PMID- 26242183
OWN - NLM
STAT- MEDLINE
DCOM- 20160401
LR  - 20231213
IS  - 1465-993X (Electronic)
IS  - 1465-9921 (Print)
IS  - 1465-9921 (Linking)
VI  - 16
IP  - 1
DP  - 2015 Aug 5
TI  - Plk1 regulates MEK1/2 and proliferation in airway smooth muscle cells.
PG  - 93
LID - 10.1186/s12931-015-0257-8 [doi]
LID - 93
AB  - BACKGROUND: Polo-like kinase 1 (Plk1) is a serine/threonine protein kinase that 
      has been implicated in the regulation of mitosis. In addition, the activation of 
      mitogen-activated protein kinase (MAPK) is a key event in the early stage of the 
      growth factor response. The role of Plk1 in MAPK phosphorylation in cells has not 
      been investigated. METHODS: Immunoblot analysis was used to evaluate Plk1 and 
      MAPK phosphorylation in cells upon stimulation with platelet-derived growth 
      factor (PDGF). We also generated stable Plk1 knockdown (KD) cells to assess the 
      role of Plk1 in MAPK activation and cell proliferation. Furthermore, we used a 
      non-phosphorylatable Plk1 mutant to determine the function of Plk1 
      phosphorylation in these processes. RESULTS: Treatment with PDGF increased Plk1 
      phosphorylation at Thr-210 (an indication of Plk1 activation) in human airway 
      smooth muscle cells. Plk1 KD attenuated the PDGF-induced phosphorylation of 
      MEK1/2 and ERK1/2 as well as cell proliferation. However, phosphorylation of 
      Raf-1 and AKT upon stimulation with PDGF was not reduced in Plk1 KD cells. 
      Furthermore, the expression of T210A Plk1 (alanine substitution at Thr-210) 
      inhibited the PDGF-stimulated MEK1/2 phosphorylation, ERK1/2 phosphorylation and 
      cell proliferation. CONCLUSIONS: Together, these findings suggest that Plk1 is 
      activated upon growth factor stimulation, which may control the activation of 
      MEK1/2 and ERK1/2, and smooth muscle cell proliferation.
FAU - Jiang, Sixin
AU  - Jiang S
AD  - The Center for Cardiovascular Sciences, Albany Medical College, 47 New Scotland 
      Avenue, MC-8, Albany, NY, 12208, USA. jiangs@mail.amc.edu.
FAU - Tang, Dale D
AU  - Tang DD
AD  - The Center for Cardiovascular Sciences, Albany Medical College, 47 New Scotland 
      Avenue, MC-8, Albany, NY, 12208, USA. tangd@mail.amc.edu.
LA  - eng
GR  - R01 HL113208/HL/NHLBI NIH HHS/United States
GR  - HL113208/HL/NHLBI NIH HHS/United States
GR  - R01 HL110951/HL/NHLBI NIH HHS/United States
GR  - R01 HL130304/HL/NHLBI NIH HHS/United States
GR  - HL-110951/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20150805
PL  - England
TA  - Respir Res
JT  - Respiratory research
JID - 101090633
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - EC 2.7.1.- (MAP2K2 protein, human)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 1)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 2)
RN  - EC 2.7.12.2 (MAP2K1 protein, human)
SB  - IM
MH  - Bronchi/cytology/physiology
MH  - Cell Cycle Proteins/*physiology
MH  - Cell Proliferation/*physiology
MH  - Humans
MH  - MAP Kinase Kinase 1/*physiology
MH  - MAP Kinase Kinase 2/*physiology
MH  - Muscle, Smooth, Vascular/cytology/physiology
MH  - Myocytes, Smooth Muscle/*physiology
MH  - Protein Serine-Threonine Kinases/*physiology
MH  - Proto-Oncogene Proteins/*physiology
MH  - Trachea/cytology/physiology
MH  - Polo-Like Kinase 1
PMC - PMC4531535
EDAT- 2015/08/06 06:00
MHDA- 2016/04/02 06:00
PMCR- 2015/08/05
CRDT- 2015/08/06 06:00
PHST- 2015/05/12 00:00 [received]
PHST- 2015/07/25 00:00 [accepted]
PHST- 2015/08/06 06:00 [entrez]
PHST- 2015/08/06 06:00 [pubmed]
PHST- 2016/04/02 06:00 [medline]
PHST- 2015/08/05 00:00 [pmc-release]
AID - 10.1186/s12931-015-0257-8 [pii]
AID - 257 [pii]
AID - 10.1186/s12931-015-0257-8 [doi]
PST - epublish
SO  - Respir Res. 2015 Aug 5;16(1):93. doi: 10.1186/s12931-015-0257-8.