Passionate scientist, breakthrough researcher and GMS faculty member John H. Schwartz, M.D. is now the Director of the renowned M.D./Ph.D. program. Dr. Schwartz’ enthusiasm for science has propelled him through a prolific career in the medical sciences field – with Boston University (BU) at its center. From his undergraduate degree in biology to his current position at GMS as a professor of medicine and member of the renal section at Boston University School of Medicine (BUSM), Dr. Schwartz has long been actively involved in the promotion of programs for his fellow scientists and students at BU. Now, as newly appointed Director of the M.D./Ph.D. program, Dr. Schwartz applies this same energy, continually striving to make the program more robust and enriching.
The M.D./Ph.D. program was already significantly strengthened in 2008 when GMS committed itself to providing M.D./Ph.D. students with full funding. This new standard for financial support, which continues to this day, ensures students complete tuition remission as well as stipends for living expenses during their graduate study years. As Director, Dr. Schwartz also works to make it possible for M.D./Ph.D. students to participate in special meetings, seminars and a retreat as well as in national conferences that focus on physician scientist training. To allow for these types of activities and to increase selectivity, the number of students supported in the M.D./Ph.D. program has been reduced to eight per year.
By training scientists in the M.D./Ph.D. program and acting as program Director, Dr. Schwartz aims to nurture and mold leaders in biomedical research and clinical practice. He maintains the philosophy that the clinical encounter is central in the generation of relevant questions that can be best explored by scientific methodology – and therefore central in producing effective physician-scientists. For this reason, the M.D./Ph.D. program emphasizes a balance between clinical and scientific training.
Dr. Schwartz grew up in Fall River, Ma. As an undergraduate at Boston University, he became interested in basic research and was involved in a National Science Foundation sponsorship program for undergraduates. He went on to earn his M.D. at the New York University School of Medicine and train in the laboratory of Dr. Philip Steinmetz at Harvard Medical School. He also completed a residency in Integral Medicine at the Beth Israel Hospital in Boston and post doctoral fellowship in Nephrology. In 1971, he became a staff member of the renal unit at the Walter Reed Army Institute of Research, eventually acting as chief of the unit from 1973 to 1977. Dr. Schwartz also acts as a mentor to physician scientists at GMS.
Dr. Schwartz has made research contributions (link out) in a number of areas including the cellular regulation of H+ transport in renal epithelia, coupling in excitable cells and pathogenesis of acute renal failure. His research is supported by grants from NIH.
Dr. Schwartz’s Research Activities:
Control Mechanisms of Acid Secretion
Renal inner medullary collecting duct cells transport protons, mediated by an H+-ATPase, and H2O, mediated by aquaporin-2 (AQP2) across their apical membrane. In our cultured line of IMCD cells, as in the kidney both of these processes are controlled by regulated exocytic insertion and endocytic retrieval of vesicles that carry either an H+-ATPase or AQP2 as cargo in their membranes, but not both. The targeting and fusion of these vesicles to the apical membrane may be mediated by SNARE proteins, the same proteins that mediate exocytosis at the synaptic membrane. However, despite the similarity of the postulated targeting-fusion system, exocytosis of H+-ATPase and AQP2 are independently regulated. Our group is evaluating how a polar renal epithelial cell target two distinct cargo-laden vesicles to the apical membrane utilizing similar docking-fusion proteins. We propose the following hypotheses which will be the focus of our current studies: 1) the minimal machinery, the SNAREpin, required for targeting and fusion of H+-ATPase or AQP2 vesicle subtypes to the apical membrane consists of a distinct set of v & t-SNAREs; 2) the cargo proteins (H+-ATPase and AQP2), per se, participate in the regulation, targeting and exocytic insertion of their carrier vesicles and 3) regulated exocytosis of these vesicles is not only initiated but proceeds by different signal cascades that modify (phosphorylate) dissimilar proteins in either the vesicles or target (apical) membrane.
Gene Expression Associated with Acute Renal Injury – Cellular Mechanisms of Injury in Acute Renal Failure
Although ischemia is a common cause of acute renal failure (ARF), the cellular pathogenesis of injury is unknown and no therapeutic interventions presently exist. Recent investigations in Dr. Borkan’s and other laboratories have suggest that the kidney in vivo and cultured cells in vitro respond to ischemia by producing a host of “stress proteins”. These proteins include the heat stress proteins (HSPs), well-known “cell protectants” that may be capable of preventing or ameliorating acute renal failure if increased prior to the insult. Current studies are intended to quantify the protection afforded by HSP 70 by selectively manipulating the content of the wild type hsp70 and several of its well-characterized mutants. This model system is being used to dissect the potential mechanisms by which HSPs protect the cell from ischemic injury. We are presently investigating the interaction between hsp70 and members of the BCL2 family, as well as identifying the events that result in mitochondrial membrane injury, a key step in triggering the apoptotic cascade that results in cell death.