Kuicheon Choi, Ph.D.
Assistant Professor, Division of Gastroenterology and Hepatology
Kuicheon Choi, Ph.D.
Department of Internal Medicine
University of Texas Medical Branch
301 University Blvd.
Galveston, TX 77555-1083
Dr. Choi received his Ph.D. in 2003 from the Integrated Department of Biology at Rutgers, the State University of New Jersey. His research over this period was on the signaling mechanism of heat stress to regulate the expression of chemokines in CNS and its biological significance. After graduation, Dr. Choi had spent 6 years as a post doctoral fellow in Dr. Shear's laboratory in NIEHS/NIH and Dr. Kurie's laboratory at UT-MD Anderson Cancer Center. During this period, his research continuously focused on the signaling mechanism involved in stress responses and its clinical application for human well-fare. Particularly, his original observation for the roles of inositol pyrophosphates on the regulation of various types of internal and external stress responses lead him to be one of the FARE2006 (Fellow Award for Research Excellence 2006) awardees at NIH in 2005. In 2009, Dr. Choi joined the Division of Gastroenterology in the Department of Internal Medicine at UTMB in order to devote his efforts to full time research.
Awards and Honors
- Poster of Distinction. Digestive Disease Week (DDW), 2011
- FARE2006 (Fellow Award for Research Excellence 2006) Award. NIH. 2005
- Fellowship. Johnson and Johnson. 2002 Summer.
- Fellowship. Johnson and Johnson. 2001.
- Carl Krauss Scholarship. Rutgers, The State University of New Jersey. 2000.
Inflammation in gastrointestinal track results in the change of contractile activity of intestinal smooth muscle. Although this change on intestinal motility is suggested to be caused by disturbance of the enteric nervous system, change on the cytokine, chemokine, and growth factor profiles, and/or modification of calcium channels, our understanding on this is still preliminary. My ultimate research interest is to answer a basic fundamental question on this; How can inflammation cause the altered motility of intestine? To answer this, my primary concern is on the Cacna1C (alpha1C). Cacna1C is a subtype of voltage-gated L type calcium channels which are known to be one of the main causes for the decreased motility in the intestine. Recently, our research group showed the decreased expression of Cacna1C in muscularis externa of distal colon in adult rats challenged with TNBS for the induction of inflammation, and this decrease was not fully recovered during the recovery from the inflammation. In spite of these observations, we do not know what mediator(s) produced during inflammation cause(s) this decreased expression of Cacna1C and what the mechanism is for the prolonged inhibition of Cacna1C. Although TNF-Î± was known to decrease the expression of Cacna1c through NF-ÎºB activation, the level of TNF-Î± in our inflammation model was not changed.
In addition, other pro-inflammatory cytokines involved in inflammation failed to inhibit the expression of Cacna1C. Production of reactive oxygen and nitrogen species is another key feature of inflammation. In cardiovascular system, CO and reactive oxygen species is known to regulate the expression of Cacna1C. One of my current researches is to characterize the roles of Nrf family members, a sensor for oxidative stress, and HMOX-1, a source for CO and sensor for oxidative DNA damage, on Cacna1c expression and motility of intestine. On the other hand, prolonged disturbance of Cacna1C expression suggests that transcription of this gene may be regulated by epigenetic mechanisms. Analysis of Cacna1C promoter with several tools used for bioinformatics showed the presences of 6 CpG islands for DNA methylation, a typical sequence for folate sensitive fragile site to make this area labile for the chromosome break during stress, and highly conserved target sites for microRNAs, particularly miR-19, miR-25, miR-26ab, miR-33, and miR-133. Second part of my on-going researches is to define the meaning and roles of these features on Cacna1C promoter. I expect our understanding on these will expand our knowledge on the mechanism for disturbed motility of intestine. This research will also have a dramatic impact on human well-fare in our society. As we know, altered motility of gastrointestinal track is one of the key components of IBS (Irritable Bowel Syndrome) which is a major cause of medical consultation among gastroenterology patients in USA.
- K. Choi, L. Ni, G. M. Jonakait (2011) Fas ligation and tumor necrosis factor alpha activation of murine astrocytes promote heat shock factor-1 activation and heat shock protein expression leading to chemokine induction and cell survival. Journal of Neurochemistry, 116(3):438-448
- K. Choi , YH Ahn, DL Gibbons, HT Tran, CJ Creighton, L Girard, JD Minna, FX Qin, JM Kurie (2009) Distinct biological roles for the notch ligands Jagged-1 and Jagged-2. Journal of Biological Chemistry, 284(26):17766-74
- L. Zhong, J. Roybal, R. Chaerkady, W. Zhang, K. Choi, C.A. Alvarez, H. Tran, S. Yan, R.M. Strieter, A. Pandey, J.M. Kurie (2008). Identification of Secreted Proteins that Mediate Cell-Cell Interaction in an In Vitro Model of the Lung Cancer Microenvironment. Cancer Research, 68, 7237-7245.
- K. Choi, E. Mollapour, J.H. Choi, and S.B. Shears (2008). Cellular Energetic Status Supervises the Synthesis of Bis-diphosphoinositol Tetrakisphosphate (InsP8), Independently of AMP-Activated Protein Kinase. Molecular Pharmacology 74(2):527-36
- J. Zhang, K. Iwanaga, K. Choi, M. Wislez, M.G. Raso, W. Wei, I.I. Wistuba, J.M. Kurie (2008) Intratumoral Epiregulin is a Marker of Advanced Disease in Non-Small Cell Lung Cancer Patients and Confers Invasive Properties on EGFR-Mutant Cells. Cancer Prevention Research, 1(3), 201-207
- K. Choi, C. Creighton, D. Stivers, N. Fujimoto, J.M. Kurie (2007) ranscriptional Profiling of Non-Small Cell Lung Cancer Cells with Activating EGFR Somatic Mutation. PlosOne, 2(11), e1226
- Cho J, K. Choi, Darden T, Reynolds PR, Petitte JN, S.B. Shears (2006) Avian multiple inositol polyphosphate phosphatase is an active phytase that can be engineered to help ameliorate the planet's "phosphate crisis". Journal of Biotech, 126, 248-259
- S. Deleu, K. Choi, J.M. Reece, and S.B. Shears (2006) Pathogenicity of Salmonella: SopE-mediated membrane ruffling is independent of inositol phosphate signals. FEBS Letters, 580, 1709-1715
- S. Deleu, K. Choi, X. Pesesse, J. Cho, M.L. Sulis, R. Parsons, S.B. Shears (2006) Physiological Levels of PTEN Control the Size of the Cellular Ins (1, 3, 4, 5, 6) P5 Pool. Cellular Signaling, 18, 488-498
- K. Choi, E. Mollapour, S.B. Shears (2005), Signal Transduction during Environmental Stress: InsP8 Operates within Highly Restricted Context. Cellular Signaling, 17, 1533-1541
- X. Pesesse, K. Choi, T. Zhang, S.B. Shears (2004), Signaling by Higher Inositol Polyphosphates. Journal of Biological Chemistry, 279 (42), 43378-43381.
The department of internal medicine is developing evidence based clinical protocols which will be available in EPIC (as order sets) for use when admitting patients with these diagnoses. Their AIM is to standardize care and decrease length of stay and readmission rates.Currently available protocols are:
- CAP - Community Acquired Pneumonia Order set
- Congestive Heart Failure (CHF)
- Chronic Obstructive Pulmonary Disease (COPD)
- Diabetic Ketoacidosis Adult, ICU
- General Medicine Admission
- Immunodeficiency Flow Panel
- MICU/CCU Admission Order Set
- Oral Analgesic Medications
- Parenteral Opioids
- Sepsis, Adult ICU
- 111 - Stroke Alert
- 112 - Stroke Activation
- 300086 - Stroke Floor Admission
- 3000000001 - Stroke Critical care without tPA
- 300088 Stroke - Transfer from Critical care to floor
- 3004002 - Stroke Discharge
All protocols can be found in the EPIC order set section.
The department of Internal Medicine has a large role in the Meaningful Use Initiative. Our participation is key for the success of the initiative. Please visit the meaningful use website for important communication and updates from the Meaningful Use Initiative.