PMID- 22801596
OWN - NLM
STAT- MEDLINE
DCOM- 20130212
LR  - 20211021
IS  - 1752-8984 (Electronic)
IS  - 1479-1641 (Print)
IS  - 1479-1641 (Linking)
VI  - 9
IP  - 4
DP  - 2012 Oct
TI  - Antisense to protein kinase C-alpha and p47phox attenuates the pro-inflammatory 
      effects of human C-reactive protein in macrophages of biobreeding diabetic rats.
PG  - 315-9
AB  - OBJECTIVE: Type 1 diabetes mellitus (T1DM) is a pro-inflammatory state 
      characterized by high C-reactive protein (CRP) levels. Previously, we showed that 
      CRP accentuated a macrophage (MO) activity in spontaneously diabetic biobreeding 
      (BB) rats and increased the MO activity of protein kinase C-alpha (PKC-alpha) and 
      p47phox. In this report, we tested the effects of molecular inhibition of CRP 
      effects on MO activity using antisense oligonucleotide (ASO) to both PKC-alpha and 
      p47phox. METHODS: Prior to administration of human C-reactive protein (hCRP) 
      daily for 3 days, ASO or scrambled ASO to either PKC-alpha or p47phox was also 
      delivered for 3 days and after killing on day 4, peritoneal MOs were isolated. 
      RESULTS: The increase in the levels of superoxide anion, interleukin (IL)-1, 
      monocyte chemoattractant protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha) 
      and IL-6 release in MOs with hCRP compared to human albumin was significantly 
      attenuated by antisense to either PKC-alpha and p47phox (p < 0.01 vs. scrambled ASO; 
      n = 5 per group). CONCLUSION: Our novel data suggest that antisense to either 
      PKC-alpha or p47phox attenuates the pro-inflammatory effects of human CRP on MOs in 
      diabetic rats.
FAU - Jialal, Ishwarlal
AU  - Jialal I
AD  - Laboratory for Atherosclerosis and Metabolic Research, Department of Pathology 
      and Laboratory Medicine, University of California at Davis, Sacramento, CA 95817, 
      USA. ishwarlal.jialal@ucdmc.ucdavis.edu
FAU - Devaraj, Sridevi
AU  - Devaraj S
LA  - eng
GR  - R01 HL074360/HL/NHLBI NIH HHS/United States
GR  - R01-HL074360/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20120716
PL  - England
TA  - Diab Vasc Dis Res
JT  - Diabetes & vascular disease research
JID - 101234011
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Oligoribonucleotides, Antisense)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 11062-77-4 (Superoxides)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 1.6.3.1 (neutrophil cytosolic factor 1)
RN  - EC 2.7.11.13 (Protein Kinase C-alpha)
SB  - IM
MH  - Animals
MH  - C-Reactive Protein/administration & dosage/*metabolism
MH  - Chemokine CCL2/metabolism
MH  - Diabetes Mellitus, Type 1/enzymology/genetics/immunology/*therapy
MH  - Disease Models, Animal
MH  - Genetic Therapy/*methods
MH  - Humans
MH  - Inflammation Mediators/administration & dosage/*metabolism
MH  - Injections, Intraperitoneal
MH  - Interleukin-1/metabolism
MH  - Interleukin-6/metabolism
MH  - Macrophages, Peritoneal/*enzymology/immunology
MH  - Male
MH  - NADPH Oxidases/genetics/*metabolism
MH  - Oligoribonucleotides, Antisense/*administration & dosage
MH  - Protein Kinase C-alpha/genetics/*metabolism
MH  - Rats
MH  - Superoxides/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC3523880
MID - NIHMS426075
COIS- Conflict of interest The authors declare that they have no conflicts of interest.
EDAT- 2012/07/18 06:00
MHDA- 2013/02/13 06:00
PMCR- 2012/12/17
CRDT- 2012/07/18 06:00
PHST- 2012/07/18 06:00 [entrez]
PHST- 2012/07/18 06:00 [pubmed]
PHST- 2013/02/13 06:00 [medline]
PHST- 2012/12/17 00:00 [pmc-release]
AID - 1479164112452165 [pii]
AID - 10.1177/1479164112452165 [doi]
PST - ppublish
SO  - Diab Vasc Dis Res. 2012 Oct;9(4):315-9. doi: 10.1177/1479164112452165. Epub 2012 
      Jul 16.