Adiponectin receptors activation performs dual effects on regulating myogenesis and adipogenesis of young and aged muscle satellite cells

Liu, Shibo; Liu, Hanghang; Liu, Yao; Zhang, Ju; Liu, Zhikai; Zheng, Zizhuo; Luo, En

doi:10.1111/cpr.13370

Cited by 6 publications

(1 citation statement)

References 55 publications

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“…For instance, APN signaling stimulates pro-osteogenic and anti‐osteoclastogenic potential of MSCs in young mice [ 60 ]. APN receptor activation improves age-related skeletal muscle dysfunction via the stimulation of aged muscle satellite cells, but shows contrary effect in young muscle satellite cells [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

Adiponectin affects the migration ability of bone marrow-derived mesenchymal stem cells via the regulation of hypoxia inducible factor 1α

Soh

Han

et al. 2023

Cell Commun Signal

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Background Bone marrow (BM) is progressively filled with adipocytes during aging process. Thus, BM adipocytes-derived adiponectin (APN) affects the function of bone marrow-derived mesenchymal stem cells (BMSCs). However, little is known about the effect of APN on migration ability of BMSCs cultured under hypoxic conditions, which is similar to the BM microenvironment. Results We found that the population and migration ability of BMSCs from APN KO mice was higher than that of WT mice due to increased stability of hypoxia inducible factor 1α (HIF1α). Stem cell factor (SCF)-activated STAT3 stimulated the induction of HIF1α which further stimulated SCF production, indicating that the SCF/STAT3/HIF1α positive loop was highly activated in the absence of APN. It implies that APN negatively regulated this positive loop by stimulating HIF1α degradation via the inactivation of GSK3β. Furthermore, APN KO BMSCs were highly migratory toward EL-4 lymphoma, and the interaction between CD44 in BMSCs and hyaluronic acid (HA) from EL-4 enhanced the migration of BMSCs. On the other hand, the migrated BMSCs recruited CD8+ T cells into the EL-4 tumor tissue, resulting in the retardation of tumor growth. Additionally, gradually increased APN in BM on the aging process affects migration and related functions of BMSCs, thus aged APN KO mice showed more significant suppression of EL-4 growth than young APN KO mice due to higher migration and recruitment of CD8+ T cells. Conclusion APN deficiency enhances CD44-mediated migration ability of BMSCs in the hypoxic conditions by the SCF/STAT3/HIF1α positive loop and influences the migration ability of BMSCs for a longer time depending on the aging process.

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Section: Discussionmentioning

confidence: 99%

Adiponectin affects the migration ability of bone marrow-derived mesenchymal stem cells via the regulation of hypoxia inducible factor 1α

Soh

Han

et al. 2023

Cell Commun Signal

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Cytokines and exosomal miRNAs in skeletal muscle–adipose crosstalk

Guo,

Quan,

Pang

et al. 2023

Trends in Endocrinology & Metabolism

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Aging alters the effect of adiponectin receptor signaling on bone marrow‐derived mesenchymal stem cells

Liu,

Zhao,

Liu

et al. 2024

Aging Cell

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Adiponectin receptor signaling represents a promising therapeutic target for age‐related conditions such as osteoporosis and diabetes. However, the literature presents conflicting evidence regarding the role of adiponectin signaling in bone homeostasis and fracture repair across different health states, ages, and disease conditions. These inconsistencies may arise from the complex endocrine and paracrine feedback mechanisms regulating adiponectin, as well as the variability in adiponectin isoforms and receptor expressions. In this study, we observed differential expression of adiponectin receptors in the bone marrow (BM) of aged mice, characterized by elevated levels of adiponectin receptor 2 and reduced levels of receptor 1, as corroborated by both single‐cell sequencing and in vivo staining. Additionally, circulating levels of adiponectin and its local expression were significantly higher in aged mice compared to younger counterparts. Treatment with adiponectin receptor agonist, AdipoRon, enhanced bone regeneration and repair in young mice by promoting osteogenesis and reducing osteoclastogenesis. Conversely, in aged mice, AdipoRon treatment led to cellular senescence, delayed bone repair, and inhibited osteogenic activity. Notably, the adiponectin receptor 1‐Wnt and adiponectin receptor 2‐MAPK and mTOR signaling pathways were differentially activated in AdipoRon‐treated BM mesenchymal stem cells from young and aged mice. Additionally, the NF‐κB, and AKT pathways were consistently downregulated in BM macrophages of both age groups following AdipoRon administration. In conclusion, aging significantly modulates the impact of adiponectin receptor signaling on BM mesenchymal stem cells. This modulation is potentially attributable to changes in receptor transcription and distribution, as well as differential activation of downstream signaling pathways.

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Adiponectin receptors activation performs dual effects on regulating myogenesis and adipogenesis of young and aged muscle satellite cells

Cited by 6 publications

References 55 publications

Adiponectin affects the migration ability of bone marrow-derived mesenchymal stem cells via the regulation of hypoxia inducible factor 1α

Adiponectin affects the migration ability of bone marrow-derived mesenchymal stem cells via the regulation of hypoxia inducible factor 1α

Cytokines and exosomal miRNAs in skeletal muscle–adipose crosstalk

Aging alters the effect of adiponectin receptor signaling on bone marrow‐derived mesenchymal stem cells

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