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Research Areas

Mohammad Asghar Mohammad Asghar, Ph.D.  | 

Research Interest

The kidney plays a pivotal role in the maintenance of sodium homeostasis and subsequently body fluid volume and blood pressure. There are several endogenous compounds including angiotensin II and dopamine, present in the kidney that help regulate sodium transporters, sodium potassium ATPase (Na,K-ATPase) and sodium-proton (Na,H)-exchanger, and maintain sodium homeostasis. Angiotensin II via AT1 receptor stimulates these transporters and facilitates sodium re-absorption while dopamine via D1 receptor inhibits these transporters and promotes sodium excretion. Appropriate functioning of these receptors is required for the maintenance of sodium homeostasis. An increase in AT1 receptor function and a decrease in D1 receptor function favor a positive sodium balance, increase in fluid volume and high blood pressure.

National Institute of Health (News Release in 2001) recognizes that sodium (salt) is a risk factor for hypertension that increases the risk for heart attack, cardiovascular events, and even death in hypertensive individuals. The risk increases with age and is true for men and women. The long-term goal of my research is to identify the role of kidney and the underlying mechanism(s) related to AT1 and D1 receptor signaling in altered sodium homeostasis contributing to high blood pressure in aging.


Tahir Hussain Richard A. Bond, Ph.D.  | 

Research Interest

Receptor theory.  Our current goals are to determine how chronic a subset of drugs classified as blockers which are termed inverse agonists, may actually increase cellular signaling.  Our specific focus at this time is examining this phenomenon in asthma. Expertise:  The classification and characterization of G protein-coupled receptors.

Lokhandwala Mustafa F. Lokhandwala, Ph.D.  | 

Research Interest

Hypertension and Antihypertensive Drug Mechanisms

Central and peripheral control of the  cardiovascular and renal function
Role of oxidative stress in cardiovascular diseases

  • receptor-G protein coupling
  • drug responsiveness
  • antioxidant supplementation

Dopamine, Dopamine Receptor Agonists and Cardiovascular Function

Dopamine receptor function in obesity, diabetes, hypertension and aging

  • Dopamine receptor mediated cellular signalling mechanisms in the proximal tubule
  • Role of kidney dopamine in fluid and electrolyte balance
  • Oxidative stress and D1 receptor signal transduction in the kidney


Knoll Brian J. Knoll, Ph.D.  | 

Research Interest

Effective asthma therapy relies on β-agonist drugs that activate β2-adrenoceptors (β2ARs) on the surfaces of cells in airway smooth muscle and epithelium. β-agonist drugs are effective in acting upon airway smooth muscle to cause bronchodilation, thereby relieving some asthma symptoms.  However, β2-agonists also may act upon airway epithelium to promote inflammation and secretion of mucous in the presence of the proinflammatory cytokine IL-13. Treatment of mice with antagonists of the β2AR, as well as deletion of the β2AR gene, reduces asthma-like symptoms in experimental mice.

We are exploring the mechanisms by which β2AR signaling in airway epithelium causes a proinflammatory effect. As one model, we use primary human airway epithelial cells grown in culture and treated pharmacologically and genetically to modify signal transducing components downstream of the β2AR and the IL-13 receptors. We employ immunoblotting, confocal microscopy, qRT-PCR and other methods to assess gene expression and the activity of signal-transducing molecules. In collaborative studies with the Bond lab, genetically modified mice are used to test hypotheses derived from the experiments with human airway epithelium.

These studies may lead to the development of new therapeutics designed to reduce airway inflammation by blockade of β2AR signaling in airway epithelium.



McConnell Bradley K. McConnell, Ph.D.  | 

Research Interest

Heart disease is the number one cause of death in the USA, affecting more than 12 million Americans. Specifically, nearly 5 million patients in the USA have heart failure; where the heart is unable to efficiently pump blood. Research interests in my laboratory focuses on the genetics and physiology of heart disease, as it relates to normal healthy hearts and to diseased hearts. In particular, our goals are to define mechanisms and to investigate strategies to improve cardiac function in heart disease.

Current research programs in my laboratory include a National Institute of Health (NIH) funded project, focused on targeted disruption of beta-adrenergic signaling to alter cardiac contractility, using transgenic murine models and viral gene transfer. In this project, we hope to better understand the signal transduction pathways (i.e. cell communication) involved in normal healthy hearts and diseased hearts. In particular, we will characterized the role on one such component of the signal transduction pathway in heart cells; the role of A-Kinase Anchoring Proteins (or simply AKAPs) that are found within the Protein Kinase A (PKA) signaling pathway. The PKA signaling pathway is commonly known to be activated by the binding of epinephrine (adrenaline) to beta-adrenergic receptors on the surface of the heart cell.

By using novel genetic approaches to study AKAPs’ role as a central and multi-component regulator of PKA signaling, our studies will yield important insights into the relationship between AKAP function, cardiac muscle signal transduction and heart disease. Other projects in the laboratory include the identification and characterization of human polymorphisms (DNA variants) that are associated with heart disease; that are found within components of the beta-adrenergic signaling pathway. These investigations will enable us to address many exciting questions in cardiovascular science, in order to fuel efforts for scientific discoveries: for the translation of basic science discoveries to clinical application and for the translation of clinically based discoveries to support basic science research.