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Lipolysis supports bone formation by providing osteoblasts with endogenous fatty acid substrates to maintain bioenergetic status

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Bone Research 2023年第4期11卷 876-894页

作者： Ananya Nandy Ron C.M.Helderman Santosh Thapa Shobana jayapalan Alison Richards Nikita Narayani Michael P.Czech clifford j.rosen Elizabeth Rendina-Ruedy Department of Medicine Division of Clinical PharmacologyVanderbilt University Medical CenterNashvilleTN 37232USA Program in Molecular Medicine University of Massachusetts Chan Medical SchoolWorcesterMA 01605USA Maine Medical Center Research Institute ScarboroughMEUSA Molecular Physiology and Biophysics Vanderbilt UniversityNashvilleTN 37232USA

Bone formation is a highly energy-demanding process that can be impacted by metabolic disorders.Glucose has been considered the principal substrate for osteoblasts,although fatty acids are also important for osteoblast function.Here,we report that osteoblasts can derive energy from endogenous fatty acids stored in lipid droplets via lipolysis and that this process is critical for bone formation.As such,we demonstrate that osteoblasts accumulate lipid droplets that are highly dynamic and provide the molecular mechanism by which they serve as a fuel source for energy generation during osteoblast maturation.Inhibiting cytoplasmic lipolysis leads to both an increase in lipid droplet size in osteoblasts and an impairment in osteoblast function.The fatty acids released by lipolysis from these lipid droplets become critical for cellular energy production as cellular energetics shifts towards oxidative phosphorylation during nutrient-depleted conditions.In vivo,conditional deletion of the ATGL-encoding gene Pnpla2 in osteoblast progenitor cells reduces cortical and trabecular bone parameters and alters skeletal lipid metabolism.Collectively,our data demonstrate that osteoblasts store fatty acids in the form of lipid droplets,which are released via lipolysis to support cellular bioenergetic status when nutrients are limited.Perturbations in this process result in impairment of bone formation,specifically reducing ATP production and overall osteoblast function.

关键词： endogenous maintain osteoblast

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Bone Remodeling and Energy Metabolism:New Perspectives

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Bone Research 2013年第1期1卷 72-84页

作者： Francisco j.A.de Paula clifford j.rosen Department of Internal Medicine School of Medicine of Ribeiro PretoUniversity of So PauloBrazil Center for Clinical and Translational Research Maine Medical Center Research InstituteUSA

Bone mineral, adipose tissue and energy metabolism are interconnected by a complex and multilevel series of networks. Calcium and phosphorus are utilized for insulin secretion and synthesis of high energy compounds. Adipose tissue store lipids and cholecalciferol, which, in turn, can influence calcium balance and energy expenditure. Hormones long-thought to solely modulate energy and mineral homeostasis may influence adipocytic function. Osteoblasts are a target of insulin action in bone. Moreover, endocrine mediators, such as osteocalcin, are synthesized in the skeleton but regulate carbohydrate disposal and insulin secretion. Finally, osteoblasts and adipocytes originate from the same mesenchymal progenitor. The mutual crosstalk between osteoblasts and adipocytes within the bone marrow microenvironment plays a crucial role in bone remodeling. In the present review we provide an overview of the reciprocal control between bone and energy metabolism and its clinical implications.

关键词： bone adipose tissue mineral metabolism energy metabolism leptin osteocalcin

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A peptide containing the receptor binding site of insulin-like growth factor binding protein-2 enhances bone mass in ovariectomized rats

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Bone Research 2018年第3期6卷 280-288页

作者： Gang Xi Christine Wai clifford j.rosen David R.Clemmons Department of Medicine University of North Carolina at Chapel HillChapel HillUSA Maine Medical Center Research Institute ScarboroughUSA

Male Igfbp2-/-mice have a significant reduction in bone mass and administration of a peptide that contains the insulin-like growth factor binding protein-2(IGFBP-2) receptor-binding domain stimulates bone formation in these animals. Female Igfbp2-/-mice do not have this phenotype but following ovariectomy(OVX) lose more bone than OVX wild-type mice. This suggests that in the absence of estrogen, IGFBP-2 is required to maintain bone mass. Therefore these studies were undertaken to determine if this peptide could stimulate bone acquisition in OVX rats. OVX rats were divided into seven treatment groups: sham animals, OVX animals, OVX animals receiving a control scrambled peptide, or one of three doses of the active peptide termed PEG-HBD-1(0.7, 2,and 6 mg·kg^(-1)) and an OVX group receiving parathyroid hormone(PTH)(50 μg·kg-1 per day). The peptides were administered for8 weeks. DXA revealed a significant reduction in femoral and tibial areal bone mineral density(aBMD) after OVX, whereas treatment with the high-dose peptide increased aBMD by 6.2% ± 2.4%(P < 0.01) compared to control peptide; similar to the increase noted with PTH(5.6% ± 3.0%, P < 0.01). Similar increases were noted with two lower doses of the peptide(3.8% ± 1.5%, P < 0.05 for low dose; 3.1% ± 1.6%, P = 0.07 for middle dose). Micro CT showed that the OVX control peptide animals had reductions of 41% and64% in femoral trabecular BV/TV and trabecular number, respectively. All three doses of the peptide increased bone volume/total volume(BV/TV) significantly, while the low and middle doses increased trabecular number. Cortical BV/TV and thickness at the midshaft increased significantly with each dose of peptide(18.9% ± 9.8%, P < 0.01 and 14.2% ± 7.9%, P < 0.01 for low dose; 23.7% ±10.7%, P < 0.001 and 15.8% ± 6.1%, P < 0.001 for middle dose; 19.0% ± 6.9%, P < 0.01 and 16.2% ± 9.7%, P < 0.001 for high dose)and with PTH(25.8% ± 9.2%, P < 0.001 and 19.4% ± 8.8%, P < 0.001). Histomorphometry showed that the lowest dose of peptide stimulated BV/TV, trabecular

关键词： insulin-like growth factor binding protein-2 OVX wild-type mice

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Metabolic programming determines the lineage-differentiation fate of murine bone marrow stromal progenitor cells

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Bone Research 2019年第4期7卷 410-423页

作者： Michaela Tencerova Elizabeth Rendina-Ruedy Ditte Neess Nils Faergeman Florence Figeac Dalia Ali Morten Danielsen Anders Haakonsson clifford j.rosen Moustapha Kassem Department of Molecular Endocrinology University of Southern Denmark and Odense University Hospital5000 OdenseDenmark Center for Molecular Medicine Maine Medical Center Research InstituteScarboroughME 04074USA Villum Center for Analytical Biosciences Department of Biochemistry and Molecular BiologyUniversity of Southern Denmark5230 OdenseDenmark MSOmics 2950 CopenhagenDenmark Department of Cellular and Molecular Medicine Novo Nordisk Foundation Center for Stem Cell Biology(DanStem)University of Copenhagen2200 CopenhagenDenmark

Enhanced bone marrow adipogenesis and impaired osteoblastogenesis have been observed in obesity,suggesting that the metabolic microenvironment regulates bone marrow adipocyte and osteoblast progenitor differentiation fate.To determine the molecular mechanisms,we studied two immortalized murine cell lines of adipocyte or osteoblast progenitors(BMSCs^adipo and BMSC^sosteo,respectively)under basal and adipogenic culture conditions.At baseline,BMSCs^adipo,and BMSCs^osteo exhibit a distinct metabolic program evidenced by the presence of specific global gene expression,cellular bioenergetics,and metabolomic signatures that are dependent on insulin signaling and glycolysis in BMSCs^osteo versus oxidative phosphorylation in BMSCs^adipo.To test the flexibility of the metabolic program,we treated BMSCsadipo with parathyroid hormone,S961(an inhibitor of insulin signaling)and oligomycin(an inhibitor of oxidative phosphorylation).The treatment induced significant changes in cellular bioenergetics that were associated with decreased adipocytic differentiation.Similarly,12 weeks of a high-fat diet in mice led to the expansion of adipocyte progenitors,enhanced adipocyte differentiation and insulin signaling in cultured BMSCs.Our data demonstrate that BMSC progenitors possess a distinct metabolic program and are poised to respond to exogenous metabolic cues that regulate their differentiation fate.

关键词： progenitor impaired programming

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Clouds:The Most Useful Metaphor of All Time?

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考试（高考英语） 2011年第12期 30-32页

作者： Rebecca j.rosen 不详

云计算、云服务,不止文学,科技也喜欢用＂云＂做比喻。

关键词：英语学习高中英语英语美文英语阅读

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A GLOBALLY CONVERGENT ALGORITHM FOR THE EUCLIDEAN MULTIPLICITY LOCATION PROBLEM

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Acta Mathematicae Applicatae Sinica 1992年第4期8卷 357-366页

作者： j.B.rosen 薛国良 Computer Science Department University of MinnesotaMinneapolisMN 55455USA Institute of Operations Research Qufu Normal University Qufu 278165 Chinahe Euclidean single facility location problem (ESFL) and the Euclidean multiplicity lo-cation problem (EMFL) are two special nonsmooth convex programming problems which haveattracted a largr literature. For the ESFL problem. there are algorithms which converge bothglobally and quadratically For the EMFL problem there are some quadratically convergentalgorithms. but for global convergencel they all need nontrivial assumptions on the problem.In this paper we present an algorithm for EMFL. With no assumption on the problem it isproved that from any initial point this algorithm generates a sequence of points which convergesto the closed convex set of optimal solutions of EMFL.

The Euclidean single facility location problem (ESFL) and the Euclidean multiplicity lo-cation problem (EMFL) are two special nonsmooth convex programming problems which haveattracted a largr literature. For the ESFL problem. there are algorithms which converge bothglobally and quadratically For the EMFL problem, there are some quadratically convergentalgorithms. but for global convergencel they all need nontrivial assumptions on the problem.In this paper, we present an algorithm for EMFL. With no assumption on the problem, it isproved that from any initial point, this algorithm generates a sequence of points which convergesto the closed convex set of optimal solutions of EMFL.

关键词： A GLOBALLY CONVERGENT ALGORITHM FOR THE EUCLIDEAN MULTIPLICITY LOCATION PROBLEM

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Finding stable multi-component materials by combining cluster expansion and crystal structure predictions

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npj Computational Materials 2023年第1期9卷 2137-2146页

作者： Adam Carlsson johanna rosen Martin Dahlqvist Materials Design Department of PhysicsChemistryand Biology(IFM)Linköping UniversitySE-58183 LinköpingSweden

A desired prerequisite when performing a quantum mechanical calculation is to have an initial idea of the atomic positions within an approximate crystal structure.The atomic positions combined should result in a system located in,or close to,an energy minimum.However,designing low-energy structures may be a challenging task when prior knowledge is scarce,specifically for large multi-component systems where the degrees of freedom are close to infinite.In this paper,we propose a method for identification of low-energy crystal structures within multi-component systems by combining cluster expansion and crystal structure predictions with density-functional theory calculations.Crystal structure prediction searches are applied to the Mo_(2)AlB_(2) and Sc2AlB_(2) ternary systems to identify candidate structures,which are subsequently used to explore the quaternary(pseudo-binary)(Mo_(x)Sc_(1–x))2AlB_(2) system through the cluster expansion formalism utilizing the ground-state search approach.Furthermore,we show that utilizing low-energy structures found within the cluster expansion ground-state search as seed structures within crystal structure predictions of(Mo_(x)Sc_(1–x))2AlB_(2) can significantly reduce the computational demands.With this combined approach,we not only correctly identified the recently discovered Mo_(4/3)Sc_(2/3)AlB_(2) i-MAB phase,comprised of in-plane chemical ordering of Mo and Sc and with Al in a Kagomélattice,but also predict additional low-energy structures at various concentrations.This result demonstrates that combining crystal structure prediction with cluster expansion provides a path for identifying low-energy crystal structures in multi-component systems by employing the strengths from both frameworks.

关键词： structure cluster crystal

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COMPOSITION OPERATORS ON BERGMAN SPACES

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Chinese Annals of Mathematics,Series B 2003年第4期24卷 433-448页

作者： j.H.clifford ZHENGDECHAO DepaxtmentofMathematicsandStatistics UniversityofMichiganatDearbornDearbornMichigan48128USA DepartmentofMathematics VanderbiltUniversityNashvilleTN37240USA.

The authors obtain function theoretic characterizations of the compactness on the standardweighted Bergman spaces of the two operators formed by multiplying a composition operatorwith the adjoint of another compositio... 详细信息

关键词：结合算子 Bergman空间正则半映射紧性角微商 Toeplitz算子广义计数函数

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Beta-adrenergic agonist protects retinal pigment epithelium against hydroxycholoroquine toxicity via c AMP-PKA signal pathway

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International journal of Ophthalmology(English edition) 2020年第4期13卷 552-559页

作者： Ruihua Zhang Dan-Ning Hu Richard rosen Eye and Vision Research Institute Department of OphthalmologyIcahn School of Medicine at Mount SinaiNew York 10029USA Department of Ophthalmology New York Eye and Ear Infirmary of Mount SinaiNew York 10003USA

AIM: To test our hypothesis that activation of protein kinase A(PKA) signal pathway by β-adrenergic agonist plays an important role in the protecting of cultured retinal pigment epithelial(RPE) cells against the hydroxychloroquine(HCQ) toxicity. METHODS: Cultured human RPE cells were treated with 1) HCQ, 2) HCQ with salbutamol(a β2-adrenergic receptor agonist), and 3) HCQ with salbutamol and a PKA inhibitor, and compared these to 4) untreated cells(controls). After treated for 24 h, cell vacuolation, cells viability, PKA and PKA kinase activity levels were determined by the measurement of the size of vacuoles using Image j software, the cell counting with a dye-exclusion testing, Western blot and PKA kinase detection, respectively. RESULTS: Cell vacuolation and cell death of cultured RPE cells were significantly increased by the treatment of HCQ. Salbutamol significantly elevated PKA and PKA activity levels and this was associated with the inhibition of the vacuolation and cell death. The PKA inhibitor significantly decreased the PKA levels and eliminated the protective effects of salbutamol on HCQ-treated RPE cells. CONCLUSION: The PKA pathway plays an important role in the protective effects of β2-adrenergic agonist on the RPE cells against HCQ toxicity. These findings reveal a novel potential strategy against HCQ retinopathy by treatment with PKA activating medications.

关键词： hydroxycholoroquine retinal pigment epithelial cells retinopathy protein kinase A vacuolation

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Engineered neuronal microtissue provides exogenous axons for delayed nerve fusion and rapid neuromuscular recovery in rats

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Bioactive Materials 2022年第12期7卷 339-353页

作者： justin C.Burrell Suradip Das Franco A.Laimo Kritika S.Katiyar Kevin D.Browne Robert B.Shultz Vishal j.Tien Phuong T.Vu Dmitriy Petrov Zarina SAli joseph M.rosen D.Kacy Cullen Center for Brain Injury&Repair Department of NeurosurgeryPerelman School of MedicineUniversity of PennsylvaniaPhiladelphiaPAUSA Department of Bioengineering School of Engineering&Applied ScienceUniversity of PennsylvaniaPhiladelphiaPAUSA Center for Neurotrauma Neurodegeneration&RestorationCorporal Michael J.Crescenz Veterans Affairs Medical CenterPhiladelphiaPA19104USA Axonova Medical LLCPhiladelphiaPAUSA Dartmouth-Hitchcock Medical Center Division of Plastic SurgeryDartmouth CollegeLebanonNHUSA

Nerve injury requiring surgical repair often results in poor functional recovery due to the inability of host axons to re-grow long distances and reform meaningful connections with the target muscle. While surgeons can re-route local axon fascicles to the target muscle, there are no technologies to provide an exogenous source of axons without sacrificing healthy nerves. Accordingly, we have developed tissue engineered neuromuscular interfaces (TE-NMIs) as the first injectable microtissue containing motor and sensory neurons in an anatomically-inspired architecture. TE-NMIs provide axon tracts that are intended to integrate with denervated distal structures and preserve regenerative capacity during prolonged periods without host innervation. Following implant, we found that TE-NMI axons promoted Schwann cell maintenance, integrated with distal muscle, and preserved an evoked muscle response out to 20-weeks post nerve transection in absence of innervation from host axons. By repopulating the distal sheath with exogenous axons, TE-NMIs also enabled putative delayed fusion with proximal host axons, a phenomenon previously not achievable in delayed repair scenarios due to distal axon degeneration. Here, we found immediate electrophysiological recovery after fusion with proximal host axons and improved axon maturation and muscle reinnervation at 24-weeks post-transection (4-weeks following delayed nerve fusion). These findings show that TE-NMIs provide the potential to improve functional recovery following delayed nerve repair.

关键词： Nerve regeneration Neuromuscular injury Muscle preservation Tissue engineering Microtissue Axon fusion

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