Kristina D. Rinker

Centre for Bioengineering Research and Education

Department of Chemical and Petroleum Engineering

• Office: CCIT 122
• Phone: 403-210-9733
• Fax: 403-210-9770 or 403-284-4852
• Email: kdrinker [at] ucalgary [dot] ca
• Research Web Site

Research

The Cellular and Molecular Bioengineering Research Laboratory (CMBRL) is located in the Calgary Centre for Innovative Technology. CMBRL research efforts are focused upon combining engineering principles with cell biology, molecular biology, and biochemistry in the investigation of the effects of physical and biochemical forces on human cell physiology. One particularly strong area of interest is vascular bioengineering targeting cardiovascular disease. Cardiovascular disease, and atherosclerosis in particular, are important research topics due to the prevalence of these conditions in western society. In Canada, cardiovascular disease is the leading cause of death, and approximately 80% of the population is at risk for developing it in some form. The annual cost to the economy is in excess of $18 billion. In an effort to extend current understanding of both cardiovascular disease and factors complicating treatment of occluded coronary arteries, CMBRL research in this area investigates the effects of blood flow and the biochemical environment upon arterial endothelial cells. The design and implementation of cultivation systems to expose cells to physiological flow is a major theme of the laboratory, and surface evaluation of cells by fluorescence microscopy and flow cytometry are routinely used. Molecular analyses, such as real-time RT-PCR and Western Blotting, are also common techniques employed to ascertain the outcomes of experiments.

Vascular Cell Experimental Models

In order to more fully evaluate the mechanisms involved in the development and progression of cardiovascular disease, in vitro experimental models of the human vasculature have been developed that are capable of supporting cell culture over a variety of time periods (hours to days). Advantages of in vitro models include the ability to directly manipulate cultivation conditions and isolate the target cells from potentially interfering effects of more complex systems. As an example, Angiotensin II is a biochemical that results in constriction of the arteries and often plays a role in essential hypertension. By using the in vitro model system, the specific effects of angiotensin II on endothelial cells may be addressed, thereby highlighting individual mechanisms contributing to disease or health. Additionally, these models may serve as good systems to determine efficacy and side effects for novel treatment options as they are developed over time.

Vascular Inflammation

The presence of endothelial cells at the interface of blood flow and the arterial lumen suggests that many factors affecting arterial health are likely to be mediated by the endothelial layer. Cardiovascular disease has been shown to be an inflammation dependent disorder initiated by endothelial up-regulation of white blood cell adhesion receptors and propagated by generation of inflammatory biochemicals (cytokines). The overall effect of these cytokines on vascular endothelial cell physiology is a result of the balance between cell-stress inhibitors and activators. The laminar shear flow found in normal artery segments has been shown to inhibit the deleterious effects of inflammatory cytokines by multiple mechanisms, and to protect against disease. Investigation of the molecular regulation involved in cytokine stimulation of vascular endothelial cells may reveal unique elements of regulatory control not previously identified. Further, examining cytokine action under both healthy flow (disease protective), disturbed flow (disease prone), and static conditions may highlight the shear stress protective function. Current studies investigating the combinations of fluid flow, fluid pressure, and cytokine addition are major components of Dr. Rinker's research program. An important point to consider when addressing vascular diseases such as atherosclerosis is how endothelial cells may be returned to a quiescent phenotype to arrest the influx of white blood cells and low-density lipoproteins that ultimately are incorporated into arterial plaques, the clinical manifestation of atherosclerosis.

Vascular endothelial cells cultivated under (A) static or (B) flow conditions.

Professional Memberships

• American Association for the Advancement of Science
• American Society for Engineering Education
• American Institute of Chemical Engineers
• Biomedical Engineering Society

Work Experience

• Assistant Professor, Centre for Bioengineering Research and Education, University of Calgary. July 2005 to present.
• Assistant Professor, Department of Chemical and Petroleum Engineering, University of Calgary. July 2005 to present.
• Assistant Professor, Chemical Engineering Department, Colorado State University. August 2000 to June, 2005.
• Interim Co-Director, Biomedical Engineering Program, Colorado State University. July 2002 to June 2003.
• Research Assistant Professor, Biomedical Engineering Department, Duke University. August 1998 to July 2000.