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Genomes and Genes | J E WergedalSummaryCountry: USA Publications
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Sca-1(+) hematopoietic cell-based gene therapy with a modified FGF-2 increased endosteal/trabecular bone formation in miceSusan L Hall
Musculoskeletal Disease Center, Jerry L Pettis Memorial V A Medical Center, Loma Linda, California 92357, USA
Mol Ther 15:1881-9. 2007..In conclusion, this study provided compelling test-of-principle evidence for the feasibility of using an Sca-1(+) cell-based ex vivo systemic FGF-2 gene therapy strategy to promote endosteal bone formation...- Mapping of the chromosome 17 BMD QTL in the F(2) male mice of MRL/MpJ x SJL/JHongrun Yu
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, CA 92357, USA
Genetica 135:59-66. 2009..There were also co-localized QTLs for femur length, femur periosteal circumference (PC) and total body bone area, suggesting possibility of pleiotropy. Runx2 and VEGFA are strong candidate genes located within this QTL region... - Prepubertal OVX increases IGF-I expression and bone accretion in C57BL/6J miceKristen E Govoni
Jerry L Pettis Memorial Veterans Affairs Medical Center, Loma Linda, California 92357, USA
Am J Physiol Endocrinol Metab 295:E1172-80. 2008.... - Targeted transgenic expression of an osteoclastic transmembrane protein-tyrosine phosphatase in cells of osteoclastic lineage increases bone resorption and bone loss in male young adult miceMatilda H C Sheng
Musculoskeletal Disease Center, Jerry L Pettis Memorial Veterans Affairs Medical Center, Loma Linda, California 92357, USA
J Biol Chem 284:11531-45. 2009..In summary, this study provides compelling in vivo evidence that PTP-oc is a positive regulator of osteoclasts... - Genetic variation in femur extrinsic strength in 29 different inbred strains of mice is dependent on variations in femur cross-sectional geometry and bone densityJon E Wergedal
Musculoskeletal Disease Center, J L Pettis Memorial V A Medical Center and Department of Medicine, Loma Linda University, Loma Linda, CA 92357, USA
Bone 36:111-22. 2005..These studies identify inbred mouse strains suitable for future studies identifying genes regulating bone geometry and mechanical properties... - Femur mechanical properties in the F2 progeny of an NZB/B1NJ x RF/J cross are regulated predominantly by genetic loci that regulate bone geometryJon E Wergedal
Musculoskeletal Disease Center, J L Pettis Memorial VA Medical Center, Loma Linda, CA 92357, USA
J Bone Miner Res 21:1256-66. 2006..Genetic analysis of an NZB/B1NJ x RF/J cross has identified QTLs for femur mechanical, geometric, and densitometric phenotypes. Most mechanical QTLs were associated with geometric QTLs, strongly suggesting common genetic regulation... - Patients with Van Buchem disease, an osteosclerotic genetic disease, have elevated bone formation markers, higher bone density, and greater derived polar moment of inertia than normalJon E Wergedal
Musculoskeletal Disease Center, J L Pettis Memorial Veterans Affairs Medical Center and Loma Linda University, Loma Linda, California 92357, USA
J Clin Endocrinol Metab 88:5778-83. 2003..None of these changes was found in Van Buchem carriers. These observations indicate that decreased expression of the SOST gene can lead to increased bone formation and to stronger bones... - Mouse genetic model for bone strength and size phenotypes: NZB/B1NJ and RF/J inbred strainsJ E Wergedal
Musculoskeletal Disease Center and Department of Medicine and Biochemistry, Loma Linda University, Loma Linda, CA 92357, USA
Bone 31:670-4. 2002..The NZB/B1NJ and RF/J mice should be an excellent model to investigate the genes that regulate femur size and strength... - High osteoblastic activity in C3H/HeJ mice compared to C57BL/6J mice is associated with low apoptosis in C3H/HeJ osteoblastsM H C Sheng
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, CA 92357, USA
Calcif Tissue Int 78:293-301. 2006..In conclusion, these studies support the premise that higher bone density and bone formation rate in C3H mice could be due in part to lower apoptosis in C3H osteoblasts... - Postnatal and pubertal skeletal changes contribute predominantly to the differences in peak bone density between C3H/HeJ and C57BL/6J miceC Richman
JL Pettis Veterans Administration Medical Center and Loma Linda University, California 92357, USA
J Bone Miner Res 16:386-97. 2001.... - Detecting novel bone density and bone size quantitative trait loci using a cross of MRL/MpJ and CAST/EiJ inbred miceH Yu
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA
Calcif Tissue Int 80:103-10. 2007..This study demonstrates the utility of crosses involving inbred strains of mice which exhibit a similar phenotype in QTL identification... - Histomorphometric studies show that bone formation and bone mineral apposition rates are greater in C3H/HeJ (high-density) than C57BL/6J (low-density) mice during growthM H Sheng
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center and Department of Medicine, Loma Linda University, CA 92357, USA
Bone 25:421-9. 1999..Consequently, these two inbred strains of mice are suitable as a model to identify genetic factors responsible for high bone formation rates... - A genomewide screening of N-ethyl-N-nitrosourea-mutagenized mice for musculoskeletal phenotypesA K Srivastava
Musculoskeletal Disease Center, Jerry L. Pettis Veterans Medical Center, and Department of Medicine, Loma Linda University, Loma Linda, CA 92357, USA
Bone 33:179-91. 2003..So far, this ENU mutagenesis program has identified four outliers that can undergo positional cloning... - Genetic regulation of femoral bone mineral density: complexity of sex effect in chromosome 1 revealed by congenic sublines of miceB Edderkaoui
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, 11201 Benton Street, and Department of Biochemistry, Loma Linda University, CA 92357, USA
Bone 41:340-5. 2007.... - Development of an MFG-based retroviral vector system for secretion of high levels of functionally active human BMP4H Peng
Department of Medicine, Loma Linda University, and Musculoskeletal Disease Center (151, Jerry L. Pettis VA Medical Center, Loma Linda, California 92357, USA
Mol Ther 4:95-104. 2001..We have developed an MFG-based retroviral vector system that causes secretion of high levels of functionally active human BMP4 protein... - Mechanical loading-induced gene expression and BMD changes are different in two inbred mouse strainsChandrasekhar Kesavan
Musculoskeletal Disease Center, Veterans Affairs Loma Linda Healthcare System, Loma Linda, CA 92357, USA
J Appl Physiol 99:1951-7. 2005..We conclude that mechanical loading-induced molecular pathways are activated to a greater extent in the B6 than in the C3H mice, resulting in a higher anabolic response in the B6 mice... - Chemical mutagenesis induced two high bone density mouse mutants map to a concordant distal chromosome 4 locusS Mohan
Musculoskeletal Disease Center 151, Loma Linda VA Healthcare Systems, Loma Linda, CA 92357, USA
Bone 41:860-8. 2007..The large phenotype in the mutant mice compared to generally observed QTL effects (<5%) would increase the probability of identifying the mutant gene... - Ex vivo gene therapy with stromal cells transduced with a retroviral vector containing the BMP4 gene completely heals critical size calvarial defect in ratsR Gysin
Department of Medicine, Loma Linda University, CA 92357, USA
Gene Ther 9:991-9. 2002..5 x 10(6) implanted BMP4 cells. In conclusion, the retroviral-based BMP4 gene therapy system that we have developed has the potential for regeneration of large skeletal defects... - Regulation of bone volume is different in the metaphyses of the femur and vertebra of C3H/HeJ and C57BL/6J miceM H C Sheng
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center and the Department of Medicine, Loma Linda University, Loma Linda, CA 92357, USA
Bone 30:486-91. 2002.... - Comparison of bone formation responses to parathyroid hormone(1-34), (1-31), and (2-34) in miceS Mohan
Musculoskeletal Disease Center, Jerry L Pettis VA Medical Center, Loma Linda, CA 92357, USA
Bone 27:471-8. 2000..In conclusion, our findings suggest that PTH(1-34) and PTH(1-31) may exhibit different anabolic effects at the periosteum vs. endosteum in the long bones of mice... - Transgenic overexpression of pregnancy-associated plasma protein-A increases the somatic growth and skeletal muscle mass in miceMark Rehage
Musculoskeletal Disease Center, J L Pettis Veterans Affairs Medical Center 151, 11201 Benton Street, Loma Linda, CA 92357, USA
Endocrinology 148:6176-85. 2007..Moreover, our studies provide the first experimental evidence that IGFBP degradation is a key determinant in modulating the local action of IGFs in muscle... - Identification of genetic loci that regulate bone adaptive response to mechanical loading in C57BL/6J and C3H/HeJ mice intercrossChandrasekhar Kesavan
Musculoskeletal Disease Center, VA Loma Linda Healthcare System, Loma Linda, CA 92357, USA
Bone 39:634-43. 2006..Knowledge of the genes underlying these loci could provide novel approaches to improve skeletal mass... - Androgens directly stimulate proliferation of bone cells in vitroC H Kasperk
Department of Medicine, Loma Linda University, CA 92357
Endocrinology 124:1576-8. 1989..We conclude that androgens can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the osteoblast-line differentiation marker ALP, presumably by an androgen receptor mediated mechanism... - Conditional deletion of insulin-like growth factor-I in collagen type 1alpha2-expressing cells results in postnatal lethality and a dramatic reduction in bone accretionKristen E Govoni
Musculoskeletal Disease Center, Jerry L Pettis Memorial Veterans Affairs Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA
Endocrinology 148:5706-15. 2007..In conclusion, both local and endocrine IGF-I actions are involved in regulating growth of various tissues including bone, but they act via different mechanisms... - Pregnancy-associated plasma protein-A increases osteoblast proliferation in vitro and bone formation in vivoXuezhong Qin
Musculoskeletal Disease Center, J L Pettis Veterans Affairs Medical Center 151, 11201 Benton Street, and Department of Medicine, Loma Linda University, California 92357, USA
Endocrinology 147:5653-61. 2006..Thus, enhancing IGF bioavailability by PAPP-A can be a powerful strategy in the treatment of certain metabolic diseases such as osteoporosis... - Digit tip regrowth and differential gene expression in MRL/Mpj, DBA/2, and C57BL/6 miceRobert B Chadwick
Musculoskeletal Disease Center, JL Pettis VA Medical Center, Molecular Genetics Division, Loma Linda, CA 92357, USA
Wound Repair Regen 15:275-84. 2007..This enhanced regrowth is likely due to strain-specific increased expression of genes involved in growth and development... - Osteoactivin is a novel osteoclastic protein and plays a key role in osteoclast differentiation and activityMatilda H C Sheng
Musculoskeletal Disease Center 151, Jerry L Pettis Memorial VA Medical Center, Loma Linda, CA 92357, USA
FEBS Lett 582:1451-8. 2008..These findings indicate that OA is a novel osteoclastic protein and plays a role in osteoclast differentiation and/or activity... - In vivo and in vitro evidence that the high osteoblastic activity in C3H/HeJ mice compared to C57BL/6J mice is intrinsic to bone cellsMatilda H C Sheng
Musculoskeletal Disease Center, Jerry L Pettis Memorial Veterans Medical Center, Loma Linda, CA 92357, USA
Bone 35:711-9. 2004.... - Local ex vivo gene therapy with bone marrow stromal cells expressing human BMP4 promotes endosteal bone formation in miceXiao S Zhang
Department of Medicine, Loma Linda University, and Gene Therapy Division, Musculoskeletal Disease Center (151, VA Loma Linda Healthcare Network, Loma Linda, CA 92357, USA
J Gene Med 6:4-15. 2004..4% at 56 days. CONCLUSIONS: The present findings support the feasibility of using ex vivo MSC-based retroviral gene therapy to induce relatively sustained new bone formation, with normal histological appearance, at endosteal bone sites... - Lack of insulin-like growth factor I exaggerates the effect of calcium deficiency on bone accretion in miceYuji Kasukawa
Musculoskeletal Disease Center, J L Petttis Veterans Administration Medical Center, 11201 Benton Street, Loma Linda, California 92357, USA
Endocrinology 144:4682-9. 2003.... - Marrow stromal cell-based cyclooxygenase 2 ex vivo gene-transfer strategy surprisingly lacks bone-regeneration effects and suppresses the bone-regeneration action of bone morphogenetic protein 4 in a mouse critical-sized calvarial defect modelK H William Lau
Musculoskeletal Disease Center 151, Jerry L Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA
Calcif Tissue Int 85:356-67. 2009..In summary, the Cox-2 ex vivo gene-transfer strategy not only lacks bone-regeneration effects but also suppresses the bone-regeneration action of BMP4 in healing of calvarial defects... - Loss of sex-specific difference in femoral bone parameters in male leptin knockout miceXiaoguang Wang
Musculoskeletal Disease Center 151, J L Pettis Memorial Veterans Administration Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA
Calcif Tissue Int 80:374-82. 2007.... - LMP-1 retroviral gene therapy influences osteoblast differentiation and fracture repair: a preliminary studyCassandra A Strohbach
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA
Calcif Tissue Int 83:202-11. 2008..These exciting, albeit preliminary, findings indicate that LMP-1-based gene therapy may potentially be a simple and effective means to enhance fracture repair that warrants further investigation... - Mapping genetic loci that regulate lipid levels in a NZB/B1NJxRF/J intercross and a combined intercross involving NZB/B1NJ, RF/J, MRL/MpJ, and SJL/J mouse strainsJon E Wergedal
Musculoskeletal Disease Center, Loma Linda VA Health Care Systems, Loma Linda, CA, USA
J Lipid Res 48:1724-34. 2007..The identification of shared loci from multiple crosses increases confidence toward finding the QTL gene... - New quantitative trait loci that regulate wound healing in an intercross progeny from DBA/1J and 129 x 1/SvJ inbred strains of miceGodfred L Masinde
Musculoskeletal Disease Center, Jerry L Pettis Memorial Veterans Administration Medical Center, Loma Linda, CA 92357, USA
Funct Integr Genomics 6:157-63. 2006..7% of the phenotype variation in ear punch healing. In conclusion, we have identified novel QTL and shown that minor interacting loci contribute significantly to wound healing in DBA x 129 mice cross... - Inactivation of insulin-like-growth factors diminished the anabolic effects of pregnancy-associated plasma protein-A (PAPP-A) on bone in miceDavid Phang
Musculoskeletal Disease Center, Loma Linda University, Loma Linda, CA 92354, United States
Growth Horm IGF Res 20:192-200. 2010..This clear definition of PAPP-A's mechanism of action is critical for future translational studies on the therapeutic application of PAPP-A... - Identification of mouse Duffy antigen receptor for chemokines (Darc) as a BMD QTL geneBouchra Edderkaoui
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, and Department of Medicine and Biochemistry, Loma Linda University, California 92357, USA
Genome Res 17:577-85. 2007.... - Effect of insulin-like growth factor-1 (IGF-1) plus alendronate on bone density during puberty in IGF-1-deficient MIDI miceL Stabnov
Musculoskeletal Disease Center, Jerry L. Pettis Veterans Administration Medical Center, Loma Linda, CA 92357, USA
Bone 30:909-16. 2002.... - Fracture healing in mice deficient in plasminogen activator inhibitor-1Charles H Rundle
Musculoskeletal Disease Center, Jerry L Pettis Memorial Veterans Administration Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA
Calcif Tissue Int 83:276-84. 2008.... - Bax deficiency in mice increases cartilage production during fracture repair through a mechanism involving increased chondrocyte proliferation without changes in apoptosisCharles H Rundle
Musculoskeletal Disease Center, Jerry L Pettis Memorial Veterans Administration Medical Center 151, 11201 Benton Street, Loma Linda, CA 92357, USA
Bone 43:880-8. 2008..The unexpected effect of Bax deficiency on chondrocyte proliferation implicates a novel regulatory function for Bax on chondrocyte proliferation during fracture repair... - Multiple genetic loci from CAST/EiJ chromosome 1 affect vBMD either positively or negatively in a C57BL/6J backgroundBouchra Edderkaoui
Musculoskeletal Disease Center, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California 92357, USA
J Bone Miner Res 21:97-104. 2006..Skeletal phenotype analyses of 10 B6.CAST-1 congenic sublines of mice have revealed evidence for the presence of three closely linked QTLs in Chr 1 that influence femoral vBMD both positively and negatively... - Regulation of phosphatidylinositol 3-kinase (PI3K)/Akt and nuclear factor-kappa B signaling pathways in dystrophin-deficient skeletal muscle in response to mechanical stretchCharu Dogra
Molecular Genetics Division, Jerry L Pettis Memorial VA Medical Center, Loma Linda, California 92357, USA
J Cell Physiol 208:575-85. 2006..Taken together, our data suggest that loss of dystrophin and/or mechanical stretch results in the up-regulation of P13K/Akt and NF-kappaB signaling pathways in skeletal muscle... - Disruption of insulin-like growth factor-I expression in type IIalphaI collagen-expressing cells reduces bone length and width in miceKristen E Govoni
Jerry L Pettis Veterans Affairs Medical Center and Loma Linda University, Loma Linda, California 92357, USA
Physiol Genomics 30:354-62. 2007..20). In conclusion, IGF-I from cells expressing procollagen type IIalphaI regulates bone accretion that occurs during postnatal growth period... - TNF-related weak inducer of apoptosis (TWEAK) is a potent skeletal muscle-wasting cytokineCharu Dogra
Musculoskeletal Disease Center, Jerry L Pettis Memorial Veterans Administration Medical Center, Loma Linda, CA 92357, USA
FASEB J 21:1857-69. 2007..Collectively, our data suggest that TWEAK induces skeletal muscle atrophy through inhibition of the PI3K/Akt signaling pathway and activation of the ubiquitin-proteasome and NF-kappaB systems... - In vivo bone formation in fracture repair induced by direct retroviral-based gene therapy with bone morphogenetic protein-4Charles H Rundle
Departments of Medicine and Biochemistry, Loma Linda University, and the Jerry L. Pettis Memorial VA Medical Center, 11201 Benton Street, Loma Linda, CA 92357, USA
Bone 32:591-601. 2003.... - Microarray analysis of gene expression during the inflammation and endochondral bone formation stages of rat femur fracture repairCharles H Rundle
Musculoskeletal Disease Center, Jerry L. Pettis V. A. Medical Center, Loma Linda, CA 92357, USA
Bone 38:521-9. 2006..These observations suggest that these genes might also regulate the scarless healing characteristic of bone regeneration by similar mechanisms... - Retroviral-based gene therapy with cyclooxygenase-2 promotes the union of bony callus tissues and accelerates fracture healing in the ratCharles H Rundle
Department of Medicine, Loma Linda University, Loma Linda, CA, USA
J Gene Med 10:229-41. 2008..An in vivo gene therapy strategy was developed to accelerate bone fracture repair... - Insulin-like growth factor-binding protein-5 induces a gender-related decrease in bone mineral density in transgenic miceDervis A M Salih
Laboratory of Molecular Signaling, The Babraham Institute, Cambridge, United Kingdom CB2 4AT
Endocrinology 146:931-40. 2005..These findings have implications for the gender-biased progression of osteoporosis... - A time course of bone response to jump exercise in C57BL/6J miceYoshihisa Umemura
School of Health and Sport Sciences, Chukyo University, Toyota, Japan
J Bone Miner Metab 20:209-15. 2002..We conclude that a shorter exercise regimen, of 3 weeks, induced a bone response that was greater than or equal to that of 4 weeks of jump exercise reported earlier... - A missense mutation in the mouse Col2a1 gene causes spondyloepiphyseal dysplasia congenita, hearing loss, and retinoschisisLeah Rae Donahue
The Jackson Laboratory, Bar Harbor, Maine 04609, USA
J Bone Miner Res 18:1612-21. 2003..In addition, SED patients have been identified with a similar molecular mutation in human COL2A1. This mouse model offers a useful tool for molecular and biological studies of bone development and pathology...