Professor Office: G323 Phone: (601) 984-1707 Fax: (601) 984-1637 E-mail: email@example.com
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Data included in AJP cover article, May 2012 (doi: 10.1152/ajpregu.00487.2011)
My laboratory is interested in the roles of endocrine (tissue-to-tissue), paracrine (cell-to-cell), and intracrine (cytoplasmic and nuclear) angiotensin II (ANG II) and its G protein-coupled receptor (GPCR) signal mechanisms in the kidney and blood pressure control. Specifically, we are currently working: 1) to determine the molecular and signaling mechanisms by which extracellular (circulating and intrarenally formed) ANG II is taken up by the proximal tubule of the kidney to act as an intracellular peptide, 2) to determine the effects and signaling mechanisms by which internalized or intracellular ANG II induces long-term genomic effects, 3) to determine the role of the sodium and hydrogen exchanger 3 (NHE3) in the proximal tubule on blood pressure responses to extracellular and intracellular ANG II; and 4) the role and signaling mechanisms of ANG II/AT1a receptors in the regulation of urine concentration. To test our hypotheses, we use complementary state of the art approaches including: 1) single proximal tubule cell intracellular microinjection of ANG II, 2) live cell multicolor fluorescent imaging, 3) intravital multi-photon functional imaging of the proximal tubule, 4) proximal tubule cells derived from wild-type or AT1a receptor-deficient (AT1a-KO) mice, 5) global and proximal tubule-specific knockout of AT1a receptors or NHE3, 6) proximal tubule-specific knockin or overexpression of an intracellular cyan fluorescent fusion of ANG II protein (ECFP/ANG II) or a fusion ANG II protein (fsANG II), which is secreted upon expression, 7) high resolution light and electron microscopic autoradiography and immunohistochemistry, and 8) molecular biology and proteomic approaches including real-time and single-cell RT-PCR, gene microarrays, phosphoproteomic and western blot analyses.
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