Bone Regulation of Insulin Secretion and Glucose Homeostasis

Endocrinology ◽  
2020 ◽  
Vol 161 (10) ◽  
Author(s):  
Patricia Ducy
Keyword(s):  
Cell Biology ◽  
Regulatory Networks ◽  
Bone Growth ◽  
Bone Cells ◽  
Protective Role ◽  
Brain Cell ◽  
Mouse Genetics ◽  
The Body ◽  
Lipocalin 2 ◽  
Inner Organs

Abstract For centuries our image of the skeleton has been one of an inert structure playing a supporting role for muscles and a protective role for inner organs like the brain. Cell biology and physiology modified this view in the 20st century by defining the constant interplay between bone-forming and bone resorbing cells that take place during bone growth and remodeling, therefore demonstrating that bone is as alive as any other tissues in the body. During the past 40 years human and, most important, mouse genetics, have allowed not only the refinement of this notion by identifying the many genes and regulatory networks responsible for the crosstalk existing between bone cells, but have redefined the role of bone by showing that its influence goes way beyond its own physiology. Among its newly identified functions is the regulation of energy metabolism by 2 bone-derived hormones, osteocalcin and lipocalin-2. Their biology and respective roles in this process are the topic of this review.

Bioactive Glass Scaffolds with Hierarchical Structure and their 3D Characterization

2010 ◽  
Vol 441 ◽  
pp. 123-137 ◽  
Author(s):  
Julian R. Jones ◽  
Peter D. Lee
Keyword(s):  
Bioactive Glass ◽  
Hierarchical Structure ◽  
Bone Growth ◽  
Bone Cells ◽  
Sol Gel ◽  
Three Dimensional ◽  
The Body ◽  
Native Bone ◽  
Degradation Rates ◽  
Hierarchical Porous

Bone tissue has evolved into hierarchical three-dimensional structures with dimensions ranging from nanometres to metres. The structure varies depending on the site in the body, which is dictated by the loading environment. Medically, bone is one of the most replaced body parts (second only to blood) but replicating these complex living hierarchical structures for the purpose of regenerating defective bone is a challenge that has yet to be overcome. A temporary template (scaffold) is needed that matches the hierarchical structure of native bone as closely as possible that is available ‘off the shelf’ for surgeons to use. After implantation the scaffold must bond to bone and stimulate not only three dimensional (3D) bone growth, but also vascularisation to feed the new bone. There are many engineering design criteria for a successful bone scaffold and bioactive glass foam scaffolds have been developed that can fulfil most of them, as they have a hierarchical porous structure, they can bond to bone, and they release soluble silica species and calcium ions that have been found to up-regulate seven families of genes in osteogenic cells. Other ions have also been incorporated to combat infection and to counteract osteoporosis. Their tailorable hierarchical structure consists of highly interconnected open spherical macropores, further, because the glass is sol-gel derived, the entire structure is nanoporous. The macropores are critical for bone and blood vessel growth, the nanopores for tailoring degradation rates and protein adsorption and for cell attachment. This chapter describes the optimised sol-gel foaming process and how bone cells respond to them. Whatever type of scaffold is used for bone regeneration, it is critically important to be able to quantify the hierarchial pore structure. The nanopore size can be quantified using gas sorption, but to obtain full information of the macropore structure, imaging must be done using X-ray microtomography and the resulting images must be quantified via 3D image analysis. These techniques are reviewed.

scholarly journals Anti-Osteoclastic Effect of Zinc Studied in MCF-7 Induced Osteoclastogenesis

2019 ◽  
Vol 9 (4-s) ◽  
pp. 94-97
Author(s):  
K Nagalakshmi ◽  
S Shila ◽  
P Rasappan
Keyword(s):  
Oxidative Stress ◽  
Bone Metastasis ◽  
Bone Cells ◽  
Bone Remodelling ◽  
Antioxidant Properties ◽  
Cathepsin K ◽  
Protective Role ◽  
The Body ◽  
Mrna Levels ◽  
Mcf 7

Bone which a key structural support of the body, undergoes dynamic micro structural remodelling all over life to control automatic stress and calcium requirement in the body. A number of risk factors including oxidative stress, apoptosis and abnormal intracellular Ca2+ metabolism have been postulated to play a function in the inception and progress of bone osteolysis. Cancer cells establish a tight relationship with the host tissue, secreting factors that stimulate or inhibit bone cells, receiving signals generated from the bone remodelling activity, and displaying some features of bone cells. This interplay between tumour and bone cells alters the physiological bone remodelling, leading to the generation of a vicious cycle that promotes bone metastasis growth. Zinc is one of the most relevant minerals to human health, because of its antioxidant properties. The present study was aimed to investigate protective role of zinc against bone metastasis. In the present study, TRAP positive multinucleated cell count was low compared to CM treated cells. Zinc treatment suppressed MCF-7 induced mRNA levels of cytoplasmic 1 (Nfatc1), TRAP and Cathepsin-K. Hence, it can be concluded that zinc decreases osteoclastogenesis induced by MCF-7 cells. Keywords: Oxidative stress; Metastasis; Bone remodelling; Zinc.

scholarly journals The Cellular Senescence Stress Response in Post-Mitotic Brain Cells: Cell Survival at the Expense of Tissue Degeneration

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 229
Author(s):  
Eric Sah ◽  
Sudarshan Krishnamurthy ◽  
Mohamed Y. Ahmidouch ◽  
Gregory J. Gillispie ◽  
Carol Milligan ◽  
...  
Keyword(s):  
Stress Response ◽  
Cell Fate ◽  
Cellular Senescence ◽  
Cell Biology ◽  
Brain Aging ◽  
Complex Stress ◽  
Brain Cell ◽  
Tissue Degeneration ◽  
Cellular Dna

In 1960, Rita Levi-Montalcini and Barbara Booker made an observation that transformed neuroscience: as neurons mature, they become apoptosis resistant. The following year Leonard Hayflick and Paul Moorhead described a stable replicative arrest of cells in vitro, termed “senescence”. For nearly 60 years, the cell biology fields of neuroscience and senescence ran in parallel, each separately defining phenotypes and uncovering molecular mediators to explain the 1960s observations of their founding mothers and fathers, respectively. During this time neuroscientists have consistently observed the remarkable ability of neurons to survive. Despite residing in environments of chronic inflammation and degeneration, as occurs in numerous neurodegenerative diseases, often times the neurons with highest levels of pathology resist death. Similarly, cellular senescence (hereon referred to simply as “senescence”) now is recognized as a complex stress response that culminates with a change in cell fate. Instead of reacting to cellular/DNA damage by proliferation or apoptosis, senescent cells survive in a stable cell cycle arrest. Senescent cells simultaneously contribute to chronic tissue degeneration by secreting deleterious molecules that negatively impact surrounding cells. These fields have finally collided. Neuroscientists have begun applying concepts of senescence to the brain, including post-mitotic cells. This initially presented conceptual challenges to senescence cell biologists. Nonetheless, efforts to understand senescence in the context of brain aging and neurodegenerative disease and injury emerged and are advancing the field. The present review uses pre-defined criteria to evaluate evidence for post-mitotic brain cell senescence. A closer interaction between neuro and senescent cell biologists has potential to advance both disciplines and explain fundamental questions that have plagued their fields for decades.

scholarly journals Neural is Fundamental: Neural Stemness as the Ground State of Cell Tumorigenicity and Differentiation Potential

2020 ◽  
Author(s):  
Ying Cao
Keyword(s):  
Ground State ◽  
Cell Biology ◽  
Regulatory Networks ◽  
Splice Variants ◽  
Tumor Biology ◽  
General Rule ◽  
Tumor Initiating Cells ◽  
Differentiation Potential ◽  
Neural Stem Progenitor Cells ◽  
Long Genes

Tumorigenesis is a complex biological phenomenon that includes extensive genetic and phenotypic heterogeneities and complicated regulatory mechanisms. In the recent few years, our studies demonstrate that tumor-initiating cells are similar to neural stem/progenitor cells in regulatory networks, tumorigenicity and pluripotent differentiation potential. In the review, I will make further discussion on these observations and propose a rule of cell biology by integrating these findings with evidence from developmental biology, tumor biology and evolution, which suggests that neural stemness underlies two coupled cell properties, tumorigenicity and pluripotent differentiation potential. Tumorigenicity and phenotypic heterogeneity in tumor is a result of acquirement of neural stemness in cells. The neural stemness property of tumor-initiating cells can hopefully integrate different concepts/hypotheses underlying tumorigenesis. Neural stem cells/neural progenitors and tumor-initiating cells share regulatory networks; both exhibit neural stemness, tumorigenicity and differentiation potential; both are dependent on expression or activation of ancestral genes (the atavistic effect); both rely primarily on aerobic glycolytic metabolism; both can differentiate into various cells or tissues that are derived from three germ layers, resembling severely disorganized or more severely degenerated process of embryonic development; both are enriched in long genes with more splice variants that provide more plastic scaffolds for cell differentiation, etc. The property of neural stemness might be a key point to understand tumorigenesis and pluripotent differentiation potential, and possibly explain certain pathological observations in tumors that have been inexplicable. Therefore, behind the complexity of tumorigenesis might be a general rule of cell biology, i.e., neural stemness represents the ground state of cell tumorigenicity and pluripotent differentiation potential.

scholarly journals Changes in Adult Rats’ Testis structure Induced by Hypothyroidism and Alleviating Role of L-Carnitine

2019 ◽  
Vol 1 (4) ◽  
pp. 13-28
Author(s):  
Abdelmonem Awad Hegazy ◽  
Manal Mohammad Morsy ◽  
Rania Said Moawad ◽  
Gehad Mohammad Elsayed
Keyword(s):  
Fatty Acids ◽  
Semen Analysis ◽  
Protective Role ◽  
The Body ◽  
Albino Rats ◽  
Adult Rats ◽  
Fatty Acids Metabolism ◽  
Group 3 ◽  
Group 2

Background Hypothyroidism is a metabolic disorder affecting the functions of many tissues in the body including the testis. Testis is rich in the polyunsaturated fatty acids content and lacks strong intrinsic antioxidant system making it prone to such oxidative stress. L-carnitine (LC) regulates long chain fatty acids metabolism; and is considered a valuable antioxidant factor. Aim It was to evaluate the effect of hypothyroidism induced by propylthiouracil (PTU) on rats’ testes and the possible protective role of LC. Methods Forty-eight adult male albino rats were used in this work. The animals were divided into three groups with sixteen animals in each. Group 1 (Control): Animals were kept without medications. Group 2 (PTU-treated): was subjected to administration of PTU; while group 3 (PTU and LC) received both PTU and LC. By the end of the experiment “30 days”, blood samples were taken for hormonal assay; then animals were anaesthetized and sacrificed. Specimens were homogenized for biochemical analysis; epididymal content of each rat was obtained immediately for semen analysis. Testes’ specimens were harvested, prepared and examined by light microscope examination. Results Induced hypothyroidism was noticed to cause histopathological, morphometric and biochemical changes in rat’s testes. LC protected the testicular specimens against such changes; it also improved the seminal quality and quantity as well as testicular structure and biochemistry. Conclusion Hypothyroidism could result in hazards to the structure of testis. Fortunately co-administration of LC might reduce such hazards.

scholarly journals Plexin-B1 mutation drives prostate cancer metastasis

2020 ◽  
Author(s):  
Boris Shorning ◽  
Neil Trent ◽  
David Griffiths ◽  
Thomas Worzfeld ◽  
Stefan Offermanns ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Metastasis ◽  
Locally Advanced ◽  
Tumour Cells ◽  
Mouse Genetics ◽  
The Body ◽  
Cancer Type ◽  
Wild Type ◽  
Tumour Spread ◽  
Mouse Prostate

AbstractProstate cancer mortality is associated with the metastatic spread of tumour cells. A better understanding of the mechanisms which allow a locally advanced tumour to disseminate around the body will identify new therapeutic targets to block this process. One of set of genes implicated in metastasis are plexins, which can promote or suppress tumour progression depending on cancer type and cellular context. We have taken a mouse genetics approach to gain insight into the role of Plexin-B1 in prostate cancer progression in vivo.We show here that genetic deletion of Plexin-B1 in PbCre+Ptenfl/flKrasG12V and PbCre+Ptenfl/flp53fl/fl mouse prostate cancer models significantly decreased metastasis. High levels of prostate epithelial cell-specific expression of wild-type Plexin-B1 in knock-in mice with a PbCre+Ptenfl/flKrasG12V background also significantly decreased metastasis. In contrast, expression of a Plexin-B1 mutant (P1597L; identified from metastatic deposits in prostate cancer patients) in prostate epithelial cells in PbCre+Ptenfl/flKrasG12V and PbCre+Ptenfl/flp53fl/fl mice significantly increased metastasis, in particular metastasis to distant sites. In line with these findings, both deletion and overexpression of wild-type Plexin-B1 reduced invasion of tumour cells into the prostate stroma, while overexpression of mutant Plexin-B1 significantly increased invasion, suggesting that Plexin-B1 has a role in the initial stages of metastasis. Invasion and metastasis also correlated with phosphorylation of myosin light chain, suggesting that Plexin-B1 signals via the Rho/ROCK pathway to promote metastasis.Our results demonstrate that mutant Plexin-B1 promotes metastasis in prostate cancer and represents a new therapeutic target to suppress tumour spread.

scholarly journals An Implanted Magnetic Microfluidic Pump for In Vivo Bone Remodeling Applications

Micromachines ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 300 ◽  
Author(s):  
Ziyu Chen ◽  
Sunggi Noh ◽  
Rhonda D. Prisby ◽  
Jeong-Bong Lee
Keyword(s):  
Bone Growth ◽  
Static Pressure ◽  
Dynamic Pressure ◽  
The Body ◽  
In Vivo Studies ◽  
Fischer 344 ◽  
Fischer 344 Rat ◽  
Pressure Modulation

Modulations of fluid flow inside the bone intramedullary cavity has been found to stimulate bone cellular activities and augment bone growth. However, study on the efficacy of the fluid modulation has been limited to external syringe pumps connected to the bone intramedullary cavity through the skin tubing. We report an implantable magnetic microfluidic pump which is suitable for in vivo studies in rodents. A compact microfluidic pump (22 mm diameter, 5 mm in thickness) with NdFeB magnets was fabricated in polydimethylsiloxane (PDMS) using a set of stainless-steel molds. An external actuator with a larger magnet was used to wirelessly actuate the magnetic microfluidic pump. The characterization of the static pressure of the microfluidic pump as a function of size of magnets was assessed. The dynamic pressure of the pump was also characterized to estimate the output of the pump. The magnetic microfluidic pump was implanted into the back of a Fischer-344 rat and connected to the intramedullary cavity of the femur using a tube. On-demand wireless magnetic operation using an actuator outside of the body was found to induce pressure modulation of up to 38 mmHg inside the femoral intramedullary cavity of the rat.

scholarly journals Insights into Arbutin Effects on Bone Cells: Towards the Development of Antioxidant Titanium Implants

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 579 ◽  
Author(s):  
Maria A. Bonifacio ◽  
Giorgia Cerqueni ◽  
Stefania Cometa ◽  
Caterina Licini ◽  
Luigia Sabbatini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Cells ◽  
Cell Damage ◽  
Protective Role ◽  
Titanium Implants ◽  
Point Of View ◽  
Differentiation Markers ◽  
Scavenging Effect ◽  
High Viability

Arbutin is a plant-derived glycosylated hydroquinone with antioxidant features, exploited to combat cell damage induced by oxidative stress. The latter hinders the osseointegration of bone prostheses, leading to implant failure. Little is known about arbutin antioxidant effects on human osteoblasts, therefore, this study explores the in vitro protective role of arbutin on osteoblast-like cells (Saos-2) and periosteum-derived progenitor cells (PDPCs). Interestingly, cells exposed to oxidative stress were protected by arbutin, which preserved cell viability and differentiation. Starting from these encouraging results, an antioxidant coating loaded with arbutin was electrosynthesized on titanium. Therefore, for the first time, a polyacrylate-based system was designed to release the effective concentration of arbutin in situ. The innovative coating was characterized from the physico-chemical and morphological point of view to achieve an optimized system, which was in vitro tested with cells. Morpho-functional evaluations highlighted the high viability and good compatibility of the arbutin-loaded coating, which also promoted the expression of PDPC differentiation markers, even under oxidative stress. These results agreed with the coatings’ in vitro antioxidant activity, which showed a powerful scavenging effect against DPPH radicals. Taken together, the obtained results open intriguing opportunities for the further development of natural bioactive coatings for orthopedic titanium implants.

scholarly journals Vascular Endothelial Cell Biology: An Update

2019 ◽  
Vol 20 (18) ◽  
pp. 4411 ◽  
Author(s):  
Krüger-Genge ◽  
Blocki ◽  
Franke ◽  
Jung
Keyword(s):  
Endothelial Cells ◽  
Cell Biology ◽  
Current Knowledge ◽  
Regional Blood Flow ◽  
Vascular Endothelial Cell ◽  
Inflammatory Cells ◽  
The Body ◽  
Arterial Tree ◽  
Foreign Materials ◽  
And Function

The vascular endothelium, a monolayer of endothelial cells (EC), constitutes the inner cellular lining of arteries, veins and capillaries and therefore is in direct contact with the components and cells of blood. The endothelium is not only a mere barrier between blood and tissues but also an endocrine organ. It actively controls the degree of vascular relaxation and constriction, and the extravasation of solutes, fluid, macromolecules and hormones, as well as that of platelets and blood cells. Through control of vascular tone, EC regulate the regional blood flow. They also direct inflammatory cells to foreign materials, areas in need of repair or defense against infections. In addition, EC are important in controlling blood fluidity, platelet adhesion and aggregation, leukocyte activation, adhesion, and transmigration. They also tightly keep the balance between coagulation and fibrinolysis and play a major role in the regulation of immune responses, inflammation and angiogenesis. To fulfill these different tasks, EC are heterogeneous and perform distinctly in the various organs and along the vascular tree. Important morphological, physiological and phenotypic differences between EC in the different parts of the arterial tree as well as between arteries and veins optimally support their specified functions in these vascular areas. This review updates the current knowledge about the morphology and function of endothelial cells, particularly their differences in different localizations around the body paying attention specifically to their different responses to physical, biochemical and environmental stimuli considering the different origins of the EC.

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