PMID- 24048733
OWN - NLM
STAT- MEDLINE
DCOM- 20140106
LR  - 20211021
IS  - 1522-1563 (Electronic)
IS  - 0363-6143 (Print)
IS  - 0363-6143 (Linking)
VI  - 305
IP  - 10
DP  - 2013 Nov 15
TI  - Antidicer RNAse activity of monocyte chemotactic protein-induced protein-1 is 
      critical for inducing angiogenesis.
PG  - C1021-32
LID - 10.1152/ajpcell.00203.2013 [doi]
AB  - Inflammatory angiogenesis involves the induction of a novel gene ZC3H12A encoding 
      monocyte chemoattractant protein-1 (MCP-1)-induced protein-1 (MCPIP1) that has 
      deubiquitinase and antidicer RNAse activities. If and how these enzymatic 
      activities of MCPIP1 mediate the biological functions of MCPIP1 are unknown. 
      Present studies with human umbilical vein endothelial cells suggest that 
      MCPIP-induced angiogenesis is mediated via hypoxia-inducible factor (HIF-1alpha), 
      vascular endothelial growth factor (VEGF), and silent information regulator 
      (SIRT-1) induction that results in the inhibition of angiogenesis inhibitor 
      thrombospondin-1. MCPIP1 expression inhibited the production of the 
      antiangiogenic microRNA (miR)-20b and -34a that repress the translation of HIF-1alpha 
      and SIRT-1, respectively. The RNase-dead MCPIP mutant D141N not only did not 
      induce angiogenesis but also failed to inhibit the production of miR-20b and -34a 
      suggesting that the antidicer RNase activity of MCPIP1 is involved in 
      MCPIP-mediated angiogenesis. Mimetics of miR-20b and -34a inhibited 
      MCPIP1-induced angiogenesis confirming that MCPIP1 suppresses the biogenesis of 
      miR-20b and -34a. Furthermore, our results indicate that MCPIP expression induces 
      nuclear translocation of HIF-1alpha. We show that under hypoxia angiogenesis is 
      mediated via induction of MCPIP1 and under normoxia, in vitro, MCPIP 
      deubiquitinates ubiquitinated HIF-1alpha and the stabilized HIF-1alpha enters the nucleus 
      to promote the transcription of its target genes, cyclooxygenase-2 and VEGF, 
      suggesting that the deubiquitinase activity of MCPIP may also promote 
      angiogenesis. The present results show for the first time that the antidicer 
      RNase activity of MCPIP1 is critical in mediating a biological function of MCPIP, 
      namely angiogenesis.
FAU - Roy, Arpita
AU  - Roy A
AD  - Burnett School of Biomedical Sciences, College of Medicine, University of Central 
      Florida, Orlando, Florida.
FAU - Zhang, Miaojun
AU  - Zhang M
FAU - Saad, Yasser
AU  - Saad Y
FAU - Kolattukudy, Pappachan E
AU  - Kolattukudy PE
LA  - eng
GR  - HL-69458/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130918
PL  - United States
TA  - Am J Physiol Cell Physiol
JT  - American journal of physiology. Cell physiology
JID - 100901225
RN  - 0 (Basic Helix-Loop-Helix Leucine Zipper Transcription Factors)
RN  - 0 (HIF1A protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (NF-kappa B)
RN  - 0 (SPZ1 protein, human)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor Ligand Superfamily Member 15)
RN  - EC 3.1.- (Ribonucleases)
RN  - EC 3.1.- (ZC3H12A protein, human)
RN  - EC 3.5.1.- (SIRT1 protein, human)
RN  - EC 3.5.1.- (Sirtuin 1)
SB  - IM
MH  - Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics/metabolism
MH  - Endothelial Cells/*metabolism/physiology
MH  - Gene Expression Regulation/physiology
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/genetics/metabolism
MH  - NF-kappa B/genetics/metabolism
MH  - Ribonucleases/genetics/*metabolism
MH  - Sirtuin 1/genetics/metabolism
MH  - Transcription Factors/genetics/*metabolism
MH  - Tumor Necrosis Factor Ligand Superfamily Member 15/genetics/metabolism
PMC - PMC3840202
OTO - NOTNLM
OT  - HIF-1alpha
OT  - MCPIP1
OT  - SIRT-1
OT  - miR-20b
OT  - miR-34a
EDAT- 2013/09/21 06:00
MHDA- 2014/01/07 06:00
PMCR- 2014/11/15
CRDT- 2013/09/20 06:00
PHST- 2013/09/20 06:00 [entrez]
PHST- 2013/09/21 06:00 [pubmed]
PHST- 2014/01/07 06:00 [medline]
PHST- 2014/11/15 00:00 [pmc-release]
AID - ajpcell.00203.2013 [pii]
AID - C-00203-2013 [pii]
AID - 10.1152/ajpcell.00203.2013 [doi]
PST - ppublish
SO  - Am J Physiol Cell Physiol. 2013 Nov 15;305(10):C1021-32. doi: 
      10.1152/ajpcell.00203.2013. Epub 2013 Sep 18.