PMID- 25821833
OWN - NLM
STAT- MEDLINE
DCOM- 20151217
LR  - 20190723
IS  - 2314-6753 (Electronic)
IS  - 2314-6745 (Print)
VI  - 2015
DP  - 2015
TI  - Pituitary adenylate cyclase-activating polypeptide protects glomerular podocytes 
      from inflammatory injuries.
PG  - 727152
LID - 10.1155/2015/727152 [doi]
LID - 727152
AB  - Diabetic nephropathy (DN) is a leading cause of end-stage kidney disease; 
      however, there are few treatment options. Inflammation plays a crucial role in 
      the initiation and/or progression of DN. Pituitary adenylate cyclase-activating 
      polypeptide (PACAP) is a neuropeptide, which was originally isolated from the 
      ovine hypothalamus and reportedly has diverse biological functions. It has been 
      reported that PACAP has renoprotective effects in different models of kidney 
      pathology. However, the specific cell types within the kidney that are protected 
      by PACAP have not yet been reported. In this study, we localized VPAC1, one of 
      the PACAP receptors, to glomerular podocytes, which also reportedly has crucial 
      roles not only in glomerular physiology but also in pathology. PACAP was 
      effective in the downregulation of proinflammatory cytokines, such as monocyte 
      chemoattractant protein-1 (MCP-1) and interleukin-6, which had been induced by 
      the activation of toll-like receptor (TLR) with lipopolysaccharide. PACAP also 
      had downregulated the expression of MCP-1 through the protein kinase A signaling 
      pathway; this led to the attenuation of the activation of extracellular 
      signal-regulated kinase and nuclear factor-kappa B signaling. Our results 
      suggested that PACAP could be a possible treatment option for DN through the use 
      of anti-inflammation effects on glomerular podocytes.
FAU - Sakamoto, Kenichi
AU  - Sakamoto K
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Kuno, Kyoko
AU  - Kuno K
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan.
FAU - Takemoto, Minoru
AU  - Takemoto M
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - He, Peng
AU  - He P
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan.
FAU - Ishikawa, Takahiro
AU  - Ishikawa T
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Onishi, Shunichiro
AU  - Onishi S
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Ishibashi, Ryoichi
AU  - Ishibashi R
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Okabe, Emiko
AU  - Okabe E
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Shoji, Mayumi
AU  - Shoji M
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Hattori, Akiko
AU  - Hattori A
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Yamaga, Masaya
AU  - Yamaga M
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Kobayashi, Kazuki
AU  - Kobayashi K
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Kawamura, Harukiyo
AU  - Kawamura H
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Tokuyama, Hirotake
AU  - Tokuyama H
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Maezawa, Yoshiro
AU  - Maezawa Y
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
FAU - Yokote, Koutaro
AU  - Yokote K
AD  - Department of Clinical Cell Biology and Medicine, Chiba University Graduate 
      School of Medicine, Japan ; Division of Diabetes, Metabolism and Endocrinology, 
      Chiba University Hospital, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150302
PL  - England
TA  - J Diabetes Res
JT  - Journal of diabetes research
JID - 101605237
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Pituitary Adenylate Cyclase-Activating Polypeptide)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Toll-Like Receptors)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/chemistry
MH  - Chemokine CCL2/metabolism
MH  - Cyclic AMP-Dependent Protein Kinases/metabolism
MH  - Down-Regulation
MH  - Inflammation/*metabolism
MH  - Interleukin-6/metabolism
MH  - Kidney/metabolism
MH  - Kidney Glomerulus/*metabolism
MH  - Lipopolysaccharides/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/metabolism
MH  - Pituitary Adenylate Cyclase-Activating Polypeptide/*metabolism
MH  - Podocytes/*metabolism
MH  - Signal Transduction
MH  - Toll-Like Receptor 4/metabolism
MH  - Toll-Like Receptors/metabolism
PMC - PMC4363873
EDAT- 2015/03/31 06:00
MHDA- 2015/12/19 06:00
PMCR- 2015/03/02
CRDT- 2015/03/31 06:00
PHST- 2014/11/14 00:00 [received]
PHST- 2015/01/15 00:00 [revised]
PHST- 2015/01/19 00:00 [accepted]
PHST- 2015/03/31 06:00 [entrez]
PHST- 2015/03/31 06:00 [pubmed]
PHST- 2015/12/19 06:00 [medline]
PHST- 2015/03/02 00:00 [pmc-release]
AID - 10.1155/2015/727152 [doi]
PST - ppublish
SO  - J Diabetes Res. 2015;2015:727152. doi: 10.1155/2015/727152. Epub 2015 Mar 2.