Fragmented Adipose Tissue Transplanted to Craniofacial Deformities Induces Bone Repair Associated with Immunoexpression of Adiponectin and Parathyroid Hormone 1-Receptor

2013 ◽  
Vol 50 (6) ◽  
pp. 639-647 ◽  
Author(s):  
Ranulfo Duarte Azevedo-Neto ◽  
Carla Castiglia Gonzaga ◽  
Tatiana Miranda Deliberador ◽  
Luiz Gustavo Klug ◽  
Lidiane Da Costa Oliveira ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Parathyroid Hormone ◽  
Bone Repair ◽  
Parathyroid Hormone 1 Receptor

scholarly journals Extracellular vesicles-released parathyroid hormone-related protein from Lewis lung carcinoma induces lipolysis and adipose tissue browning in cancer cachexia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenjun Hu ◽  
Hairong Xiong ◽  
Zeyuan Ru ◽  
Yan Zhao ◽  
Yali Zhou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Parathyroid Hormone ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Cancer Cachexia ◽  
Lewis Lung ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Tissue Browning

AbstractCancer cachexia is a metabolic disorder characterized by skeletal muscle wasting and white adipose tissue browning. Specific functions of several hormones, growth factors, and cytokines derived from tumors can trigger cachexia. Moreover, adipose tissue lipolysis might explain weight loss that occurs owing to cachexia. Extracellular vesicles (EVs) are involved in intercellular communication. However, whether EVs participate in lipolysis induced by cancer cachexia has not been thoroughly investigated. Using Lewis lung carcinoma (LLC) cell culture, we tested whether LLC cell-derived EVs can induce lipolysis in 3T3-L1 adipocytes. EVs derived from LLC cells were isolated and characterized biochemically and biophysically. Western blotting and glycerol assay were used to study lipolysis. LLC cell-derived EVs induced lipolysis in vivo and vitro. EVs fused directly with target 3T3-L1 adipocytes and transferred parathyroid hormone-related protein (PTHrP), activating the PKA signaling pathway in 3T3-L1 adipocytes. Blocking PTHrP activity in LLC-EVs using a neutralizing antibody and by knocking down PTHR expression prevented lipolysis in adipocytes. Inhibiting the PKA signaling pathway also prevents the lipolytic effects of EVs. In vivo, suppression of LLC-EVs release by knocking down Rab27A alleviated white adipose tissue browning and lipolysis. Our data showed that LLC cell-derived EVs induced adipocyte lipolysis via the extracellular PTHrP-mediated PKA pathway. Our data demonstrate that LLC-EVs induce lipolysis in vitro and vivo by delivering PTHrP, which interacts with PTHR. The lipolytic effect of LLC-EVs was abrogated by PTHR knockdown and treatment with a neutralizing anti-PTHrP antibody. Together, these data show that LLC-EV-induced lipolysis is mediated by extracellular PTHrP. These findings suggest a novel mechanism of lipid droplet loss and identify a potential therapeutic strategy for cancer cachexia.

Effect of cell therapy with osteoblasts differentiated from bone marrow or adipose tissue stromal cells on bone repair

2019 ◽  
Vol 14 (12) ◽  
pp. 1107-1119 ◽  
Author(s):  
Gileade P Freitas ◽  
Helena B Lopes ◽  
Alann T P Souza ◽  
Paula G F P Oliveira ◽  
Adriana L G Almeida ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Adipose Tissue ◽  
Cell Therapy ◽  
Bone Formation ◽  
Bone Tissue ◽  
Stromal Cells ◽  
Bone Repair ◽  
Calvarial Bone ◽  
Adipose Tissue Stromal Cells ◽  
Phosphate Buffered Saline

Aim: The aim of this study was to investigate the effect of local injection of osteoblasts differentiated from bone marrow (BM-OB) or adipose tissue (AT-OB) mesenchymal stromal cells on bone tissue formation. Materials & methods: Defects were created in rat calvaria and injected with BM-OB or AT-OB and phosphate-buffered saline without cells were injected as control. Bone formation was evaluated 4 weeks postinjection. Results: Injection of BM-OB or AT-OB resulted in higher bone formation than that obtained with control. The bone tissue induced by cell injections exhibited similar mechanical properties as those of pristine calvarial bone, and its molecular cues suggested the occurrence of a remodeling process. Conclusion: Results of this study demonstrated that cell therapy with osteoblasts induced significant bone formation that exhibited the same quality as that of pre-existent bone.

scholarly journals Small Molecule Inhibition of the Na+/H+ Exchange Regulatory Factor 1 and Parathyroid Hormone 1 Receptor Interaction

Biochemistry ◽  
2014 ◽  
Vol 53 (37) ◽  
pp. 5916-5922 ◽  
Author(s):  
Jeremy M. Fitzpatrick ◽  
Maria Pellegrini ◽  
Patrick R. Cushing ◽  
Dale F. Mierke
Keyword(s):  
Parathyroid Hormone ◽  
Small Molecule ◽  
Receptor Interaction ◽  
Regulatory Factor ◽  
Small Molecule Inhibition ◽  
Parathyroid Hormone 1 Receptor

Parathyroid Hormone Senses Extracellular Calcium To Modulate Endocrine Signaling upon Binding to the Family B GPCR Parathyroid Hormone 1 Receptor

2018 ◽  
Vol 13 (8) ◽  
pp. 2347-2358 ◽  
Author(s):  
Kelly J. Culhane ◽  
Morgan E. Belina ◽  
Jeremiah N. Sims ◽  
Yingying Cai ◽  
Yuting Liu ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Extracellular Calcium ◽  
The Family ◽  
Parathyroid Hormone 1 Receptor ◽  
Endocrine Signaling

Parathyroid hormone receptor stimulation induces human adipocyte lipolysis and browning

2021 ◽  
Vol 184 (5) ◽  
pp. 687-697
Author(s):  
Peter Breining ◽  
Steen B Pedersen ◽  
Mads Kjolby ◽  
Jacob B Hansen ◽  
Niels Jessen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Parathyroid Hormone ◽  
Receptor Gene ◽  
Receptor Expression ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Cell Models ◽  
Receptor Stimulation ◽  
Receptor Gene Expression

Objective Activation of brown adipose tissue is a promising strategy to treat and prevent obesity and obesity-related disorders. Activation of uncoupling protein 1 (UCP1) leads to uncoupled respiration and dissipation of stored energy as heat. Induction of UCP1-rich adipocytes in white adipose tissue, a process known as ‘browning’, serves as an alternative strategy to increase whole body uncoupling capacity. Here, we aim to assess the association between parathyroid hormone (PTH) receptor expression and UCP1 expression in human adipose tissues and to study PTH effects on human white and brown adipocyte lipolysis and UCP1 expression. Design A descriptive study of human neck adipose tissue biopsies substantiated by an interventional study on human neck-derived adipose tissue cell models. Methods Thermogenic markers and PTH receptor gene expression are assessed in human neck adipose tissue biopsies and are related to individual health records. PTH-initiated lipolysis and thermogenic gene induction are assessed in cultured human white and brown adipocyte cell models. PTH receptor involvement is investigated by PTH receptor silencing. Results PTH receptor gene expression correlates with UCP1 gene expression in the deep-neck adipose tissue in humans. In cell models, PTH receptor stimulation increases lipolysis and stimulates gene transcription of multiple thermogenic markers. Silencing of the PTH receptor attenuates the effects of PTH indicating a direct PTH effect via this receptor. Conclusion PTH 1 receptor stimulation by PTH may play a role in human adipose tissue metabolism by affecting lipolysis and thermogenic capacity.

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