573) 876-0708

Mary Jenkins
jenkinsmg@health.missouri.edu
(573) 882-7299

Jeff Hoelscher
hoelscherj@health.missouri.edu
(573) 884-1608

Derek Thompson
thompsonder@health.missouri.edu
(573) 882-3323

Justin Kelley (Photographer)
kelleyju@health.missouri.edu
(573) 882-5786
Pager (573) 397-9289


Web Communications
University of Missouri Health System
One Hospital Drive, MA204G, DC018.00
Columbia, MO 65212
(573) 884-0298

Rich Gleba
glebar@health.missouri.edu
(573) 884-0298

Laura Gerding, APR
gerdingla@health.missouri.edu
(573) 882-9193

Velvet Hasner
hasnerv@health.missouri.edu
(573) 884-1115



Printer Friendly
Follow us on Twitter!   Facebook   YouTube Videos   Instagram   Pinterest  
Website created and maintained by the Office of Communications. Contact the MU School of Medicine.
Revised: July 07, 2015 - Copyright © 2014 - Curators of the University of Missouri. All rights reserved. DMCA and other copyright information. An equal opportunity/access/affirmative action/pro-disabled and veteran employer.