Vipul C. Chitalia, M.D., Ph.D.
Assistant Professor
Boston University School of Medicine
Dept of Medicine
Nephrology Section

MD, Seth G.S. Medical College
MBBS, Lokmanya Tilak Medical College and Hospital
DM, Seth G.S. Medical College



Our laboratory focuses on the role of post-translational modifications of proteins, especially polyubiquitnation of the key mediators of vascular pathologies in diseases such as cancer and renal failure. While these diseases are discrete, several fundamental biological processes remain similar. Through a highly collaborative network, our laboratory harnesses the power of various cellular and molecular biological tools, relevant animal models (zebrafish and mice), computational methods and machine-learning techniques and strives to validate these findings and hypotheses in humanized models or human samples from large data bases, which highlights the translational nature of our approach.

A. Vascular diseases in kidney failure: Close to 20 million Americans or 10% of US population suffer from the chronic kidney disease (CKD). Among plethora of cardiovascular manifestations, CKD patients are particularly at high risk for both venous and arterial thrombosis, especially after vascular injury (endovascular injury such as angioplasty or stents; and surgical injury such as arteriovenous fistula creation) in CKD patients. This area of CKD management warrants urgent investigation due to lack of risk predictors and CKD-specific therapeutic targets.
Renal failure results in the retention of several chemical compounds, which unleash cellular toxicity, and hence called uremic solutes/toxins. While investigating the molecular pathogenesis of uremic toxicity, our laboratory was the first to demonstrate the prothrombotic propensity of indolic uremic solutes, which inhibits the ubiquitination of tissue factor, a bona fide member of the extrinsic coagulation pathway. Further investigation revealed Aryl Hydrocarbon Receptor (AHR) pathway as a critical mediator of tissue factor ubiquitination and thrombosis. Leveraging the ligand and the mediator, our lab aims to gain a deeper understanding into the mechanism of this unique uremic thrombosis axis (uremic solutes- AHR- TF- thrombosis) and to develop biomarkers and novel compounds to improve the management of the CKD patients with thrombosis after interventions in various vascular beds including coronary artery and arteriovenous fistula, etc.
Thrombosis being a dynamic and the multicomponent process, our laboratory has taken a holistic approach, under the co-directorship of Drs. Chitalia and Ravid, the Department of Medicine of BUSM and established a Thrombosis and Hemostasis ARC, which is a multidisciplinary platform of cell and molecular biologists, clinicians (cardiologists, vascular medicine, nephrologists and hematologists), computational biologists, biomedical engineers and statisticians and mathematicians to investigate various facets of thrombosis. http://www.bumc.bu.edu/evanscenteribr/the-arcs/the-arcs/

B. Angiogenesis: Angiogenesis, a process of generation of novel blood vessel is fundamental during the development and in various diseases such as cancer. Wnt signaling, a highly conserved oncogenic pathway is critical in angiogenesis. Beta catenin is the prime mediator of Wnt activation. Focusing on the ubiquitination and proteasomal degradation of beta catenin, our previous work had described Jade-1, as an E3 ligases of wild-type beta catenin. Our recent efforts have specifically focused on c-Cbl as an E3 ligase for the mutant beta catenin and for the transcriptionally active beta catenin in the nucleus. These two species of beta catenin, once considered resistant to degradation are effectively downregulated by c-Cbl. Thus, c-Cbl is a unique E3 ligase of tumorigenic beta catenin, which is involved in several cancers including colorectal cancer pathogenesis. Leveraging the cancer animal models and human cancer samples including machine learning based quantitative histology! techniques, our group investigates the colorectal cancer pathogenesis to gain deeper understanding of the role of E3 ligases of beta catenin E3 ligases in various cancers.

Graduate Faculty (Primary Mentor of Grad Students)
Boston University School of Medicine, Division of Graduate Medical Sciences


Active Staff Hospital Privileges
Boston Medical Center
Medicine



2016 Boston University : Outstanding Mentor award for UROP mentoring
2015-2017 Boston University School of Medicine: Evan’s Junior Faculty Merit Award
2007 Boston University School of Medicine: Annual Evan’s Research Day award
2005 Boston University School of Medicine: Annual Evan’s Research Day award
1998-1999 International Society of Nephrology: International Society of Nephrology Fellowship award
1995 University of Bombay: Gold medal Postdoctoral examination in Nephrology
1990-1992 University of Bombay: Merit Scholarship, Government of India
1987 University of Bombay: Charles Moorhead Prize



Thrombotic complication of uremia: role of prothrombotic uremic solutes
03/16/2016 - 02/28/2020 (PI)
NIH-NHLBI
5R01HL132325-02

Role of c-Cbi in Colon Cancer
07/01/2014 - 04/30/2019 (PI)
NIH-NCI
5R01CA175382-04

Role of Wnt Signaling in Uremia-induced Endothelial Dysfunction
06/14/2009 - 06/30/2014 (PI)
NIH-NIDDK
5K08 DK080946-04

Role of Wnt Signaling in uremia-induced endothelial dysfunction
07/01/2009 - 06/30/2013 (PI)
National Kidney Fdtn

Role of Jade-1 in Wnt Signaling
07/01/2006 - 06/30/2008 (PI)
Polycystic Kidney Disease Fdtn

Research Fellowship--Polycystic Kidney Disease
07/01/2003 - 06/30/2005 (PI)
National Kidney Fdtn



Yr Title Project-Sub Proj Pubs
2017 Thrombotic complication of uremia: role of prothrombotic uremic solutes 5R01HL132325-02
2017 Role of c-Cbl in Colon cancer 5R01CA175382-04
2016 Thrombotic complication of uremia: role of prothrombotic uremic solutes 1R01HL132325-01
2016 Role of c-Cbl in Colon cancer 5R01CA175382-03
2015 Role of c-Cbl in Colon cancer 5R01CA175382-02
2014 Role of c-Cbl in Colon cancer 1R01CA175382-01A1
2013 Role of Wnt signaling in uremia-induced entothelial dysfunction 5K08DK080946-05 8
2012 Role of Wnt signaling in uremia-induced entothelial dysfunction 5K08DK080946-04 8
2011 Role of Wnt signaling in uremia-induced entothelial dysfunction 5K08DK080946-03 8
2010 Role of Wnt signaling in uremia-induced entothelial dysfunction 5K08DK080946-02 8
Showing 10 of 11 results. Show All Results
Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

  1. Abbonante V, Chitalia V, Rosti V, Leiva O, Matsuura S, Balduini A, Ravid K. Up-regulation of lysyl oxidase and adhesion to collagen of human megakaryocytes and platelets in primary myelofibrosis. Blood. 2017 Jun 07.View Related Profiles. PMID: 28592432.
  2. Shashar M, Siwak J, Tapan U, Lee SY, Meyer RD, Parrack P, Tan J, Khatami F, Francis J, Zhao Q, Hartshorn K, Kolachalama VB, Rahimi N, Chitalia V. c-Cbl mediates the degradation of tumorigenic nuclear ß-catenin contributing to the heterogeneity in Wnt activity in colorectal tumors. Oncotarget. 2016 11 01; 7(44):71136-71150.View Related Profiles. PMID: 27661103; DOI: 10.18632/oncotarget.12107;.
  3. Moshe Shashar, Jamaica Siwak, Umit Tapan, Shin Yin Lee, Rosana D. Meyer, Paige Parrack, Josenia Tan, Fatemeh Khatami, Jean Francis, Qing Zhao, Kevan Hartshorn, Vijaya B. Kolachalama, Nader Rahimi and Vipul Chitalia. c-Cbl mediates the degradation of tumorigenic nuclear ß-catenin contributing to the heterogeneity in Wnt activity in colorectal tumors. Oncotarget. 2016; (Epub). View Publication
  4. Arafa E, Bondzie PA, Rezazadeh K, Meyer RD, Hartsough E, Henderson JM, Schwartz JH, Chitalia V, Rahimi N. TMIGD1 is a novel adhesion molecule that protects epithelial cells from oxidative cell injury. Am J Pathol. 2015 Oct; 185(10):2757-67.View Related Profiles. PMID: 26342724; PMCID: PMC4607757; DOI: 10.1016/j.ajpath.2015.06.006;.
  5. Srinivasan S, Chitalia V, Meyer RD, Hartsough E, Mehta M, Harrold I, Anderson N, Feng H, Smith LE, Jiang Y, Costello CE, Rahimi N. Hypoxia-induced expression of phosducin-like 3 regulates expression of VEGFR-2 and promotes angiogenesis. Angiogenesis. 2015 Oct; 18(4):449-62.View Related Profiles. PMID: 26059764; PMCID: PMC4600037; DOI: 10.1007/s10456-015-9468-3;.
  6. Shivanna S, Kolandaivelu K, Shashar M, Belghasim M, Al-Rabadi L, Balcells M, Zhang A, Weinberg J, Francis J, Pollastri MP, Edelman ER, Sherr DH, Chitalia VC. The Aryl Hydrocarbon Receptor is a Critical Regulator of Tissue Factor Stability and an Antithrombotic Target in Uremia. J Am Soc Nephrol. 2016 Jan; 27(1):189-201.View Related Profiles. PMID: 26019318; PMCID: PMC4696580; DOI: 10.1681/ASN.2014121241;.
  7. Vipul Chitalia. Good-in-good-out: Diet modification in chronic kidney disease. Science Translational Medicine. 2015; 7(280):280. View Publication
  8. Shivanna S, Harrold I, Shashar M, Meyer R, Kiang C, Francis J, Zhao Q, Feng H, Edelman ER, Rahimi N, Chitalia VC. The c-Cbl ubiquitin ligase regulates nuclear ß-catenin and angiogenesis by its tyrosine phosphorylation mediated through the Wnt signaling pathway. J Biol Chem. 2015 May 15; 290(20):12537-46.View Related Profiles. PMID: 25784557; PMCID: PMC4432275; DOI: 10.1074/jbc.M114.616623;.
  9. Shashar M, Francis J, Chitalia V. Thrombosis in the uremic milieu--emerging role of "thrombolome". Semin Dial. 2015 Mar-Apr; 28(2):198-205.View Related Profiles. PMID: 24962903; PMCID: PMC4407993; DOI: 10.1111/sdi.12255;.
  10. Voyvodic PL, Min D, Liu R, Williams E, Chitalia V, Dunn AK, Baker AB. Loss of syndecan-1 induces a pro-inflammatory phenotype in endothelial cells with a dysregulated response to atheroprotective flow. J Biol Chem. 2014 Apr 4; 289(14):9547-59. PMID: 24554698; PMCID: PMC3975006; DOI: 10.1074/jbc.M113.541573;.
Showing 10 of 34 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 27 publications over 15 distinct years, with a maximum of 5 publications in 2015

YearPublications
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19981
19991
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20051
20082
20101
20112
20122
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20142
20155
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20171
In addition to these self-described keywords below, a list of MeSH based concepts is available here.

Chronic Kidney Disease
E3 Ubiquitin Ligase
Thrombosis
Uremic Vascular Disease
Wnt Signaling

I am an Assistant Professor of Medicine at Boston University School of Medicine and an affiliate of Biomedical Engineering at Harvard-MIT Division of Science and Technology, MIT. I am also an attending nephrologist covering renal consults and dialysis and kidney transplant in-patients services at Boston Medical Center. Teaching is my passion and I consider it as my honor to be able to contribute in the training of next generation of physicians, scientists and physician-scientists. I strongly believe that a true mentor is one who inspires passion from within and empowers a mentee to find his or her own path of success. Spanning over entire spectrum, our laboratory has trained several undergraduate students, graduate students and post doctoral fellows, of which several are clinical fellows from renal, cardiovascular and hematology-oncology specialties. Our laboratory has not only US researchers, but has students and post doctoral fellows from Europe, Middle East and Asia creating a truly international learning environment. I have been awarded 2016 Outstanding Mentor Award from the undergraduate research opportunity program (UROP) of Boston University and been nominated for best research mentoring award at BUSM.

Available to Mentor as: (Review Mentor Role Definitions):
  • Advisor
  • Career Mentor
  • Education Mentor
Contact for Mentoring:
  • Email (see 'Contact Info')


650 Albany St Evans Biomed Research Ctr
Boston MA 02118
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