Directory > Faculty
Nara Parameswaran
, Ph.D.
 |
Assistant
Professor of Physiology
|
Broadly, our laboratory is interested in receptor biology and
signal transduction in the context of inflammatory diseases. Inflammation
is implicated in a number of diseases including cardiovascular
diseases (e.g. atherosclerosis), musculoskeletal diseases (e.g.
arthritis), cancer, renal diseases, neurological disorders, as
well as in conditions such as septicemia. In recent years, crucial
breakthroughs have occurred in the understanding of innate immunity
and inflammatory processes in many diseases. Important discoveries
include the role of Toll-like receptors (receptors that mediate
signaling and pathophysiology from microbial products and possibly
from endogenous ligands) and tumor necrosis factor receptors in
many disease processes where inflammation is a key component.
In fact, these receptors are therapeutic drug targets in a number
of these diseases. Currently, our work focuses on the regulation
of these receptors and the signaling pathways particularly in
macrophages (cell type that plays a pivotal role in innate immunity
and inflammation). We are especially focusing our work on the
role of two major protein families, namely arrestins and G-protein
coupled receptor kinases (GRKs) in receptor signaling in macrophages.
Arrestins and GRKs were originally discovered in the context of
G-protein coupled receptor (GPCR) signaling. Recent studies have
implicated a much broader role for these two protein families.
Our goals for the next few years are to identify the biochemical
and molecular mechanisms by which arrestins and GRKs regulate
receptor biology and signaling pathways in macrophages and also
to test the mechanisms by which these signaling pathways mediate
inflammation. Using a number of different approaches including
RNA interference, proteomics and knockout mice strategy, we are
currently testing how arrestins and GRKs regulate macrophage signaling
and biology (such as cytokine production, phagocytosis, and macrophage
survival/death). Understanding the mechanisms by which macrophage
biology is regulated will help us devise strategies to therapeutically
target some of these critical pathways in inflammatory diseases
including atherosclerosis and arthritis.
Selected Publications (last five years):
1. K.J. Loneiwski, S. Patial, and N. Parameswaran. SENSITIVITY
OF TLR-4 AND -7-INDUCED NFkB1 P105-TPL2-ERK PATHWAY TO TNF-RECEPTOR-ASSOCIATED-FACTOR-6
REVEALED BY RNAI IN MOUSE MACROPHAGES. 2007 Jul (Epub 2007 May
15), Molecular Immunology 44, 3715-3723.
2. N. Parameswaran, C. Pao, K. Leonhard, D.S. Kang, M. Kratz,
S. Ley, and J.L. Benovic. ARRESTIN-2 AND G-PROTEIN COUPLED RECEPTOR
KINASE-5 INTERACT WITH NFB1 p105 AND NEGATIVELY REGULATE LIPOPOLYSACCHARIDE-STIMULATED
ERK1/2 ACTIVATION IN MACROPHAGES. 2006 Nov (Epub 2006 Sep 15)
Journal of Biological Chemistry 10; 281(45):34159-70.
3. N. Parameswaran and W. S. Spielman. RAMPs: The past, present,
and future. 2006 Nov; (Epub 2006 Sep 28) Trends in Biochemical
Sciences (TIBS), 31(11):631-8
4. J.M. Bomberger, W.S. Spielman, C.S. Hall, E. Weinmann and
N. Parameswaran. RAMP ISOFORM-SPECIFIC REGULATION OF ADRENOMEDULLIN
RECEPTOR TRAFFICKING BY NHERF-1. 2005 June, (Epub 2005 April1),
Journal of Biological Chemistry, 280(25): 23926-23935.
5. J.M. Bomberger, N. Parameswaran, C.S. Hall, N. Aiyar, and
W.S. Spielman. NOVEL FUNCTION FOR RECEPTOR ACTIVITY MODIFYING
PROTEINS (RAMPs) IN POST-ENDOCYTIC TRAFFICKING. 2005 Mar (Epub
2004 Dec 21) Journal of Biological Chemistry, 280(10): 9297-307.
6. N. Parameswaran, W.S. Spielman, D.P. Brooks, and P. Nambi.
OKADAIC ACID STIMULATES CASPASE-LIKE ACTIVITIES AND INDUCES APOPTOSIS
OF CULTUTED RAT MESANGIAL CELLS. 2004, Molecular and Cellular
Biochemistry, 260: 7-11.
7. N. Parameswaran, C.S. Hall, J. Bomberger, and W.S. Spielman.
REGULATION OF ADRENOMEDULLIN SIGNALING IN KIDNEY INTERSTITIAL
FIBROBLASTS. 2003, Cellular Physiology and Biochemistry, 13: 391-400.
8. N. Parameswaran, C.S. Hall, J. Bomberger, H.V. Sparks, D.B.
Jump, and W.S. Spielman. NEGATIVE GROWTH EFFECTS OF CIGLITAZONE
ON KIDNEY MESANGIAL CELLS AND INTERSTITIAL FIBROBLASTS: ROLE OF
PPAR-. 2003, Kidney and Blood Pressure research, 26(1), 2-9.
9. N. Parameswaran, C.S. Hall, L.R. McCabe, and W.S. Spielman.
ADRENOMEDULLIN INCREASES AP-1 EXPRESSION AND ACTIVITY IN RAT MESANGIAL
CELLS VIA ACTIVATION OF PROTEIN KINASE-A AND P38 MAPK. 2003, Cellular
Physiology and Biochemistry, 13: 367-374.
10. N. Parameswaran, C.S. Hall, B.C. Bock, H.V. Sparks, K.A.
Gallo, and W.S. Spielman. MIXED LINEAGE KINASE 3 INHIBITS PHORBOL
MYRISTOYL ACETATE-INDUCED DNA SYNTHESIS BUT NOT OSTEOPONTIN EXPRESSION
IN RAT MESANGIAL CELLS. 2002, Molecular and Cellular Biochemistry,
241: 37-43.
11. N. Aiyar, J. Disa, Z. Ao, D. Xu, A. Surya, K. Pillarisetti,
N. Parameswaran, S. K. Gupta, S. A. Douglas and P. Nambi. MOLECULAR
CLONING AND PHARMACOLOGICAL CHARACTERIZATION OF BOVINE CALCITONIN
RECEPTOR –LIKE RECEPTOR FROM BOVINE AORTIC ENDOTHELIAL CELLS.
2002, Biochemical Pharmacology, 63: 1949-1959.
12. V. Nowak, N. Parameswaran, C.S. Hall, N. Aiyar, H.V. Sparks,
and W.S. Spielman. A NOVEL REGULATION OF ADRENOMEDULLIN RECEPTOR
BY PDGF IN MESANGIAL CELLS- ROLE OF RECEPTOR ACTIVITY MODIFYING
PROTEIN-3. 2002. American Journal of Physiology-Cell Physiology,
282: C1322-C1331.
13. N. Parameswaran, C.S. Hall, B.C. Bock, H.V. Sparks, K.A.
Gallo, and W.S. Spielman. MIXED LINEAGE KINASE 3 INHIBITS PLATELET-DERIVED
GROWTH FACTOR-STIMULATED DNA SYNTHESIS AND MATRIX MRNA EXPRESSION
IN MESANGIAL CELLS. 2002, Cellular Physiology and Biochemistry,
12 (5-6): 325-334.
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