Inhibitors of Growth 1b Suppresses Peroxisome Proliferator-Activated Receptor-β/δ Expression Through Downregulation of Hypoxia-Inducible Factor 1α in Osteoblast Differentiation

Qu, Bo; Zhao, Hong; Gong, Kai; Sheng, Jun; Wu, Hong‐Hua; Deng, Song; Huang, Gang; Ma, Zehui; Pan, Xian-Ming

doi:10.1089/dna.2015.3020

Cited by 4 publications

(2 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Observations on the mutual regulation of expression between PPARβ/δ and homeostatic hypoxia inducible factor-1α (HIF-1α) also support this statement [113]. Some natural compounds, such as dioscin (a saponin), and mangiferine (a xanthone glucoside), have up-regulated another isoform, PPARγ in osteoarthritic cartilage and chondrocytes.…”

Section: Metabolic Regulator Pparβ/δ Is a Putative Link Between Omentioning

confidence: 96%

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

Kovács

Vajda

Nagy

2019

IJMS

153

View full text Add to dashboard Cite

Cartilage and the bordering subchondral bone form a functionally active regulatory interface with a prominent role in osteoarthritis pathways. The Wnt and the OPG-RANKL-RANK signaling systems, as key mediators, interact in subchondral bone remodeling. Osteoarthritic osteoblasts polarize into two distinct phenotypes: a low secretory and an activated, pro-inflammatory and anti-resorptive subclass producing high quantities of IL-6, PGE2, and osteoprotegerin, but low levels of RANKL, thus acting as putative effectors of subchondral bone sclerosis. Wnt agonists, Wnt5a, Wisp-1 initiate excessive bone remodeling, while Wnt3a and 5a simultaneously cause loss of proteoglycans and phenotype shift in chondrocytes, with decreased expression of COL2A, aggrecan, and Sox-9. Sclerostin, a Wnt antagonist possesses a protective effect for the cartilage, while DKK-1 inhibits VEGF, suspending neoangiogenesis in the subchondral bone. Experimental conditions mimicking abnormal mechanical load, the pro-inflammatory milieu, but also a decreased OPG/RANKL ratio in the cartilage, trigger chondrocyte apoptosis and loss of the matrix via degradative matrix metalloproteinases, like MMP-13 or MMP-9. Hypoxia, an important cofactor exerts a dual role, promoting matrix synthesis via HIF-1α, a Wnt silencer, but turning on HIF-2α that enhances VEGF and MMP-13, along with aberrant collagen expression and extracellular matrix deterioration in the presence of pro-inflammatory cytokines.

show abstract

Section: Metabolic Regulator Pparβ/δ Is a Putative Link Between Omentioning

confidence: 96%

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

Kovács

Vajda

Nagy

2019

IJMS

153

View full text Add to dashboard Cite

show abstract

“…Notably, Inoue and coworkers have reported the crosstalk of the PPARβ/δ and hypoxia-inducible factor HIF-1α signaling axes in ECs upon hypoxia-induced migration [ 82 ]. During osteoblast differentiation PPARβ/δ is regulated in a HIF-1α-dependent manner [ 83 ]. In addition, PPARβ/δ regulates HIF-1α expression via calcineurin promoter binding [ 84 ].…”

Section: Pparβ/δ Controls Basic Mechanisms Of Wound Healing and Rementioning

confidence: 99%

PPARβ/δ: Linking Metabolism to Regeneration

Magadum

Engel

2018

IJMS

View full text Add to dashboard Cite

In contrast to the general belief that regeneration is a rare event, mainly occurring in simple organisms, the ability of regeneration is widely distributed in the animal kingdom. Yet, the efficiency and extent of regeneration varies greatly. Humans can recover from blood loss as well as damage to tissues like bone and liver. Yet damage to the heart and brain cannot be reversed, resulting in scaring. Thus, there is a great interest in understanding the molecular mechanisms of naturally occurring regeneration and to apply this knowledge to repair human organs. During regeneration, injury-activated immune cells induce wound healing, extracellular matrix remodeling, migration, dedifferentiation and/or proliferation with subsequent differentiation of somatic or stem cells. An anti-inflammatory response stops the regenerative process, which ends with tissue remodeling to achieve the original functional state. Notably, many of these processes are associated with enhanced glycolysis. Therefore, peroxisome proliferator-activated receptor (PPAR) β/δ—which is known to be involved for example in lipid catabolism, glucose homeostasis, inflammation, survival, proliferation, differentiation, as well as mammalian regeneration of the skin, bone and liver—appears to be a promising target to promote mammalian regeneration. This review summarizes our current knowledge of PPARβ/δ in processes associated with wound healing and regeneration.

show abstract

The novel small molecule E0924G dually regulates bone formation and bone resorption through activating the PPARδ signaling pathway to prevent bone loss in ovariectomized rats and senile mice

Li,

Liu,

Han

et al. 2024

Bioorganic Chemistry

View full text Add to dashboard Cite

Inhibitors of Growth 1b Suppresses Peroxisome Proliferator-Activated Receptor-β/δ Expression Through Downregulation of Hypoxia-Inducible Factor 1α in Osteoblast Differentiation

Cited by 4 publications

References 31 publications

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis

PPARβ/δ: Linking Metabolism to Regeneration

The novel small molecule E0924G dually regulates bone formation and bone resorption through activating the PPARδ signaling pathway to prevent bone loss in ovariectomized rats and senile mice

Contact Info

Product

Resources

About