Biography
Educational History:
Nephrology Training.
1984-1988. Yale University School of Medicine, New Haven, CT. Major field of study: Nephrology. MD Residency.
1978-1982. Pahlavi (currently Shiraz) University School of Medicine, Shiraz, Iran. Major field of study: Internal Medicine. MD.
1978. Pahlavi University School of Medicine, Shiraz, Iran. Major field of study: Medicine.
Employment History:
Professor. 2019-present. Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM.
Staff Nephrologist. 2019-present. Veterans Administration Hospital, Albuquerque, NM. Vice Chair for Research. 2013-2019. Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH.
Director, Division of Nephrology and Hypertension. 2000-2013. University of Cincinnati College of Medicine, Cincinnati, OH.
Professor of Medicine. 1998-2019. University of Cincinnati College of Medicine, Cincinnati, OH.
Director of Research. 1995-2000. Division of Nephrology, University of Cincinnati College of Medicine, Cincinnati, OH.
Associate Professor of Medicine. 1995-1998. University of Cincinnati College of Medicine, Cincinnati, OH.
Staff Nephrologist. 1995-2019. Veterans Administration Hospital, Cincinnati, OH. Associate Professor of Medicine. 1992-1995. Indiana University School of Medicine, Indianapolis, IN.
Staff Nephrologist. 1988-1995. Veterans Administration Hospital, Indianapolis, IN. Associate Professor of Medicine. 1992-1995. Indiana University School of Medicine, Indianapolis, IN.
Assistant Professor of Medicine. 1988-1992. Indiana University School of Medicine, Indianapolis, IN.
Personal Statement
I received my medical degree and residency training at Pahlavi University (currently called Shiraz Medical School) in Shiraz, Iran. Subsequently, I came to the United States in 1984 and started my fellowship in nephrology at Yale University. Since finishing my fellowship in 1988, I have been an assistant and then associate professor at Indiana University and VA Medical Center in Indianapolis (1988-1995), a professor at the University of Cincinnati and VA Medical Center in Cincinnati (1995-2019) and currently a professor at the University of New Mexico and VA Medical Center in Albuquerque NM (2019-present). My scientific dedication to research on kidney disease has remained a continuum for over 37 years.
My research activities over the last 37 years have focused on two main areas. One area is devoted to the characterization and identification of transporters and molecules responsible for electrolyte and acid-base transport and blood pressure control, with the ultimate goal of ascertaining their role in health and disease states. We have cloned 6 novel genes involved in acid base regulation and electrolyte transport in kidney and gastrointestinal tract and have generated 14 genetically engineered mouse models that lack one or 2 genes. My laboratory was instrumental in cloning and characterizing the first mammalian sodium bicarbonate cotransporter (NBC1) in 1997. Another major contribution of my lab was identifying the functional identity of pendrin as a Cl-/HCO3- exchanger (in 2001) and discovering its compensatory role in salt absorption in the absence of the thiazide sensitive sodium chloride cotransporter NCC (2012). My laboratory was the first to identify SLC26A6 (PAT1) as the major apical Cl-/HCO3- exchanger in small intestine (2001). Our recent studies have identified novel mechanisms that are critical to the kidney cystogenesis in Tuberous Sclerosis. Another major area of research in my lab focuses on identifying and characterizing molecules that play a critical role in the pathogenesis of kidney or liver damage in ischemia reperfusion (I/R), septic or toxic injury. We have specifically identified three genes, SSAT (spermidine/spermine N1-acetyltransferase), SMOX (spermine oxidase) and TSP1 (thrombospondin 1) as novel mediators of tissue damage in I/R, endotoxin or toxic injury in kidney, liver or heart. Our research demonstrated that polyamine catabolism (mediated by SSAT and SMOX) and polyamine catabolites play crucial roles in in the mediation of cell and tissue injury in these injury models. We have further shown that SSAT deficiency reduces the severity of organ damage in several models of kidney or liver injury. Overall, 215 peer reviewed articles have been published from my laboratory. We have extensive experience with various experimental methods aimed at examining the mechanisms of kidney cystogenesis in TSC, ascertaining the role of enhanced fructose in salt absorption in the small intestine and kidney tubules, and the pathogenesis of hypertension in metabolic syndrome in rodents.
Original research or scholarly articles in refereed journals (From a total of 226 articles):
NCBI Bibliography available at: https://www.ncbi.nlm.nih.gov/myncbi/1J9O8tsH7Y5AW/bibliography/public/
Areas of Specialty
1. Identification and characterization of SLC26 chloride transporters/exchangers and determination of their roles in gastrointestinal tract and kidney tubules physiology.
2. Identification of the Transcription factor FOXi1 in the pathogenesis of kidney cystogenesis in Tuberous Sclerosis.
3. Identification of fructose transporter in the intestine and its role in fructose-induced hypertension.
4. Cloning and characterization of the Na+: HCO3- cotransporters (NBCs).
5. Identification of novel genes that play critical roles in the pathogenesis of ischemic reperfusion or nephrotoxic injury in the kidney and liver.
Achievements & Awards
Professional Honors:
Senior Clinician Scientist Investigator Award (2022-2030). Veterans Health Administration Department.
James Heady Endowed Professorship in Medicine. 2007-2019. University of Cincinnati College of Medicine, Cincinnati, OH.
Key Publications
Journal Article
Barone, Sharon, Zahedi, Kamyar, Brooks, Marybeth, Henske, Elizabeth, P. Yang, Yirong, Zhang, Erik, Bissler, John, J. Yu, Jane, J. Soleimani, Manoocher, 2021 Kidney intercalated cells and the transcription factor FOXi1 drive cystogenesis in tuberous sclerosis complex PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, vol. 118, Issue 6
Journal Article
Do, Catherine , Vasquez, P, Soleimani, Manoocher, 2022 Metabolic Alkalosis: Pathogenesis, Diagnosis and Treatment (Core Curriculum).
Journal Article
Barone, Sharon, Zahedi, Kamyar, Soleimani, Manoocher, 2023 Identification of an Electrogenic 2Cl-/H+ Exchanger, ClC5, as a Chloride-Secreting Transporter Candidate in Kidney Cyst Epithelium in Tuberous Sclerosis.
Journal Article
Soleimani, Manoocher, Zahedi, Kamyar, Barone, Sharon , 2023 Pathogenesis of Hypertension in Metabolic Syndrome: The Role of Fructose and Salt.
Journal Article
Zahedi, Kamyar, Barone, Sharon, Soleimani, Manoocher, 2022 Renal Transcriptome and Metabolome in Mice with Principal Cell-Specific Ablation of the Tsc1 Gene: Derangements in Pathways Associated with Cell Metabolism, Growth and Acid Secretion.
Gender
Male
Languages
- Persian
- English
Research and Scholarship
1. Burnham CE, Amlal H, Wang Z, Shull GE, Soleimani M. Cloning and functional expression of a human kidney Na+: HCO3- cotransporter. J Biol Chem 272(31):19111-19114, 1997.
2. Wang Z, Petrovic S, Mann E, Soleimani M. Identification of an apical Cl-/HCO3- exchanger in the small intestine. Am J Physiol Gastrointest Liver Physiol 282(3): G573-G579, 2002.
3. Soleimani M, Barone S, Xu J, Shull GE, Siddiqui F, Zahedi K, Amlal H. Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure. Proc Natl Acad Sci USA.109(33):13368-73,2012.
Barone S, Zahedi K, Brooks M, Henske EP, Yang Y, Zhang E, Bissler JJ, Yu JJ, 4. Soleimani M. Kidney intercalated cells and the transcription factor FOXi1 drive cystogenesis in tuberous sclerosis complex. Proc Natl Acad Sci U S A. 2021 Feb 9; 118(6):e2020190118. PMID: 33536341; PMCID: PMC8017711; DOI: 10.1073/pnas.2020190118
5. Barone S, Fussell SL, Singh AK, Lucas F, Xu J, Kim C, Wu X, Yu Y, Amlal H, Seidler U, Zuo J, Soleimani M. Slc2a5 (Glut5) is essential for the absorption of fructose in the intestine and generation of fructose-induced hypertension. J Biol Chem. 284(8):5056-66, 2009. DOI: 10.1074/jbc.M808128200