scholarly journals Low magnitude vibration alleviates age-related bone loss by inhibiting cell senescence of osteogenic cells in naturally senescent rats

Aging ◽  
2021 ◽  
Author(s):  
Jirui Wen ◽  
Mingyue Bao ◽  
Min Tang ◽  
Xueling He ◽  
Xinghong Yao ◽  
...  
Keyword(s):  
Bone Loss ◽  
Cell Senescence ◽  
Osteogenic Cells ◽  
Age Related ◽  
Low Magnitude

Targeting Cell Senescence for the Treatment of Age-Related Bone Loss

2019 ◽  
Vol 17 (2) ◽  
pp. 70-85 ◽  
Author(s):  
Robert J. Pignolo ◽  
Rebekah M. Samsonraj ◽  
Susan F. Law ◽  
Haitao Wang ◽  
Abhishek Chandra
Keyword(s):  
Bone Loss ◽  
Cell Senescence ◽  
Age Related

scholarly journals The Dual Role of Vitamin K2 in “Bone-Vascular Crosstalk”: Opposite Effects on Bone Loss and Vascular Calcification

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1222
Author(s):  
Domitilla Mandatori ◽  
Letizia Pelusi ◽  
Valeria Schiavone ◽  
Caterina Pipino ◽  
Natalia Di Pietro ◽  
...  
Keyword(s):  
Bone Loss ◽  
Vascular Calcification ◽  
Vascular System ◽  
The Elderly ◽  
Food Supplement ◽  
Vitamin K2 ◽  
Bioactive Molecules ◽  
Calcium Deposition ◽  
Age Related

Osteoporosis (OP) and vascular calcification (VC) represent relevant health problems that frequently coexist in the elderly population. Traditionally, they have been considered independent processes, and mainly age-related. However, an increasing number of studies have reported their possible direct correlation, commonly defined as “bone-vascular crosstalk”. Vitamin K2 (VitK2), a family of several natural isoforms also known as menaquinones (MK), has recently received particular attention for its role in maintaining calcium homeostasis. In particular, VitK2 deficiency seems to be responsible of the so-called “calcium paradox” phenomenon, characterized by low calcium deposition in the bone and its accumulation in the vessel wall. Since these events may have important clinical consequences, and the role of VitK2 in bone-vascular crosstalk has only partially been explained, this review focuses on its effects on the bone and vascular system by providing a more recent literature update. Overall, the findings reported here propose the VitK2 family as natural bioactive molecules that could be able to play an important role in the prevention of bone loss and vascular calcification, thus encouraging further in-depth studies to achieve its use as a dietary food supplement.

The archaeology of osteoporosis

2001 ◽  
Vol 4 (2) ◽  
pp. 263-269 ◽  
Author(s):  
Gordon Turner-Walker ◽  
Unni Syversen ◽  
Simon Mays
Keyword(s):  
Bone Loss ◽  
Femoral Neck ◽  
Young Women ◽  
Rapid Decline ◽  
Mineral Density ◽  
Medieval Women ◽  
Age Related ◽  
Pregnancy And Lactation ◽  
Post Menopausal ◽  
The Uk

The application of medical scanning technologies to archaeological skeletons provides novel insights into the history and potential causes of osteoporosis. The present study investigated bone mineral density (BMD) in medieval skeletons from England and Norway. Comparisons between the two adult populations found no statistically significant differences. This compares with a modern fracture incidence for the femoral neck in women from Norway that is almost three times that in the UK. The pattern of age-related bone loss in medieval men was similar to that seen in men today. In contrast, the pattern in medieval women differed from that of modern young women. On average, medieval women experienced a decrease in BMD at the femoral neck of approximately 23 per cent between the ages of 22 and 35. These losses were partially recovered by age 45, after which BMD values show a decline consistent with post-menopausal bone loss in modern western women. A possible explanation of the rapid decline in BMD in young medieval women is bone loss in connection with pregnancy and lactation in circumstances of insufficient nutrition.

scholarly journals CB2 cannabinoid receptor agonist enantiomers HU-433 and HU-308: An inverse relationship between binding affinity and biological potency

2015 ◽  
Vol 112 (28) ◽  
pp. 8774-8779 ◽  
Author(s):  
Reem Smoum ◽  
Saja Baraghithy ◽  
Mukesh Chourasia ◽  
Aviva Breuer ◽  
Naama Mussai ◽  
...  
Keyword(s):  
Bone Loss ◽  
Binding Affinity ◽  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Osteoclast Differentiation ◽  
Protective Mechanism ◽  
Binding Studies ◽  
Age Related ◽  
Comparative Binding ◽  
Biological Potency

Activation of the CB2 receptor is apparently an endogenous protective mechanism. Thus, it restrains inflammation and protects the skeleton against age-related bone loss. However, the endogenous cannabinoids, as well as Δ9-tetrahydrocannabinol, the main plant psychoactive constituent, activate both cannabinoid receptors, CB1 and CB2. HU-308 was among the first synthetic, selective CB2 agonists. HU-308 is antiosteoporotic and antiinflammatory. Here we show that the HU-308 enantiomer, designated HU-433, is 3–4 orders of magnitude more potent in osteoblast proliferation and osteoclast differentiation culture systems, as well as in mouse models, for the rescue of ovariectomy-induced bone loss and ear inflammation. HU-433 retains the HU-308 specificity for CB2, as shown by its failure to bind to the CB1 cannabinoid receptor, and has no activity in CB2-deficient cells and animals. Surprisingly, the CB2 binding affinity of HU-433 in terms of [3H]CP55,940 displacement and its effect on [35S]GTPγS accumulation is substantially lower compared with HU-308. A molecular-modeling analysis suggests that HU-433 and -308 have two different binding conformations within CB2, with one of them possibly responsible for the affinity difference, involving [35S]GTPγS and cAMP synthesis. Hence, different ligands may have different orientations relative to the same binding site. This situation questions the usefulness of universal radioligands for comparative binding studies. Moreover, orientation-targeted ligands have promising potential for the pharmacological activation of distinct processes.

Cross-sectional assessment of age-related bone loss in men: the MINOS study

Bone ◽  
2000 ◽  
Vol 26 (2) ◽  
pp. 123-129 ◽  
Author(s):  
P Szulc ◽  
F Marchand ◽  
F Duboeuf ◽  
P.D Delmas
Keyword(s):  
Bone Loss ◽  
Cross Sectional ◽  
Age Related

scholarly journals Hypothalamic leptin gene therapy reduces body weight without accelerating age-related bone loss

2015 ◽  
Vol 227 (3) ◽  
pp. 129-141 ◽  
Author(s):  
Russell T Turner ◽  
Michael Dube ◽  
Adam J Branscum ◽  
Carmen P Wong ◽  
Dawn A Olson ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Body Weight ◽  
Bone Loss ◽  
Bone Mass ◽  
Bone Turnover ◽  
Cancellous Bone ◽  
Mass Density ◽  
Female Rats ◽  
Bone Mass Density ◽  
Age Related

Excessive weight gain in adults is associated with a variety of negative health outcomes. Unfortunately, dieting, exercise, and pharmacological interventions have had limited long-term success in weight control and can result in detrimental side effects, including accelerating age-related cancellous bone loss. We investigated the efficacy of using hypothalamic leptin gene therapy as an alternative method for reducing weight in skeletally-mature (9 months old) female rats and determined the impact of leptin-induced weight loss on bone mass, density, and microarchitecture, and serum biomarkers of bone turnover (CTx and osteocalcin). Rats were implanted with cannulae in the 3rd ventricle of the hypothalamus and injected with either recombinant adeno-associated virus encoding the gene for rat leptin (rAAV-Leptin,n=7) or a control vector encoding green fluorescent protein (rAAV-GFP,n=10) and sacrificed 18 weeks later. A baseline control group (n=7) was sacrificed at vector administration. rAAV-Leptin-treated rats lost weight (−4±2%) while rAAV-GFP-treated rats gained weight (14±2%) during the study. At study termination, rAAV-Leptin-treated rats weighed 17% less than rAAV-GFP-treated rats and had lower abdominal white adipose tissue weight (−80%), serum leptin (−77%), and serum IGF1 (−34%). Cancellous bone volume fraction in distal femur metaphysis and epiphysis, and in lumbar vertebra tended to be lower (P<0.1) in rAAV-GFP-treated rats (13.5 months old) compared to baseline control rats (9 months old). Significant differences in cancellous bone or biomarkers of bone turnover were not detected between rAAV-Leptin and rAAV-GFP rats. In summary, rAAV-Leptin-treated rats maintained a lower body weight compared to baseline and rAAV-GFP-treated rats with minimal effects on bone mass, density, microarchitecture, or biochemical markers of bone turnover.

scholarly journals Acute myeloid leukemia induces protumoral p16INK4a-driven senescence in the bone marrow microenvironment

Blood ◽  
2019 ◽  
Vol 133 (5) ◽  
pp. 446-456 ◽  
Author(s):  
Amina M. Abdul-Aziz ◽  
Yu Sun ◽  
Charlotte Hellmich ◽  
Christopher R. Marlein ◽  
Jayna Mistry ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Myeloid Leukemia ◽  
Stromal Cells ◽  
Myeloid Leukemia ◽  
Stromal Cell ◽  
Cell Senescence ◽  
Senescent Phenotype ◽  
Age Related ◽  
Acute Myeloid

Abstract Acute myeloid leukemia (AML) is an age-related disease that is highly dependent on the bone marrow (BM) microenvironment. With increasing age, tissues accumulate senescent cells, characterized by an irreversible arrest of cell proliferation and the secretion of a set of proinflammatory cytokines, chemokines, and growth factors, collectively known as the senescence-associated secretory phenotype (SASP). Here, we report that AML blasts induce a senescent phenotype in the stromal cells within the BM microenvironment and that the BM stromal cell senescence is driven by p16INK4a expression. The p16INK4a-expressing senescent stromal cells then feed back to promote AML blast survival and proliferation via the SASP. Importantly, selective elimination of p16INK4a+ senescent BM stromal cells in vivo improved the survival of mice with leukemia. Next, we find that the leukemia-driven senescent tumor microenvironment is caused by AML-induced NOX2-derived superoxide. Finally, using the p16-3MR mouse model, we show that by targeting NOX2 we reduced BM stromal cell senescence and consequently reduced AML proliferation. Together, these data identify leukemia-generated NOX2-derived superoxide as a driver of protumoral p16INK4a-dependent senescence in BM stromal cells. Our findings reveal the importance of a senescent microenvironment for the pathophysiology of leukemia. These data now open the door to investigate drugs that specifically target the “benign” senescent cells that surround and support AML.

scholarly journals The Role of AOPP in Age-Related Bone Loss and the Potential Benefits of Berry Anthocyanins

Nutrients ◽  
2017 ◽  
Vol 9 (7) ◽  
pp. 789 ◽  
Author(s):  
◽  
◽  
Keyword(s):  
Bone Loss ◽  
Age Related ◽  
Potential Benefits ◽  
Berry Anthocyanins
Sign in / Sign up

Export Citation Format

Share Document