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Tesi sul tema "Bone resorption – Molecular aspects"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 1 febbraio 2022

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1

Cheng, Tak Sum. "Molecular identification and characterization of novel osteoclast V-ATPase subunits." University of Western Australia. School of Surgery and Pathology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0068.

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[Truncated abstract] Osteoclasts are multinucleated giant cells responsible for the resorption of the mineralized bone matrix during the process of bone remodelling. During activation towards bone resorption, polarization of the osteoclast results in the formation of a unique plasma membrane, the ruffled border, the actual resorptive organelle of the osteoclast. Through this domain protons are actively pumped into the resorption lacuna creating an acidic microenvironment that favours the dissolution of the mineralized bone matrix. The polarised secretion of protons is carried out by the action

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2

Wang, Cathy Ting-Peng. "Molecular dissection of RANKL signaling pathways in osteoclasts." University of Western Australia. School of Surgery and Pathology, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0037.

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[Truncated abstract] Bone remodeling is intricately regulated by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. The elevation in osteoclast number and/or activity is a major hallmark of several common pathological bone disorders including post-menopausal osteoporosis, osteoarthritis, Paget's disease, and tumour-mediated osteolysis. Receptor activator of nuclear factor kappa B ligand (RANKL) is a key cytokine for osteoclast differentiation and activation. The association of RANKL to its cognate receptor, RANK, which is expressed on osteoclast precursors and mature o

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3

Irani, Dilshad Minocher. "Role of the surface associated material of Eikenella corrodens in bone resorption associated with periodontal disease : a research thesis submitted in fulfilment of the requirements for the degree of Master of Science in Dentistry." Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09DSM/09dsmi65.pdf.

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4

Tan, Jamie We-Yin. "The investigation of RANKL TNF-like core domain by truncation mutation." University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0032.

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Osteoclasts are multinucleated cells found exclusively in bone and are derived from the haematopoietic cells of monocytes/macrophage lineage. The cell-to-cell interaction between osteoblastic/stromal cells and osteoclast precursor cells is necessary for osteoclastogenesis. Receptor Activator of NF-κB ligand (RANKL) was identified as a membrane-bound TNF ligand family member that is the ‘master’ cytokine expressed on osteoblastic/stromal cells, which stimulate osteoclastogenesis through cell-to-cell contact with osteoclast precursors. RANKL is considered to be a factor that is necessary and suf

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5

Hou, Peng. "Matrix metalloproteinases in the osteoclast, with special emphasis on the molecular cloning and the functional role of matrix metalloproteinase-12." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287350.

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6

Peng, Songlin, and 彭松林. "Investigation of the cellular and molecular mechanisms for the dual effect of strontium on bone." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45585167.

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7

Tkachenko, Evgeniy. "Measures of Individual Resorption Cavities in Three-Dimensional Images in Cancellous Bone." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1301413780.

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8

Burger, Nicolaas Daniel Lombard. "Failure analysis of ultra-high molecular weight polyethyelene acetabular cups." Pretoria : [s.n.], 2005. http://upetd.up.ac.za/thesis/available/etd-12142006-134036.

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9

Mbimba, Thomas S. Jr. "TRAFICKING PROTEIN PARTICLE COMPLEX (TRAPPC) -9:A NOVEL PROTEIN REGULATOR OF NF-kB MEDIATED BONE FORMATION AND RESORPTION." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1448841594.

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10

Cheng, Yin-wo, and 鄭燕和. "Molecular basis for the increased osteoblast activity in a mouse modelwith hyperostosis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B34612981.

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11

Lotz, Ethan M. "Designing Biomimetic Implant Surfaces to Promote Osseointegration under Osteoporotic Conditions by Revitalizing Mechanisms Coupling Bone Resorption to Formation." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5908.

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Abstract (sommario):

In cases of compromised bone remodeling like osteoporosis, insufficient osseointegration occurs and results in implant failure. Implant retention relies on proper secondary fixation, which is developed during bone remodeling. This process is disrupted in metastatic bone diseases like osteoporosis. Osteoporosis is characterized low bone mass and bone strength resulting from either accelerated osteoclast-mediated bone resorption or impaired osteoblast-mediated bone formation. These two processes are not independent phenomena. In fact, osteoporosis can be viewed as a breakdown of the cellular com

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12

Sherwood, Jennifer J. "Effect of weight bearing exercise on hormonal growth factors." Virtual Press, 1994. http://liblink.bsu.edu/uhtbin/catkey/897491.

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Age-related bone loss is a serious public health problem affecting 15 to 20 million people in the United States (1). In the last decade, several studies have investigated the effects of repeated bouts of exercise on bone density. Although this increase in bone density is mediated via hormones and/or cellular metabolites few studies have linked the increase in bone density with changes in these hormones or metabolites. Therefore, the purpose of this study was to determine the effect of a single bout of weight bearing exercise on the growth factors that alter bone metabolism. Seven healthy femal

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13

Dai, Zhijie, and 戴志洁. "The role of sodium/myo-inositol cotransporter 1 and myo-inositol in osteogenesis and bone formation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43783533.

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14

Lee, B. C. Bob, and 李卜駿. "Probing the molecular mechanisms of how polymorphisms in Cerberus-likeresult in low bone mineral density." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39793771.

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15

Shu, Sherry T. "Pathogenesis and Treatments of Humoral Hypercalcemia of Malignancy in Adult T-Cell Leukemia/Lymphoma Induced by Human T Lymphotropic Virus Type 1." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1245283708.

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16

Belibasakis, Georgios N. "Cellular and molecular responses of periodontal connective tissue cells to Actinobacillus actinomycetemcomitans cytolethal distending toxin." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-345.

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17

Kotadiya, Preeyal. "Regulation Of Osteoclast Function By Alpha Gene Tropomyosins, TM-2/3 And TM-5a/5b." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250612152.

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18

Himes, Evan Robert. "The role of STAT3 in osteoclast mediated bone resorption." Thesis, 2014. http://hdl.handle.net/1805/4841.

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Abstract (sommario):

Indiana University-Purdue University Indianapolis (IUPUI)<br>Signal Transducer and Activator of Transcription 3 (STAT3) is known to be related to bone metabolism. Mutation of STAT3 causes a rare disorder in which serum levels of IgE are elevated. This causes various skeletal problems similar to osteoporosis. To examine the effect of STAT3 in the osteoclast, we obtained two osteoclast specific STAT3 knockout mouse models: one using the CTSK promoter to drive Cre recombinase and another using a TRAP promoter. Examination of these mice at 8 weeks of age revealed a decreased trabecular bone vo

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19

Farrow, Emily. "Molecular Genetic Analysis of FGF23 Bioactivity in the Bone-Kidney Endocrine Axis." Thesis, 2009. http://hdl.handle.net/1805/1890.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Heritable disorders of phosphate handling are the most common cause of hypophosphatemic rickets in developed countries. Isolated renal phosphate wasting and subsequent low serum phosphate concentrations may result from a number of genetic disorders that include: autosomal dominant hypophosphatemic rickets (ADHR), X-linked hypophosphatemic rickets (XLH), and autosomal recessive hypophosphatemic rickets (ARHR). Fibroblast growth factor-23 (FGF23), identified as the causative gene in ADHR, is produced in bone and plays a central role in

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20

"Bone marrow-derived macrophage myofibroblast transition (MMT) in renal fibrosis." 2012. http://library.cuhk.edu.hk/record=b5549424.

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背景：纤维化是各种因素导致肾脏慢性损伤的最终病理过程，是决定肾功能转归的关键因素。肌纤维母细胞作为构成肾脏纤维化组织的主要细胞成分，其来源尚不清楚。本研究认为骨髓来源的巨噬细胞向肌纤维母细胞转分化（MMT）可能是肾脏纤维化中肌纤维母细胞的主要来源。我们分别在慢性肾脏病患者的肾活检组织和小鼠单侧输料管梗阻模型（UUO）中验证这一假说。<br>方法：我们用激光共聚焦技术和流式细胞染色的方法检测小鼠UUO肾脏和患者肾活检组织中的MMT细胞(F4/80⁺α-SMA⁺或CD68⁺α-SMA⁺)。为了验证骨髓来源的MMT在肾纤维化中的重要作用，UUO模型分别在以下小鼠进行：1）去除骨髓的C57BL/6J小鼠，给予或不给予绿色荧光蛋白（GFP）标记的骨髓细胞移植；2）GFP⁺骨髓的嵌合体小鼠；3）巨噬细胞敲除或不敲除的lysM-Cre/DTR小鼠；4）GFP⁺Smad3⁺/⁺ 或GFP⁺Smad3⁻/⁻骨髓的嵌合体小鼠。我们用实时定量PCR和Western blot检测小鼠肾组织collagen-I和α-SMA水平。另外，我们观察MMT细胞和PDGFR-β⁺ pericytes, CD45⁺collagen I⁺ fibrocytes的关系。最后，通过观察GFP⁺Smad3⁻/⁻骨髓嵌合体小鼠UUO模型肾纤维化程度和TGF-β1刺激下TGF-β受体II或Smad3敲除的骨髓巨噬细胞MMT的不同进

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21

Anuradha, Valiya Kambrath. "Testing the reliability and selectivity of different bone-cell-specific Cre- expressing mouse models for studying bone cell metabolism." Thesis, 2015. http://hdl.handle.net/1805/7942.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>The Cre/loxP system is a tool for targeted recombination of DNA. For applying Cre recombinase-mediated genome modifications, there is a requirement for reliable, high-fidelity, and specific transgenic expression of the Cre recombinase. This study focuses on the reliability of different bone cell specific Cre models in the Cre/loxP system. In this study, DMP1-Cre transgenic mouse which has a transgene driven by DMP1 promotor that allows Cre-expression only in late stage osteoblasts and osteocytes was used. Ctsk-Cre mouse with a driven

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22

"Role of Aqp1, Sm51 and GATA6 in differentiation and migration of bone marrow derived mesenchymal stem cells." 2013. http://library.cuhk.edu.hk/record=b5884485.

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Abstract (sommario):

Meng, Fanbiao.<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 2013.<br>Includes bibliographical references (leaves 114-138).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Abstract also in Chinese.

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23

Rhodes, Steven David. "Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects." Thesis, 2014. http://hdl.handle.net/1805/3793.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Skeletal manifestations including short stature, osteoporosis, kyphoscoliosis, and tibial dysplasia cumulatively affect approximately 70% of patients with neurofibromatosis type 1 (NF1). Tibial pseudarthrosis, the chronic non-union of a spontaneous fracture, is a debilitating skeletal malady affecting young children with NF1. These non-healing fractures respond poorly to treatment and often require amputation of the affected limb due to limited understanding of the causative mechanisms. To better understand the cellular and molecula

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24

"Roles of CRBP1, N-cadherin and SOX11 in differentiation and migration of bone marrow-derived mesenchymal stem cells." 2012. http://library.cuhk.edu.hk/record=b5549603.

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前言：間充質幹細胞容易擴增並且能分化為成骨細胞、軟骨細胞和脂肪細胞，並且能對炎症、感染和損傷做出反應，並且遷移到相應的組織部位。這些特性使間充質幹細胞成為骨骼組織工程學中非常重要的細胞來源。外周血間充質幹細胞是一種存在於血液中的間充質幹細胞，而主要的間充質幹細胞存在與骨髓中，被稱之為骨髓間充質幹細胞。在我們實驗室之前的研究中通過DNA微陣列發現外周血間充質幹細胞中很多基因的表達與骨髓間充質幹細胞有很大區別。這其中的一些基因可能參與調控間充質幹細胞的分化和歸巢，我們從中挑選了三個變化比較明顯的基因--CRBP1, N-cadherin和 SOX11做進一步研究。本研究的目的在於研究CRBP1, N-cadherin和 SOX11在骨髓間充質幹細胞分化和遷移中的作用及相關機理。<br>方法：培養的骨髓間充質幹細胞來源於6-8周大小的SD大鼠。細胞的表型經過多分化潛能測試（成骨分化，成脂分化和成軟骨分化）和流式細胞儀檢驗。克隆大鼠的CRBP1, N-cadherin和SOX11基因到慢病毒載體。而且還設計了針對CRBP1和 N-cadherin的shRNA及非特異性對照shRNA。慢病毒由暫態轉染293FT細胞產生。細胞遷移實驗採用了BD Falcon的細胞遷移系統（cell culture insert）。實驗採用了定量PCR、免疫共沉澱、western雜交和雙螢光報告檢驗。對於體內實

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25

Zhou, Hongkang. "The essential role of Stat3 in bone homeostasis and mechanotransduction." Thesis, 2014. http://hdl.handle.net/1805/6190.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Signal Transducer and Activator of Transcription 3 (Stat3) is a transcription factor expressed in bone and joint cells that include osteoblasts, osteocytes, osteoclasts, and chondrocytes. Stat3 is activated by a variety of cytokines and growth factors, including IL-6/gp130 family cytokines. These cytokines not only regulate the differentiation of osteoblasts and osteoclasts, but also regulate proliferation of chondrocytes through Stat3 activation. In 2007, mutations of Stat3 have been confirmed to cause a rare human immunodeficiency

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26

Dumaual, Carmen Michelle. "Expression and Function of the PRL Family of Protein Tyrosine Phosphatase." 2013. http://hdl.handle.net/1805/3248.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>The PRL family of enzymes constitutes a unique class of protein tyrosine phosphatase, consisting of three highly homologous members (PRL-1, PRL-2, and PRL-3). Family member PRL-3 is highly expressed in a number of tumor types and has recently gained much interest as a potential prognostic indicator of increased disease aggressiveness and poor clinical outcome for multiple human cancers. PRL-1 and PRL-2 are also known to promote a malignant phenotype in vitro, however, prior to the present study, little was known about their express

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27

"Phenotypic and molecular characterization of mice deficient in protein kinase A regulatory subunit type 1A (prkar1a) and catalytic subunit A (prkaca)." Thesis, 2010. http://library.cuhk.edu.hk/record=b6074857.

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A population of stromal cells that retains osteogenic capacity in adult bone (adult bone stromal cells or aBSCs) exists and is under intense investigation in relation to osteogenesis and relevant pathology. aBSCs may be different from their embryonic or neonatal counterparts, and are influenced by species-/age-specific and other factors. Mice heterozygous for a null allele of prkar1a (Prkar1a+/-, a gene encoding for cyclic adenosine mono-phosphate (cAMP)-dependent regulatory subunit of protein kinase A (PKA), developed bone lesions that resembled fibrous dysplasia (FD) originated from cAMP-re

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28

Tanataweethum, Nida. "Mechanical property and biocompatibility of PLLA coated DCPD composite scaffolds." Thesis, 2014. http://hdl.handle.net/1805/4448.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Dicalcium phosphate dihydrate (DCPD) cements have been used for bone repair due to its excellent biocompatibility and resorbability. However, DCPD cements are typically weak and brittle. To overcome these limitations, the sodium citrate used as a setting regulator and the coating of poly-L-lactide acid (PLLA) technique have been proposed in this study. The first purpose of this thesis is to develop composite PLLA/DCPD scaffolds with enhanced toughness by PLLA coating. The second purpose is to examine the biocompatibility of the scaf

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29

Martin, Holly René. "Mechanism of Transformation and Therapeutic Targets for Hematological Neoplasms Harboring Oncogenic KIT Mutation." Thesis, 2014. http://hdl.handle.net/1805/5503.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Gain-of-function mutations in the KIT receptor tyrosine kinase have been associated with highly malignant human neoplasms. In particular, an acquired somatic mutation at codon 816 in the second catalytic domain of KIT involving an aspartic acid to valine substitution is found in patients with systemic mastocytosis (SM) and acute myeloid leukemia (AML). The presence of this mutation in SM and AML is associated with poor prognosis and overall survival. This mutation changes the conformation of the KIT receptor resulting in altered subs

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