PMID- 24008336
OWN - NLM
STAT- MEDLINE
DCOM- 20131223
LR  - 20211021
IS  - 1521-0103 (Electronic)
IS  - 0022-3565 (Print)
IS  - 0022-3565 (Linking)
VI  - 347
IP  - 2
DP  - 2013 Nov
TI  - MCP-1-induced protein promotes endothelial-like and angiogenic properties in 
      human bone marrow monocytic cells.
PG  - 288-97
LID - 10.1124/jpet.113.207316 [doi]
AB  - Monocytic cells enhance neovascularization by releasing proangiogenic mediators 
      and/or by transdifferentiating into endothelial-like cells. However, the 
      mechanisms that govern this transdifferentiation process are largely unknown. 
      Recently, monocyte chemotactic protein-1 (MCP-1)-induced protein (MCPIP) has been 
      identified as a novel CCCH-type zinc-finger protein expressed primarily in 
      monocytic cells. Here, we analyzed whether MCPIP might exert angiogenic effects 
      by promoting differentiation of monocytic cells into endothelial cell (EC)-like 
      phenotype. The expression of MCPIP increased during MCP-1-induced 
      transdifferentiation in human bone marrow mononuclear cells (BMNCs). Knockdown of 
      MCPIP with small interfering RNA (siRNA) abolished MCP-1-induced expression of EC 
      markers Flk-1 and Tie-2 in human BMNCs. BMNCs transfected with MCPIP expression 
      vector displayed EC-like morphology accompanied by downregulation of monocytic 
      markers CD14 and CD11b, upregulation of EC markers Flk-1 and Tie-2, induction of 
      cadherin (cdh)-12 and -19, activation of endoplasmic reticulum (ER) stress, and 
      autophagy. Knockdown of cdh-12 or cdh-19 markedly inhibited MCPIP-induced 
      enhancement of cell attachment and EC-marker expression. Inhibition of ER stress 
      by tauroursodeoxycholate abolished MCPIP-induced expression of EC markers. 
      Inhibition of autophagy by knockdown of Beclin-1 with siRNA or by an autophagy 
      inhibitor 3'-methyladenine inhibited MCPIP-induced expression of EC markers. 
      Expression of MCPIP in BMNCs enhanced uptake of acetylated low-density 
      lipoprotein (acLDL), formation of EC-colony, incorporation of cells into 
      capillary-like structure on Matrigel, and exhibited increased neovascularization 
      in the ischemic hindlimb in mice. These results demonstrate that MCPIP may be an 
      important regulator of inflammatory angiogenesis and provide novel mechanistic 
      insights into the link between MCP-1 and cardiovascular diseases.
FAU - Niu, Jianli
AU  - Niu J
AD  - Burnett School of Biomedical Sciences, College of Medicine, University of Central 
      Florida, Orlando, Florida (J N., O.Z., Y.S., P.E.K.); Department of 
      Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, 
      Hunan, People's Republic of China (K.W.).
FAU - Wang, Kangkai
AU  - Wang K
FAU - Zhelyabovska, Olga
AU  - Zhelyabovska O
FAU - Saad, Yasser
AU  - Saad Y
FAU - Kolattukudy, Pappachan E
AU  - Kolattukudy PE
LA  - eng
GR  - R01 HL069458/HL/NHLBI NIH HHS/United States
GR  - R56 HL069458/HL/NHLBI NIH HHS/United States
GR  - HL69458/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130905
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Cytokines)
RN  - 0 (Drug Combinations)
RN  - 0 (Laminin)
RN  - 0 (Proteoglycans)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Transcription Factors)
RN  - 119978-18-6 (matrigel)
RN  - 9007-34-5 (Collagen)
RN  - EC 3.1.- (Ribonucleases)
RN  - EC 3.1.- (ZC3H12A protein, human)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Cell Culture Techniques
MH  - Cell Line
MH  - Cell Transdifferentiation/*physiology
MH  - Cell Transplantation
MH  - Collagen
MH  - Cytokines/immunology
MH  - Drug Combinations
MH  - Endothelial Cells/cytology/*metabolism
MH  - Endothelium, Vascular/immunology/*metabolism
MH  - Hindlimb/blood supply
MH  - Humans
MH  - Ischemia/therapy
MH  - Laminin
MH  - Mice
MH  - Monocytes/cytology/*metabolism/transplantation
MH  - *Neovascularization, Physiologic/immunology
MH  - Proteoglycans
MH  - RNA, Small Interfering/genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Ribonucleases
MH  - Transcription Factors/genetics/*physiology
PMC - PMC3807059
EDAT- 2013/09/07 06:00
MHDA- 2013/12/24 06:00
PMCR- 2014/11/01
CRDT- 2013/09/07 06:00
PHST- 2013/09/07 06:00 [entrez]
PHST- 2013/09/07 06:00 [pubmed]
PHST- 2013/12/24 06:00 [medline]
PHST- 2014/11/01 00:00 [pmc-release]
AID - jpet.113.207316 [pii]
AID - JPET_207316 [pii]
AID - 10.1124/jpet.113.207316 [doi]
PST - ppublish
SO  - J Pharmacol Exp Ther. 2013 Nov;347(2):288-97. doi: 10.1124/jpet.113.207316. Epub 
      2013 Sep 5.