Activation of Protein Kinase G (PKG) Reduces Neointimal Hyperplasia, Inhibits Platelet Aggregation, and Facilitates Re-endothelialization View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-11-11

AUTHORS

Ju-Young Kim, Han-Mo Yang, Joo-Eun Lee, Baek-Kyung Kim, Sooryeonhwa Jin, Jaewon Lee, Kyung-Woo Park, Hyun-Jai Cho, Yoo-Wook Kwon, Hae-Young Lee, Hyun-Jae Kang, Byung-Hee Oh, Young-Bae Park, Hyo-Soo Kim

ABSTRACT

In spite of its great success in reducing restenosis, drug-eluting stent (DES) has unfavorable aspects such as stent thrombosis and delayed re-endothelialization. We examined the effects of PKG activation by Exisulind on neointimal formation, platelet aggregation, and re-endothelialization. Exisulind significantly reduced VSMCs viability, cell cycle progression, migration, and neointimal hyperplasia after vascular injury in rat carotid arteries. Interestingly, in contrast to the effect on VSMC viability, Exisulind did not reduce the viability of endothelial cells. Increased PKG activity by Exisulind inhibited PDGF-stimulated phenotype change of VSMCs from a contractile to a synthetic form. Conversely, the use of PKG inhibitor or gene transfer of dominant-negative PKG reversed the effects of Exisulind, resulting in the increased viability of VSMCs and neointimal formation. In addition, Exisulind facilitated the differentiation of peripheral blood mononuclear cells to endothelial lineage via PKG pathway, while inhibiting to VSMCs lineage, which was correlated with the enhanced re-endothelialization in vivo. Finally, Exisulind reduced platelet aggregation, which was mediated via PKG activation. This study demonstrated that Exisulind inhibits neointimal formation and platelet aggregation while increasing re-endothelialization via PKG pathway. These findings suggest that Exisulind could be a promising candidate drug of DES for the prevention of restenosis without other complications. More... »

PAGES

36979

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep36979

DOI

http://dx.doi.org/10.1038/srep36979

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1010680941

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27833146


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30 schema:description In spite of its great success in reducing restenosis, drug-eluting stent (DES) has unfavorable aspects such as stent thrombosis and delayed re-endothelialization. We examined the effects of PKG activation by Exisulind on neointimal formation, platelet aggregation, and re-endothelialization. Exisulind significantly reduced VSMCs viability, cell cycle progression, migration, and neointimal hyperplasia after vascular injury in rat carotid arteries. Interestingly, in contrast to the effect on VSMC viability, Exisulind did not reduce the viability of endothelial cells. Increased PKG activity by Exisulind inhibited PDGF-stimulated phenotype change of VSMCs from a contractile to a synthetic form. Conversely, the use of PKG inhibitor or gene transfer of dominant-negative PKG reversed the effects of Exisulind, resulting in the increased viability of VSMCs and neointimal formation. In addition, Exisulind facilitated the differentiation of peripheral blood mononuclear cells to endothelial lineage via PKG pathway, while inhibiting to VSMCs lineage, which was correlated with the enhanced re-endothelialization in vivo. Finally, Exisulind reduced platelet aggregation, which was mediated via PKG activation. This study demonstrated that Exisulind inhibits neointimal formation and platelet aggregation while increasing re-endothelialization via PKG pathway. These findings suggest that Exisulind could be a promising candidate drug of DES for the prevention of restenosis without other complications.
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38 Increased PKG activity
39 PDGF-stimulated phenotype change
40 PKG activation
41 PKG activity
42 PKG inhibitor
43 PKG pathway
44 Re-Endothelialization
45 VSMC
46 VSMC viability
47 VSMCs lineage
48 VSMCs viability
49 activation
50 activity
51 addition
52 aggregation
53 artery
54 aspects
55 blood mononuclear cells
56 candidate drugs
57 carotid artery
58 cell cycle progression
59 cells
60 changes
61 complications
62 contractile
63 contrast
64 cycle progression
65 differentiation
66 dominant-negative PKG
67 drug-eluting stents
68 drugs
69 effect
70 effects of exisulind
71 endothelial cells
72 endothelial lineage
73 exisulind
74 findings
75 form
76 formation
77 gene transfer
78 great success
79 hyperplasia
80 inhibitors
81 inhibits platelet aggregation
82 injury
83 kinase G
84 lineages
85 migration
86 mononuclear cells
87 neointimal formation
88 neointimal hyperplasia
89 pathway
90 peripheral blood mononuclear cells
91 phenotype changes
92 platelet aggregation
93 prevention
94 prevention of restenosis
95 progression
96 promising candidate drug
97 protein kinase G
98 rat carotid artery
99 restenosis
100 spite
101 stent thrombosis
102 stents
103 study
104 success
105 synthetic form
106 thrombosis
107 transfer
108 unfavorable aspects
109 use
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