Adipose tissue, angiogenesis and angio-MIR under physiological and pathological conditions

Stefano, Anna Barbara Di; Massihnia, Daniela; Grisafi, Federica; Castiglia, Marta; Toia, Francesca; Montesano, Luigi; Russo, Antonio; Moschella, Francesco; Cordova, Adriana

doi:10.1016/j.ejcb.2018.11.005

Cited by 20 publications

(16 citation statements)

References 151 publications

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“…We posit that AdECs, as major initiators, effectors, and regulators of metabolic stress, might be a central determinant of unhealthy AT growth. Some metabolites, proteins, miRNAs serve as messengers in the communication between adipocytes and AdECs [ 103–108 ]. Recently, one surprising discovery revealed that extracellular vesicles might be carriers of the above-mentioned signal molecules derived from AdECs, which then target adipocytes to adapt to metabolic statues [ 109 ].…”

Section: Discussionmentioning

confidence: 99%

Adipose endothelial cells mastering adipose tissues metabolic fate

Liao

Ran

et al. 2022

Adipocyte

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Dynamic communication within adipose tissue depends on highly vascularized structural characteristics to maintain systemic metabolic homoeostasis. Recently, it has been noted that adipose endothelial cells (AdECs) act as essential bridges for biological information transmission between adipose-resident cells. Hence, paracrine regulators that mediate crosstalk between AdECs and adipose stromal cells were summarized. We also highlight the importance of AdECs to maintain adipocytes metabolic homoeostasis by regulating insulin sensitivity, lipid turnover and plasticity. The differential regulation of AdECs in adipose plasticity often depends on vascular density and metabolic states. Although choosing pro-angiogenic or anti-angiogenic therapies for obesity is still a matter of debate in clinical settings, the growing numbers of drugs have been confirmed to play an anti-obesity effect by affecting vascularization. Pharmacologic angiogenesis intervention has great potential as therapeutic strategies for obesity.

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Section: Discussionmentioning

confidence: 99%

Adipose endothelial cells mastering adipose tissues metabolic fate

Liao

Ran

et al. 2022

Adipocyte

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“…As mentioned above, recent evidences highlighted a role of miRNAs in angiogenesis. Among the others, miR126 controls angiogenesis and regulates the formation and maintenance of new vessels ( 21 ) by targeting 3’UTR mRNAs of SPRED1 and PIK3R2, both negative regulators of the VEGF pathway ( 23 , 60 ). Here, we report, for the first time, that the administration of T2, through the regulation of miR126, can preserve the physiological angiogenesis and the vascular integrity in condition of increased fat mass and inflammation by regulating the above-mentioned genes.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the stimulation of an unhealthy angiogenesis leads to an increased nutrient intake into the adipocytes and recruitment of inflammation mediators at the tissue level. In this way, a vicious circle is established in which the activation of angiogenesis determines a further increase in adipocyte volume and, subsequently, an increase in the inflammatory state of adipose tissue ( 21 ). Many molecules have been implicated as positive regulators of angiogenesis, among them vascular endothelial growth factor (VEGF) is a pivotal angiogenic factor ( 22 ).…”

Section: Introductionmentioning

confidence: 99%

3,5-Diiodo-L-Thyronine (T2) Administration Affects Visceral Adipose Tissue Inflammatory State in Rats Receiving Long-Lasting High-Fat Diet

et al. 2021

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3,5-diiodo-thyronine (T2), an endogenous metabolite of thyroid hormones, exerts beneficial metabolic effects. When administered to overweight rats receiving a high fat diet (HFD), it significantly reduces body fat accumulation, which is a risk factor for the development of an inflammatory state and of related metabolic diseases. In the present study, we focused our attention on T2 actions aimed at improving the adverse effects of long-lasting HFD such as the adipocyte inflammatory response. For this purpose, three groups of rats were used throughout: i) receiving a standard diet for 14 weeks; ii) receiving a HFD for 14 weeks, and iii) receiving a HFD for 14 weeks with a simultaneous daily injection of T2 for the last 4 weeks. The results showed that T2 administration ameliorated the expression profiles of pro- and anti-inflammatory cytokines, reduced macrophage infiltration in white adipose tissue, influenced their polarization and reduced lymphocytes recruitment. Moreover, T2 improved the expression of hypoxia markers, all altered in HFD rats, and reduced angiogenesis by decreasing the pro-angiogenic miR126 expression. Additionally, T2 reduced the oxidative damage of DNA, known to be associated to the inflammatory status. This study demonstrates that T2 is able to counteract some adverse effects caused by a long-lasting HFD and to produce beneficial effects on inflammation. Irisin and SIRT1 pathway may represent a mechanism underlying the above described effects.

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“…In this study, we focused on the functions of miR-486 on osteogenesis. Previously, miR-486 have been known as a tumor suppressor and were found decreased in several cancers such as lung cancer, gastric adenocarcinoma and so on [29][30][31]. Apart from the effects in carcinogenesis, miR-486 is an important content in extracellular vehicles (EVs).…”

Section: Discussionmentioning

confidence: 99%

MiR-486-3p promotes osteogenic differentiation of BMSCs by targeting CTNNBIP1 and activating Wnt/β-catenin pathway

Zhang

Jiang

et al. 2021

Preprint

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Background Dysfunction in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) leads to bone loss/osteoporosis. CTNNBIP1 (Catenin beta interacting protein 1) is an inhibitor of Wnt/β-catenin signaling, whose role in osteogenesis remains elusive. This study aims to reveal the effects of miR-486-3p/CTNNBIP1 in osteogenesis. Methods Bone marrow samples from control and osteoporosis patients were collected and ovariectomy was performed on mice and levels of CTNNBIP1 and miR-486-3p levels were assessed. Dual-luciferase reporter assay was used to confirm their interactions. MiR-486-3p mimics/inhibitor or CTNNBIP1 overexpression lentivirus were transfected in human BMSCs (hBMSCs) and then osteogenic assay was performed. Alizarin red S (ARS) and Alkaline phosphatase (ALP) intensity with osteogenic gene expression including Runx2, Alp, Bglap and OCN was measured. Key proteins in Wnt/β-catenin pathway including active β-catenin, Bcl-2 and Cyclin D1 were assessed. Results CTNNBIP1, an inhibitor of Wnt/β-catenin signaling was upregulated while miR-486-3p was downregulated in ovariectomized (OVX) mice. CTNNBIP1 was confirmed as a target of miR-486-3p. MiR-486-3p overexpression promoted but miR-486-3p knockdown suppressed osteogenic differentiation and Wnt/β-catenin pathway. Rescue experiments further elucidated that the negative effects of CTNNBIP1 overexpression on osteoblastic differentiation and canonical Wnt signaling could be reversed by miR-486-3p mimics. Conclusion This study demonstrated that miR-486-3p sponges CTNNBIP1 thus activating Wnt/β-catenin signaling pathway to promote osteogenesis of BMSCs.

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Adipose tissue, angiogenesis and angio-MIR under physiological and pathological conditions

Cited by 20 publications

References 151 publications

Adipose endothelial cells mastering adipose tissues metabolic fate

Adipose endothelial cells mastering adipose tissues metabolic fate

3,5-Diiodo-L-Thyronine (T2) Administration Affects Visceral Adipose Tissue Inflammatory State in Rats Receiving Long-Lasting High-Fat Diet

MiR-486-3p promotes osteogenic differentiation of BMSCs by targeting CTNNBIP1 and activating Wnt/β-catenin pathway

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