Osteostatin improves the Osteogenic differentiation of mesenchymal stem cells and enhances angiogenesis through HIF-1α under hypoxia conditions in vitro

Wu, Dongjin; Liu, Liyan; Fu, Sheng-Long; Zhang, Jun

doi:10.1016/j.bbrc.2022.02.085

Cited by 8 publications

(6 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, hypoxia signals increase the number of Type H vessels and enhance endochondral angiogenesis and osteogenesis [ 150 ]. Osteostatin (OST), mainly expressed in bone marrow, induces BMSCs osteogenic differentiation and promotes the proliferation, migration, and angiogenesis of Type H ECs via the HIF-1α/VEGF pathway under hypoxia conditions [ 153 , 154 ]. These results suggest that HIF-1α/VEGF pathway regulates angiogenesis and osteogenesis by connecting Type H ECs and osteoblasts in the skeletal system ( Figure 4 ).…”

Section: Hif-1α/vegf Pathway Regulates Type H Vessels Coupling Of Ang...mentioning

confidence: 99%

HIF-1α Regulates Bone Homeostasis and Angiogenesis, Participating in the Occurrence of Bone Metabolic Diseases

Tang

et al. 2022

Cells

View full text Add to dashboard Cite

In the physiological condition, the skeletal system’s bone resorption and formation are in dynamic balance, called bone homeostasis. However, bone homeostasis is destroyed under pathological conditions, leading to the occurrence of bone metabolism diseases. The expression of hypoxia-inducible factor-1α (HIF-1α) is regulated by oxygen concentration. It affects energy metabolism, which plays a vital role in preventing bone metabolic diseases. This review focuses on the HIF-1α pathway and describes in detail the possible mechanism of its involvement in the regulation of bone homeostasis and angiogenesis, as well as the current experimental studies on the use of HIF-1α in the prevention of bone metabolic diseases. HIF-1α/RANKL/Notch1 pathway bidirectionally regulates the differentiation of macrophages into osteoclasts under different conditions. In addition, HIF-1α is also regulated by many factors, including hypoxia, cofactor activity, non-coding RNA, trace elements, etc. As a pivotal pathway for coupling angiogenesis and osteogenesis, HIF-1α has been widely studied in bone metabolic diseases such as bone defect, osteoporosis, osteonecrosis of the femoral head, fracture, and nonunion. The wide application of biomaterials in bone metabolism also provides a reasonable basis for the experimental study of HIF-1α in preventing bone metabolic diseases.

show abstract

Section: Hif-1α/vegf Pathway Regulates Type H Vessels Coupling Of Ang...mentioning

confidence: 99%

HIF-1α Regulates Bone Homeostasis and Angiogenesis, Participating in the Occurrence of Bone Metabolic Diseases

Tang

et al. 2022

Cells

View full text Add to dashboard Cite

show abstract

“…HIF-1α protein is steady under hypoxic conditions and activates transcription of multiple genes involved in glycolysis, fatty acid metabolism, mitochondrial metabolism, and cell cycle regulation (45). Stem cells or progenitor cells of some organs are relatively hypoxic and maintain their normal physiological functions by stabilizing the HIF-1α subunit (46). In 2012, researchers found that hypoxia promoted cardiomyocyte dedifferentiation and myocardial regeneration in adult zebrafish, and HIF-1α played the important role in this (19).…”

Section: Hypoxia Regulates Metabolic Reprograming To Promote Cardiac ...mentioning

confidence: 99%

Metabolic Regulation of Cardiac Regeneration

Duan

Liu²,

Zhan

2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

The mortality due to heart diseases remains highest in the world every year, with ischemic cardiomyopathy being the prime cause. The irreversible loss of cardiomyocytes following myocardial injury leads to compromised contractility of the remaining myocardium, adverse cardiac remodeling, and ultimately heart failure. The hearts of adult mammals can hardly regenerate after cardiac injury since adult cardiomyocytes exit the cell cycle. Nonetheless, the hearts of early neonatal mammals possess a stronger capacity for regeneration. To improve the prognosis of patients with heart failure and to find the effective therapeutic strategies for it, it is essential to promote endogenous regeneration of adult mammalian cardiomyocytes. Mitochondrial metabolism maintains normal physiological functions of the heart and compensates for heart failure. In recent decades, the focus is on the changes in myocardial energy metabolism, including glucose, fatty acid, and amino acid metabolism, in cardiac physiological and pathological states. In addition to being a source of energy, metabolites are becoming key regulators of gene expression and epigenetic patterns, which may affect heart regeneration. However, the myocardial energy metabolism during heart regeneration is majorly unknown. This review focuses on the role of energy metabolism in cardiac regeneration, intending to shed light on the strategies for manipulating heart regeneration and promoting heart repair after cardiac injury.

show abstract

“…PTHrP can be post-translationally processed to generate several bioactive fragments: an N-terminal fragment (aa 1–36), containing a sequence that activates parathyroid hormone receptor type 1 (PTH1R); three mid-region fragments, involved in calcium mobilization; and a C-terminal fragment (aa 107–139) [ 7 , 8 , 9 ]. The highly conserved C-terminal region, specifically the penta-peptide sequence Thr-Arg-Ser-Ala-Trp (aa 107–111), known as osteostatin, has been documented to induce bone anabolism and the activation of vascular endothelial growth [ 10 ], osteogenic differentiation of mesenchymal stem cells [ 11 ], and enhancement of bone regeneration in rat and rabbit models of bone defects [ 12 , 13 ] independently of PTH1R activation. Both the N- and C-terminal domains of PTHrP have been shown to provide protection against the production of reactive oxygen species (ROS) induced by the oxidative stress agent H 2 O 2 in both murine and human osteoblastic cells [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Osteostatin Mitigates Gouty Arthritis through the Inhibition of Caspase-1 Activation and Upregulation of Nrf2 Expression

Catalán,

Carceller,

Terencio

et al. 2024

IJMS

View full text Add to dashboard Cite

Gouty arthritis results from monosodium urate (MSU) crystal deposition in joints, initiating (pro)-interleukin (IL)-1β maturation, inflammatory mediator release, and neutrophil infiltration, leading to joint swelling and pain. Parathyroid hormone-related protein (107–111) C-terminal peptide (osteostatin) has shown anti-inflammatory properties in osteoblasts and collagen-induced arthritis in mice, but its impact in gouty arthritis models remains unexplored. We investigated the effect of osteostatin on pyroptosis, inflammation, and oxidation in macrophages, as well as its role in the formation of calcium pyrophosphate dihydrate crystals and MSU-induced gouty arthritis in mice models. Osteostatin ameliorated pyroptosis induced by lipopolysaccharide and adenosine 5′-triphosphate (LPS + ATP) in mice peritoneal macrophages by reducing the expression of caspase-1, lactate dehydrogenase release, and IL-1β and IL-18 secretion. Additionally, IL-6 and tumor necrosis factor-α (TNF-α) were also decreased due to the reduced activation of the NF-κB pathway. Furthermore, osteostatin displayed antioxidant properties in LPS + ATP-stimulated macrophages, resulting in reduced production of mitochondrial and extracellular reactive oxygen species and enhanced Nrf2 translocation to the nuclei. In both models of gouty arthritis, osteostatin administration resulted in reduced pro-inflammatory cytokine production, decreased leukocyte migration, and reduced caspase-1 and NF-κB activation. These results highlight the potential of osteostatin as a therapeutic option for gouty arthritis.

show abstract

Osteostatin improves the Osteogenic differentiation of mesenchymal stem cells and enhances angiogenesis through HIF-1α under hypoxia conditions in vitro

Cited by 8 publications

References 37 publications

HIF-1α Regulates Bone Homeostasis and Angiogenesis, Participating in the Occurrence of Bone Metabolic Diseases

HIF-1α Regulates Bone Homeostasis and Angiogenesis, Participating in the Occurrence of Bone Metabolic Diseases

Metabolic Regulation of Cardiac Regeneration

Osteostatin Mitigates Gouty Arthritis through the Inhibition of Caspase-1 Activation and Upregulation of Nrf2 Expression

Contact Info

Product

Resources

About