Procyanidins mitigate osteoarthritis pathogenesis by, at least in part, suppressing vascular endothelial growth factor signaling

Angela Wang, Daniel J. Leong, Zhiyong He, Lin Xu, Lidi Liu, Sun Jin Kim, David M. Hirsh, John A. Hardin, Neil J. Cobelli, Hui (Herb) Sun

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Procyanidins are a family of plant metabolites that have been suggested to mitigate osteoarthritis pathogenesis in mice. However, the underlying mechanism is largely unknown. This study aimed to determine whether procyanidins mitigate traumatic injury-induced osteoarthritis (OA) disease progression, and whether procyanidins exert a chondroprotective effect by, at least in part, suppressing vascular endothelial growth factor signaling. Procyanidins (extracts from pine bark), orally administered to mice subjected to surgery for destabilization of the medial meniscus, significantly slowed OA disease progression. Real-time polymerase chain reaction revealed that procyanidin treatment reduced expression of vascular endothelial growth factor and effectors in OA pathogenesis that are regulated by vascular endothelial growth factor. Procyanidin-suppressed vascular endothelial growth factor expression was correlated with reduced phosphorylation of vascular endothelial growth factor receptor 2 in human OA primary chondrocytes. Moreover, components of procyanidins, procyanidin B2 and procyanidin B3 exerted effects similar to those of total procyanidins in mitigating the OA-related gene expression profile in the primary culture of human OA chondrocytes in the presence of vascular endothelial growth factor. Together, these findings suggest procyanidins mitigate OA pathogenesis, which is mediated, at least in part, by suppressing vascular endothelial growth factor signaling.

Original languageEnglish (US)
Article number2065
JournalInternational Journal of Molecular Sciences
Volume17
Issue number12
DOIs
StatePublished - Dec 9 2016

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Proanthocyanidins
pathogenesis
Osteoarthritis
Vascular Endothelial Growth Factor A
progressions
Chondrocytes
mice
Disease Progression
effectors
polymerase chain reaction
Vascular Endothelial Growth Factor Receptor-2
phosphorylation
Phosphorylation
Tibial Meniscus
metabolites
gene expression
Polymerase chain reaction
destabilization
Metabolites
Intercellular Signaling Peptides and Proteins

Keywords

  • Chondroprotection
  • Nutraceuticals
  • Osteoarthritis
  • Pine bark extract
  • Post-traumatic osteoarthritis
  • Procyanidins
  • VEGF

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Computer Science Applications
  • Spectroscopy
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

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title = "Procyanidins mitigate osteoarthritis pathogenesis by, at least in part, suppressing vascular endothelial growth factor signaling",
abstract = "Procyanidins are a family of plant metabolites that have been suggested to mitigate osteoarthritis pathogenesis in mice. However, the underlying mechanism is largely unknown. This study aimed to determine whether procyanidins mitigate traumatic injury-induced osteoarthritis (OA) disease progression, and whether procyanidins exert a chondroprotective effect by, at least in part, suppressing vascular endothelial growth factor signaling. Procyanidins (extracts from pine bark), orally administered to mice subjected to surgery for destabilization of the medial meniscus, significantly slowed OA disease progression. Real-time polymerase chain reaction revealed that procyanidin treatment reduced expression of vascular endothelial growth factor and effectors in OA pathogenesis that are regulated by vascular endothelial growth factor. Procyanidin-suppressed vascular endothelial growth factor expression was correlated with reduced phosphorylation of vascular endothelial growth factor receptor 2 in human OA primary chondrocytes. Moreover, components of procyanidins, procyanidin B2 and procyanidin B3 exerted effects similar to those of total procyanidins in mitigating the OA-related gene expression profile in the primary culture of human OA chondrocytes in the presence of vascular endothelial growth factor. Together, these findings suggest procyanidins mitigate OA pathogenesis, which is mediated, at least in part, by suppressing vascular endothelial growth factor signaling.",
keywords = "Chondroprotection, Nutraceuticals, Osteoarthritis, Pine bark extract, Post-traumatic osteoarthritis, Procyanidins, VEGF",
author = "Angela Wang and Leong, {Daniel J.} and Zhiyong He and Lin Xu and Lidi Liu and Kim, {Sun Jin} and Hirsh, {David M.} and Hardin, {John A.} and Cobelli, {Neil J.} and Sun, {Hui (Herb)}",
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T1 - Procyanidins mitigate osteoarthritis pathogenesis by, at least in part, suppressing vascular endothelial growth factor signaling

AU - Wang, Angela

AU - Leong, Daniel J.

AU - He, Zhiyong

AU - Xu, Lin

AU - Liu, Lidi

AU - Kim, Sun Jin

AU - Hirsh, David M.

AU - Hardin, John A.

AU - Cobelli, Neil J.

AU - Sun, Hui (Herb)

PY - 2016/12/9

Y1 - 2016/12/9

N2 - Procyanidins are a family of plant metabolites that have been suggested to mitigate osteoarthritis pathogenesis in mice. However, the underlying mechanism is largely unknown. This study aimed to determine whether procyanidins mitigate traumatic injury-induced osteoarthritis (OA) disease progression, and whether procyanidins exert a chondroprotective effect by, at least in part, suppressing vascular endothelial growth factor signaling. Procyanidins (extracts from pine bark), orally administered to mice subjected to surgery for destabilization of the medial meniscus, significantly slowed OA disease progression. Real-time polymerase chain reaction revealed that procyanidin treatment reduced expression of vascular endothelial growth factor and effectors in OA pathogenesis that are regulated by vascular endothelial growth factor. Procyanidin-suppressed vascular endothelial growth factor expression was correlated with reduced phosphorylation of vascular endothelial growth factor receptor 2 in human OA primary chondrocytes. Moreover, components of procyanidins, procyanidin B2 and procyanidin B3 exerted effects similar to those of total procyanidins in mitigating the OA-related gene expression profile in the primary culture of human OA chondrocytes in the presence of vascular endothelial growth factor. Together, these findings suggest procyanidins mitigate OA pathogenesis, which is mediated, at least in part, by suppressing vascular endothelial growth factor signaling.

AB - Procyanidins are a family of plant metabolites that have been suggested to mitigate osteoarthritis pathogenesis in mice. However, the underlying mechanism is largely unknown. This study aimed to determine whether procyanidins mitigate traumatic injury-induced osteoarthritis (OA) disease progression, and whether procyanidins exert a chondroprotective effect by, at least in part, suppressing vascular endothelial growth factor signaling. Procyanidins (extracts from pine bark), orally administered to mice subjected to surgery for destabilization of the medial meniscus, significantly slowed OA disease progression. Real-time polymerase chain reaction revealed that procyanidin treatment reduced expression of vascular endothelial growth factor and effectors in OA pathogenesis that are regulated by vascular endothelial growth factor. Procyanidin-suppressed vascular endothelial growth factor expression was correlated with reduced phosphorylation of vascular endothelial growth factor receptor 2 in human OA primary chondrocytes. Moreover, components of procyanidins, procyanidin B2 and procyanidin B3 exerted effects similar to those of total procyanidins in mitigating the OA-related gene expression profile in the primary culture of human OA chondrocytes in the presence of vascular endothelial growth factor. Together, these findings suggest procyanidins mitigate OA pathogenesis, which is mediated, at least in part, by suppressing vascular endothelial growth factor signaling.

KW - Chondroprotection

KW - Nutraceuticals

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KW - Post-traumatic osteoarthritis

KW - Procyanidins

KW - VEGF

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