My laboratory studies intracellular signaling regulating contraction, relaxation and proliferation of airway smooth muscle with particular emphasis on G protein coupled receptor mediated signaling. Airway smooth muscle is the principle contractile component of airways, and contraction and relaxation of ASM regulate airway diameter. Any alteration in ASM function results in bronchoconstriction and difficulty in breathing. Therefore, ASM acts as a primary therapeutic target in obstructive airway diseases such as asthma and COPD. Delineating novel receptors and signaling mechanisms that regulate ASM function would provide basis for developing newer and better drugs to treat asthma.  Current projects are listed below.

• Understanding age-dependent changes in airway smooth muscle function
• Bitter taste receptor signaling in airway smooth muscle with a particular emphasis on compartmentalized signaling in airway smooth muscle cells
• Determining the role of small non-coding RNAs derived from tRNA and rRNA in the physiological and pathological conditions in airway cells.
• Discovering the role of diacylglycerol kinase in the regulation of airway functions and explore diacylglycerol kinase as potential therapeutic target in asthma.
• Developing and characterizing novel methods for inhibiting AP-1 transcription factor in airway smooth muscle cells in an attempt to establish the utility of these approaches to mitigate features of airway remodeling in asthma.
• Delineate cross-talk between obesity and GPCR signaling in airway cells.
• Developing and characterizing allosteric modulators of beta 2 adrenergic receptors that promote Gs-biased signaling and function in airway smooth muscle.

These projects are funded by NIH/NHLBI/NIAID