Walter Boron

Last updated
Walter F. Boron
Born(1949-11-18)November 18, 1949
Alma mater Saint Louis University, Washington University in St. Louis
Scientific career
Institutions Case Western Reserve University
Academic advisors Emile L. Boulpaep, Albert Roos

Walter F. Boron (born November 18, 1949) [1] is an American scientist and the 72nd president of the American Physiological Society (from 1999 to 2000). [2] He was Secretary-General of the International Union of Physiological Sciences. [3] Additionally, Boron is co-editor, along with Emile L. Boulpaep, of the textbook Medical Physiology and Concise Medical Physiology. He is a former editor-in-chief of two leading physiology journals, Physiological Reviews and Physiology .

Contents

Education

Boron obtained his AB degree in chemistry, summa cum laude from Saint Louis University in 1971. He then joined the Medical Scientist Training Program at Washington University School of Medicine, where he received his M.D. and Ph.D. degrees in 1977 under the mentorship of Albert Roos. [4] [5] During this time, Boron also collaborated with Paul De Weer and John M. Russell . Boron joined Yale University as a postdoctoral fellow with Emile L. Boulpaep in the Department of Physiology, from 1978 to 1980.

Career

Boron is the David N. and Inez Myers/Antonio Scarpa Professor and Chair of the Department of Physiology and Biophysics at Case Western Reserve University. [6] He is also Professor of Medicine and Professor of Biochemistry. Since 2016, he has been Executive Director of PhD programs at the School of Medicine. He briefly served as Interim Chair of the Department of Biochemistry (from 2017 to 2018). Previously, he was a member of the faculty of Yale University (from 1989-2007), serving three 3-year terms as Chair of the Department of Cellular and Moleculary Physiology from 1989 through 1998.

Boron's lifelong research interest has been pH (acid-base) homeostasis. With his colleagues, he was the first to demonstrate cell-pH regulation, developed the first mathematical model of cell-pH regulation, discovered several sodium-coupled/bicarbonate cotransporters (the NBCs), was the first to clone the DNA encoding an NBC, discovered the sensing of molecular carbon dioxide and bicarbonate, and introduced several paradigms for studying cellular acid-base physiology. His laboratory has elucidated the mechanisms and control of acid-base transport in kidney tubules, and pH regulation in neurons and glial cells from the central nervous system. [7] [8] discovered and cloned several bicarbonate transporters, [9] elucidated the sensing of molecular carbon dioxide and bicarbonate, [10] [2] and introduced several experimental paradigms for studying cellular acid-base physiology. [11] [2]

While studying pH regulation in cells from the stomach, Boron and his colleagues became the first to describe a membrane that does not permit the penetration of carbon dioxide. This result led to the discovery of the first gas channel (a protein channel in a cell membrane that is permeable to a gas), namely aquaporin-1. Boron's group has extended its interest to understanding mechanisms of gas movement through aquaporins, Rh proteins, and other membrane proteins, and the physiological significance of these movements.

Professional awards

Boron was a Searle Scholar from 1981 to 1984. He received the Homer Smith Award from the American Society of Nephrology in 2005, the Sharpey-Schafer Award from The Physiological Society (London) in 2008, and the Palade Gold Medal (shared with William Catterall and Richard Tsien) from Wayne State University in 2010. In 2014, Boron received an honorary doctorate from Aarhus University in Denmark, and was elected to the National Academy of Medicine. He was appointed Distinguished University Professor at Western Reserve University in 2020.

Entrepreneurship

Boron and Marc Pelletier co-founded Aeromics Corporation, which discovered the first high-affinity blocker of an aquaporin water blocker. This drug, which has now passed Phase 1 clinical trials, greatly slows the movement of water into the brain (cerebral edema) in models of stroke in mice and rats, and greatly improves clinical outcome. In addition, Boron, George Farr, and Paul Schlather founded Remsenwood Associates, an umbrella company that has created JanusQ, LLC.

Books

Related Research Articles

<span class="mw-page-title-main">Pacemaker potential</span>

In the pacemaking cells of the heart (e.g., the sinoatrial node), the pacemaker potential (also called the pacemaker current) is the slow, positive increase in voltage across the cell's membrane (the membrane potential) that occurs between the end of one action potential and the beginning of the next action potential. This increase in membrane potential is what causes the cell membrane, which typically maintains a resting membrane potential around -65 mV, to reach the threshold potential and consequently fire the next action potential; thus, the pacemaker potential is what drives the self-generated rhythmic firing (automaticity) of pacemaker cells, and the rate of change (i.e., the slope) of the pacemaker potential is what determines the timing of the next action potential and thus the intrinsic firing rate of the cell. In a healthy sinoatrial node (SAN, a complex tissue within the right atrium containing pacemaker cells that normally determine the intrinsic firing rate for the entire heart), the pacemaker potential is the main determinant of the heart rate. Because the pacemaker potential represents the non-contracting time between heart beats (diastole), it is also called the diastolic depolarization. The amount of net inward current required to move the cell membrane potential during the pacemaker phase is extremely small, in the order of few pAs, but this net flux arises from time to time changing contribution of several currents that flow with different voltage and time dependence. Evidence in support of the active presence of K+, Ca2+, Na+ channels and Na+/K+ exchanger during the pacemaker phase have been variously reported in the literature, but several indications point to the “funny”(If) current as one of the most important.(see funny current). There is now substantial evidence that also sarcoplasmic reticulum (SR) Ca2+-transients participate to the generation of the diastolic depolarization via a process involving the Na–Ca exchanger.

<span class="mw-page-title-main">Porosome</span> Structure in eukaryotic cell membrane

Porosomes are cup-shaped supramolecular structures in the cell membranes of eukaryotic cells where secretory vesicles transiently dock in the process of vesicle fusion and secretion. The transient fusion of secretory vesicle membrane at a porosome, base via SNARE proteins, results in the formation of a fusion pore or continuity for the release of intravesicular contents from the cell. After secretion is complete, the fusion pore temporarily formed at the base of the porosome is sealed. Porosomes are few nanometers in size and contain many different types of protein, especially chloride and calcium channels, actin, and SNARE proteins that mediate the docking and fusion of the vesicles with the cell membrane. Once the vesicles have docked with the SNARE proteins, they swell, which increases their internal pressure. They then transiently fuse at the base of the porosome, and these pressurized contents are ejected from the cell. Examination of cells following secretion using electron microscopy, demonstrate increased presence of partially empty vesicles following secretion. This suggested that during the secretory process, only a portion of the vesicular contents are able to exit the cell. This could only be possible if the vesicle were to temporarily establish continuity with the cell plasma membrane, expel a portion of its contents, then detach, reseal, and withdraw into the cytosol (endocytose). In this way, the secretory vesicle could be reused for subsequent rounds of exo-endocytosis, until completely empty of its contents.

References

  1. Walter Boron Curriculum Vitae
  2. 1 2 3 "Walter F. Boron". Presidents. American Physiological Society. Retrieved 23 March 2015. 72nd APS President (1999-2000)
  3. IUPS Council
  4. The American Physiological Society
  5. University, Wayne State (19 September 2017). "Walter F. Boron M.D., Ph.D. - Physiology - Wayne State University". physiology.med.wayne.edu. Retrieved 2018-03-31.
  6. Department of Physiology and Biophysics, Case Western Reserve University
  7. Russell, John M.; Boron, Walter F. (1976). "Role of chloride transport in regulation of intracellular pH". Nature. 264 (5581): 73–4. Bibcode:1976Natur.264...73R. doi:10.1038/264073a0. PMID   12472. S2CID   4275104.
  8. Thomas, RC (September 1984). "Experimental displacement of intracellular pH and the mechanism of its subsequent recovery". The Journal of Physiology. 354 (Suppl): 3P–22P. doi:10.1113/jphysiol.1984.sp015397. PMC   1193568 . PMID   6434728.
  9. Aalkjaer, C; Boedtkjer, E; Choi, I; Lee, S (October 2014). "Cation-coupled bicarbonate transporters". Comprehensive Physiology. 4 (4): 1605–37. doi:10.1002/cphy.c130005. PMC   4768804 . PMID   25428855.
  10. Boron, Walter F.; De Weer, Paul (1976). "Active proton transport stimulated by CO2/HCO3−, blocked by cyanide". Nature. 259 (5540): 240–1. Bibcode:1976Natur.259..240B. doi:10.1038/259240a0. PMID   2874. S2CID   4276509.
  11. Boron, Walter F. (2006). "Acid-Base Transport by the Renal Proximal Tubule". Journal of the American Society of Nephrology. 17 (9): 2368–82. doi: 10.1681/ASN.2006060620 . PMID   16914536.

Further reading