Parathyroid hormone ameliorates osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity through p38 <scp>MAPK</scp> signaling

Wang, Yuli; Huang, Lintong; Qin, Ziyue; Yuan, Hua; Li, Bing; Pan, Yongchu; Wang, Xiaoqian; Du, Xin; Hao, Shushu; Du, Yifei; Wang, Ruixia; Shen, Yi

doi:10.1002/iub.2420

Cited by 4 publications

(4 citation statements)

References 44 publications

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“…Mechanistically, PTH activates both the p38 and c-Jun N-terminal kinases-mitogen-activated protein kinases (JNK-MAPK) signaling pathways by upregulating the phosphorylation of their respective subunits. It has been observed that a selective inhibitor targeting either p38 or JNK-MAPK signaling can weaken the effects of PTH on promoting increased osteogenic differentiation in SSCs [ 77 , 78 ]. However, in osteoarthritis (OA) patients, PTH (1-34) has been observed to inhibit the expression of type X collagen (COL10) and stimulate the expression of COL2 in SSCs.…”

Section: The Direct Interactions Of Pth With Bm Cellsmentioning

confidence: 99%

PTH and the Regulation of Mesenchymal Cells within the Bone Marrow Niche

Liu,

Rosen

2024

Cells

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Parathyroid hormone (PTH) plays a pivotal role in maintaining calcium homeostasis, largely by modulating bone remodeling processes. Its effects on bone are notably dependent on the duration and frequency of exposure. Specifically, PTH can initiate both bone formation and resorption, with the outcome being influenced by the manner of PTH administration: continuous or intermittent. In continuous administration, PTH tends to promote bone resorption, possibly by regulating certain genes within bone cells. Conversely, intermittent exposure generally favors bone formation, possibly through transient gene activation. PTH’s role extends to various aspects of bone cell activity. It directly influences skeletal stem cells, osteoblastic lineage cells, osteocytes, and T cells, playing a critical role in bone generation. Simultaneously, it indirectly affects osteoclast precursor cells and osteoclasts, and has a direct impact on T cells, contributing to its role in bone resorption. Despite these insights, the intricate mechanisms through which PTH acts within the bone marrow niche are not entirely understood. This article reviews the dual roles of PTH—catabolic and anabolic—on bone cells, highlighting the cellular and molecular pathways involved in these processes. The complex interplay of these factors in bone remodeling underscores the need for further investigation to fully comprehend PTH’s multifaceted influence on bone health.

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Section: The Direct Interactions Of Pth With Bm Cellsmentioning

confidence: 99%

PTH and the Regulation of Mesenchymal Cells within the Bone Marrow Niche

Liu,

Rosen

2024

Cells

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“…The different glucose concentrations might account for the perplexing findings, which need further investigation. The dephosphorylation of p38 and suppressed p38-MAPK pathway have also been found to correlate with the impaired BMSCs osteogenesis under HG conditions ( 154 ). The potential regulatory of JNK in this process is less well understood.…”

Section: Impaired Bmscs Osteogenesis Under Hg Conditionsmentioning

confidence: 99%

Osteogenesis of bone marrow mesenchymal stem cell in hyperglycemia

Luo

Zhao

2023

Front. Endocrinol.

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Diabetes mellitus (DM) has been shown to be a clinical risk factor for bone diseases including osteoporosis and fragility. Bone metabolism is a complicated process that requires coordinated differentiation and proliferation of bone marrow mesenchymal stem cells (BMSCs). Owing to the regenerative properties, BMSCs have laid a robust foundation for their clinical application in various diseases. However, mounting evidence indicates that the osteogenic capability of BMSCs is impaired under high glucose conditions, which is responsible for diabetic bone diseases and greatly reduces the therapeutic efficiency of BMSCs. With the rapidly increasing incidence of DM, a better understanding of the impacts of hyperglycemia on BMSCs osteogenesis and the underlying mechanisms is needed. In this review, we aim to summarize the current knowledge of the osteogenesis of BMSCs in hyperglycemia, the underlying mechanisms, and the strategies to rescue the impaired BMSCs osteogenesis.

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“…PTH enhances the MSC survival rate by inhibiting their aging and apoptosis ( 81 ) and promotes MSC differentiation toward osteogenesis rather than adipogenesis ( 82 ). In the fight against glucolipotoxicity, PTH can promote osteogenic differentiation of BMSCs by activating the p38 MAPK signaling pathway ( 83 ). Moreover, in vivo studies have shown that human parathyroid hormone ( 1 – 34 ) has a positive effect on bone fracture healing in T2DM ( 84 ).…”

Section: Biochemical Cuesmentioning

confidence: 99%

Challenges to Improve Bone Healing Under Diabetic Conditions

2022

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Diabetes mellitus (DM) can affect bone metabolism and the bone microenvironment, resulting in impaired bone healing. The mechanisms include oxidative stress, inflammation, the production of advanced glycation end products (AGEs), etc. Improving bone healing in diabetic patients has important clinical significance in promoting fracture healing and improving bone integration. In this paper, we reviewed the methods of improving bone healing under diabetic conditions, including drug therapy, biochemical cues, hyperbaric oxygen, ultrasound, laser and pulsed electromagnetic fields, although most studies are in preclinical stages. Meanwhile, we also pointed out some shortcomings and challenges, hoping to provide a potential therapeutic strategy for accelerating bone healing in patients with diabetes.

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Parathyroid hormone ameliorates osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity through p38 MAPK signaling

Cited by 4 publications

References 44 publications

PTH and the Regulation of Mesenchymal Cells within the Bone Marrow Niche

PTH and the Regulation of Mesenchymal Cells within the Bone Marrow Niche

Osteogenesis of bone marrow mesenchymal stem cell in hyperglycemia

Challenges to Improve Bone Healing Under Diabetic Conditions

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