My research goal is to understand how inflammation caused by the innate immune system regulates hypertension and associated vascular tissue damage. The innate immune system detects pathogens and cellular injury through molecular receptors, such as toll-like receptors (TLRs), and initiates several signaling pathways in response. We have found that a branch of the TLR pathways also regulates hypertension in animal models. Mice with mutation in a specific adaptor protein (TRIF) of the TLR do not develop hypertension upon angiotensin II treatment, whereas deletion of another major adaptor protein MyD88 results in enhanced inflammatory gene expression and hypertension.
Thus, the MyD88 pathways may attenuate the TRIF-dependent hypertension. Our current research efforts are directed to determine the effective organ and tissues where these events take place. To this end, we are using an integrated approach utilizing:
Whole animal physiology
Genetically engineered animals
Immunological methods including bone marrow transfer
Molecular biological approaches of gene expression and mass spectrometry.