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Dr. Rajaie Namas publishes research on mouse livers

Mouse livers may not sound exciting to some, but Dr. Rajaie Namas, a second-year internal medicine resident at Hurley Medical Center, found them fascinating — at least at the cellular level.

The Grand Blanc resident's latest research findings stemmed from his work with hypoxic hepatocytes in mice — oxygen-starved liver cells as may occur in humans under inflammatory conditions such as ischemia reperfusion and hemorrhagic shock.

Ischemia is restricted blood flow to an area, such as the liver, which can occur after an injury. Reperfusion is the resupply of blood to that area, which itself can cause injury. Hemorrhagic shock is the loss of fluid from circulation as a result of blood loss, such as from a traumatic injury or internal bleeding.

Specifically, Namas and his colleagues were investigating the expression of cell death protein BNIP3 in the mice's hypoxic hepatocytes, as well as the role that HIF-1a plays in the upregulation of BNIP3 in mice with hypoxic stress. BNIP3 is a member of a unique family of death-inducing mitochondrial proteins. HIF-1a is part of the class of hypoxia inducible factors and encodes a protein found in mammalian cells at low oxygen concentrations. It plays an essential role in cellular and systemic responses to hypoxia. Upregulation is an increase in the expression of a gene.

Hypoxic stress increases the formation of the BNIP3 homodimer and decreases the amount of the monomeric form of BNIP3 in primary mouse hepatocytes. In short, this gene plays an important role in liver transplant ischemia and reperfusion, as well as in hemorrhagic shock.

Some day in the future, humans with liver hypoxia may receive a selective treatment developed as a result of these findings.

"Targeting this gene could have a great effect on patients with transplant and in hemorrhagic shock patients in the field," said Namas, adding that it could help in various settings, such as during trauma or elective surgeries.

Namas was recently selected chief resident starting July 1 in Hurley Medical Center's Internal Medicine Residency Training Program.

"What I like in this project and in any project at the molecular level is, as a physician treating patients, that it's great to get ideas from bedside and to go back to bench to try to do your best to treat and heal the people that are in need of your help. What I believe in as a physician is to 'innovate and don't imitate,'" he said.

Namas' paper about the research was published online ahead of print in the peer-reviewed journal Shock in May 2011. The paper, titled Hypoxia-Induced Overexpression of BNIP3 Is Not Dependent on HIF1a  in Mouse Hepatocytes, can be found at http://journals.lww.com/shockjournal/Abstract/publishahead/Hypoxia_Induced_Overexpression_of_BNIP3_Is_Not.99175.aspx.

Hurley Medical Center is a 443-bed premier public teaching hospital in the heart of Genesee County. As the region's only level one trauma center, burn center and the highest-level neonatal intensive care unit available in Genesee County, Hurley is a recognized leader in clinical care and education. It has affiliations with Michigan State University, the UM-Ann Arbor, the UM-Flint, Mott Community College and Henry Ford Health System. Hurley, founded in 1908, provides patient care for more than 100,000 people annually.

(Note: This report is provided as a service to our readers and a service to the group or individual mentioned in the release. Usually, only minor editing is done. The group or individual is responsible for all information provided.)

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