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Volume 7, Issue 2 (Suppl)
J Clin Exp Pathol, an open access journal
ISSN:2161-0681
Pathology and Molecular Diagnosis 2017
June 26-27, 2017
Page 29
Notes:
conference
series
.com
June 26-27, 2017 San Diego, USA
13
th
International conference on
Pathology and Molecular Diagnosis
Polo-like kinase 1 (Plk1) in smooth muscle and allergic asthma
S
mooth muscle contraction and cell proliferation are critical for the pathogenesis of airway hyper-responsiveness and
hyperplasia of allergic asthma. Polo-like kinase 1 (Plk1) is a serine/threonine protein kinase that has been implicated in
mitosis and cytokinesis. The role of Plk1 in smooth muscle contraction and cell growth has not been previously investigated.
Here, stimulation with acetylcholine induces Plk1 phosphorylation at Thr-210 (an indication of Plk1 activation) in smooth
muscle. Contractile stimulation also activates Plk1 in live smooth muscle cells as evidenced by changes in fluorescence
resonance energy transfer signal of a Plk1 sensor. Plk1 is necessary for smooth muscle force development. Plk1 regulates
airway smooth muscle contraction by affecting vimentin phosphorylation at Ser-56, but without modulating myosin light
chain phosphorylation. Plk1 phosphorylation is mediated by Ste20-like kinase (SLK), a serine/threonine protein kinase that
has been implicated in spindle orientation and microtubule organization during mitosis. Moreover, Plk1 is indispensable
for airway smooth muscle cell proliferation. Plk1 knockdown by lentivirus-mediated shRNA attenuates the growth factor-
induced phosphorylation of MEK1/2 and ERK1/2. However, Plk1 knockdown does not affect the phosphorylation of Raf-
1or AKT. Finally, smooth muscle conditional knockout of Plk1 attenuates airway resistance, airway smooth muscle hyper-
reactivity and hyperplasia in a murine model of allergic asthma. Taken together, these findings suggest that Plk1 is critical for
the regulation of smooth muscle contraction and cell proliferation. Plk1 regulates smooth muscle contraction by controlling
vimentin phosphorylation, whereas, it orchestrates cell proliferation by modulating the MAPK pathway. Plk1 contributes to
the pathogenesis of allergic asthma. Plk1 may be a pharmacological target for the development of new therapy to treat asthma.
Biography
Dale D Tang has received training at the University of Texas Southwestern Medical Center at Dallas in 1990s. He is a Professor of the Department of Molecular
and Cellular Physiology at Albany Medical College, New York, USA. He is Director of Cytoskeletal Signaling and Asthma Research Program at the school. He is an
Associate Editor of BMC
Respiratory Research
and an Editorial Board Member of
Nature Scientific Reports
. His research focuses on the role and mechanism of
cytoskeleton-associated proteins in smooth muscle in vitro and the pathogenesis of asthma and hypertension in vivo. He has published >70 peer-reviewed articles
in journals including the
Journal of Biological Chemistry and Circulation Research.
TangD@mail.amc.eduDale D Tang, J Clin Exp Pathol 2017, 7:2 (Suppl)
DOI: 10.4172/2161-0681-C1-033
Dale D Tang
Albany Medical College, USA