Professor and Paratrooper

Kevin Kit Parker (ENG’89), a U.S. Army paratrooper and a Harvard professor, and his research team have upended the conventional wisdom about the cause of traumatic brain injury. Photo courtesy of Kevin Kit Parker

Kevin Kit Parker doesn’t exactly look or sound like a Harvard professor. Measuring in at 6’5”, he sports a beat-up pair of jeans and speaks in a booming Southern drawl, often peppering his remarks with self-deprecating humor as he describes his path from rural Conyers, Ga., to Cambridge, Mass.

It all began junior year of high school, when a red recruitment brochure from Boston University arrived in the mail. Interested in biology and gadgets from an early age and impressed by the reputation of the College of Engineering’s biomedical engineering department, Parker applied to BU. But when he arrived in Boston a year later, he felt lost.

“It was a big change to be dropped off at 140 Bay State Road,” he recalls. “I had never taken a taxicab before I came up here. Someone at Logan had to take me to the cab stand and show me how to hail a cab.”

Parker (ENG’89) is now Tarr Family Professor of Bioengineering and Applied Physics at Harvard University. He led a research team that in 2011 upended the conventional wisdom about the cause of traumatic brain injury (TBI).

Whether triggered by a collision on a football field in Nebraska or blast waves from an improvised explosive device in Iraq, TBI affects millions of people each year, often resulting in long-term neurological disorders such as Parkinson’s or Alzheimer’s disease. Scientists had maintained that TBI was caused by the puncturing of membranes surrounding nerve cells in the brain, leading to the cells’ eventual breakdown.

Parker and his team showed the real mechanism behind TBI is a class of cell-signaling, cell membrane–crossing proteins called integrins that when disrupted by trauma set off a chain reaction that causes the brain’s neural network to collapse—and in some cases, causes blood vessels in the brain to constrict. The research, published in leading journals in August 2011, could yield new drug therapies that first responders could apply in the immediate aftermath of injury to limit long-term damage.

Parker has more than an academic interest in TBI. In addition to being a researcher, he is also a U.S. Army paratrooper who completed two tours of duty in Afghanistan, and he has seen the effects of TBI on blast victims. Concerned about these soldiers’ future health prospects, he began studying TBI at the behest of a fellow soldier, Colonel Geoffrey Ling, a U.S. Army neurologist specializing in brain trauma. Ling oversees TBI research funding at the Defense Advanced Research Projects Agency (DARPA) of the U.S. Department of Defense.

To better understand the mechanisms behind TBI and investigate potential drug treatments at the cellular level, Parker and his Disease Biophysics Group used tissue engineering techniques to construct a micro-tissue model of the brain’s vascular system out of human blood vessels and rat nerve cells. They then subjected the model to forces strong enough to mimic blast waves known to cause TBI, but weak enough to prevent the cell membranes from tearing apart. Their “concussion-on-a-chip” experiments, which are ongoing, revealed the same kinds of structural changes in neurons and blood vessel cells as those observed in the brains of TBI victims.

“The paradigm for brain injury is that the membrane of the nerve cell gets ripped open and the cell dies,” says Parker. “But the membrane of a neuron is like the skin on a hound dog—it’s floppy and not a good conduit of mechanical energy, so it doesn’t always tear in trauma.”

Parker and his colleagues showed that integrin-mediated cell trauma results in the activation of completely normal signaling pathways within a cell. In other words, the cell, or neuron, can survive the blast.

“If the cell’s still alive, there’s a treatment opportunity,” he maintains. “Our ultimate goal is to identify drug targets and arm the pharmaceutical industry for the long run with a tool set for TBI drug discovery.”

The TBI research is part of a very broad portfolio of projects Parker spearheads. His group’s projects range from creating miniature 3-D human organs-on-chips to developing biodegradable protein “nanofabrics” used to treat wounds to probing the protein networks that enable cuttlefish to camouflage themselves.

Impulsiveness, boldness, and good timing

As a BU freshman, after agonizing over kingdoms and phylums in his introductory biology class, Parker dropped the course. Over the next four years, however, his rocky beginning gave way to feeling at home at BU. He established enduring friendships and a foundation for a multifaceted career as an engineer-educator.

“Academics were definitely not one of the highlights of my career,” he says. Nonetheless, he made it through four years, soaking up the influence of some memorable faculty members, most notably Asim Yildiz, a former ENG aerospace and mechanical engineering professor, who taught thermodynamics. “Even though I was academically a train wreck,” Parker says, “he included me in discussions with graduate students and postdocs and saw promise in me.”

When Yildiz became ill during Parker’s senior year, he would walk to the professor’s house once a week to drink hot tea and work math problems. “He taught me about pursuing science and engineering for the sheer knowledge, not for prestigious awards,” Parker recalls. “I look at his photograph every once in a while to make sure I am on the right track.”

Drawing on his experiences at BU, Parker rose to his current position on the Harvard faculty through a combination of impulsiveness, boldness, and good timing. After graduating from ENG without a plan, he went on a summer road trip with his father, passing through Nashville, Tenn. While his father idled in the hot car outside Vanderbilt University, Parker stopped in to meet the mechanical engineering department chair, convincing him to accept him into the graduate program on a trial basis. He spent the next several years learning such things as the biophysics of hearts and the evaluation of airplane parts—while completing ROTC training and becoming commissioned as an army infantry officer.

After earning an MS in mechanical engineering in 1993 and a PhD in applied physics in 1998, Parker applied for a postdoctoral fellowship in pathology under vascular biology specialist Don Ingber at Boston Children’s Hospital. When he received a rejection letter, Parker immediately wrote back insisting that Ingber’s group accept him and prepare for his arrival. Within a week he received a call from Ingber’s office asking if he was still available.

After working with Ingber for three years and as a postdoc in biomedical engineering at the Johns Hopkins School of Medicine, Parker was offered a faculty position at Harvard in 2001. Then came September 11. He delayed joining the Harvard faculty for a year to serve in the army, completing the first of two tours of duty in Afghanistan.

When Parker received the email message from DARPA early in his tenure at Harvard suggesting that he investigate traumatic brain injury, he quickly recalled Ingber’s focus on integrin signaling and suspected that it might play a key role in TBI.

“I called DARPA back and said, ‘I think I’ve got an angle,’” Parker says. “I then went to Starbucks with an undergraduate student and sketched my hypothesis on a napkin. It took several years to prove, but we nailed it. I should have bought a lottery ticket that day.”

Mark Dwortzan can be reached at dwortzan@bu.edu.

A version of this article was originally published in the fall 2012 ENGineer magazine.