Pioglitazone Ameliorates Smooth Muscle Cell Proliferation in Cuff-Induced Neointimal Formation by Both Adiponectin-Dependent and -Independent Pathways View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-10-05

AUTHORS

Tetsuya Kubota, Naoto Kubota, Hiroyuki Sato, Mariko Inoue, Hiroki Kumagai, Tomokatsu Iwamura, Iseki Takamoto, Tsuneo Kobayashi, Masao Moroi, Yasuo Terauchi, Kazuyuki Tobe, Kohjiro Ueki, Takashi Kadowaki

ABSTRACT

The aim of this study is to elucidate to what degree adiponectin is involved in TZD-mediated amelioration of neointimal formation. We investigated the effect of 3- or 8-weeks’ pioglitazone on cuff-induced neointimal formation in adiponectin-deficient (APN-KO) and wild-type (WT) mice. Pioglitazone for 3 weeks reduced neointimal formation in the WT mice with upregulation of the plasma adiponectin levels, but failed to reduce neointimal formation in the APN-KO mice, suggesting that pioglitazone suppressed neointimal formation by adiponectin-dependent mechanisms. Pioglitazone for 3 weeks suppressed vascular smooth muscle cell (VSMC) proliferation and increased AdipoR2 expression in the WT mice. In vitro, globular adiponectin activated AMPK through both AdipoR1 and AdipoR2, resulting in the inhibition of VSMC proliferation. Interestingly, 8-weeks’ pioglitazone was reduced neointimal formation in APN-KO mice to degree similar to that seen in the WT mice, suggesting that pioglitazone can also suppress neointimal formation via a mechanism independent of adiponectin. Pioglitazone for 8 weeks completely abrogated the increased VSMC proliferation, along with a reduction of cyclin B1 and cyclin D1 expressions and cardiovascular risk profile in the APN-KO mice. In vitro, pioglitazone suppressed these expressions, leading to inhibition of VSMC proliferation. Pioglitazone suppresses neointimal formation via both adiponectin-dependent and adiponectin-independent mechanisms. More... »

PAGES

34707

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep34707

DOI

http://dx.doi.org/10.1038/srep34707

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1044916954

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27703271


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25 schema:description The aim of this study is to elucidate to what degree adiponectin is involved in TZD-mediated amelioration of neointimal formation. We investigated the effect of 3- or 8-weeks’ pioglitazone on cuff-induced neointimal formation in adiponectin-deficient (APN-KO) and wild-type (WT) mice. Pioglitazone for 3 weeks reduced neointimal formation in the WT mice with upregulation of the plasma adiponectin levels, but failed to reduce neointimal formation in the APN-KO mice, suggesting that pioglitazone suppressed neointimal formation by adiponectin-dependent mechanisms. Pioglitazone for 3 weeks suppressed vascular smooth muscle cell (VSMC) proliferation and increased AdipoR2 expression in the WT mice. In vitro, globular adiponectin activated AMPK through both AdipoR1 and AdipoR2, resulting in the inhibition of VSMC proliferation. Interestingly, 8-weeks’ pioglitazone was reduced neointimal formation in APN-KO mice to degree similar to that seen in the WT mice, suggesting that pioglitazone can also suppress neointimal formation via a mechanism independent of adiponectin. Pioglitazone for 8 weeks completely abrogated the increased VSMC proliferation, along with a reduction of cyclin B1 and cyclin D1 expressions and cardiovascular risk profile in the APN-KO mice. In vitro, pioglitazone suppressed these expressions, leading to inhibition of VSMC proliferation. Pioglitazone suppresses neointimal formation via both adiponectin-dependent and adiponectin-independent mechanisms.
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32 APN-KO mice
33 AdipoR1
34 AdipoR2
35 AdipoR2 expression
36 B1
37 D1 expression
38 TZDs
39 VSMC proliferation
40 WT mice
41 adiponectin
42 adiponectin levels
43 adiponectin-dependent mechanism
44 aim
45 amelioration
46 cardiovascular risk profile
47 cell proliferation
48 cuff
49 cyclin B1
50 cyclin D1 expression
51 effect
52 expression
53 formation
54 globular adiponectin
55 independent pathways
56 inhibition
57 levels
58 mechanism
59 mice
60 muscle cell proliferation
61 neointimal formation
62 pathway
63 pioglitazone
64 plasma adiponectin levels
65 profile
66 proliferation
67 reduction
68 risk profile
69 smooth muscle cell proliferation
70 study
71 upregulation
72 vascular smooth muscle cell proliferation
73 weeks
74 wild-type mice
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