Prominent publications by Ahlke Heydemann

KOL Index score: 12467

Chondrogenesis can occur during a bone repair process, which is related to several growth factors. Transforming growth factor beta 1 (TGF-beta 1) downregulates the expression of type II collagen by chondrocytes in vitro, but injection of TGF-beta 1 into the periosteum in vivo increases type II collagen mRNA levels and initiates chondrogenesis. We examined the effect of TGF-beta 1 on collagen gene expression in a bovine periosteum-derived cell culture system to evaluate its direct effect ...

Conocido por Growth Factor |  collagen expression |  beta 1 |  alkaline phosphatase |  cultured cells
KOL Index score: 11766

Pluripotent bone marrow-derived side population (BM-SP) stem cells have been shown to repopulate the hematopoietic system and to contribute to skeletal and cardiac muscle regeneration after transplantation. We tested BM-SP cells for their ability to regenerate heart and skeletal muscle using a model of cardiomyopathy and muscular dystrophy that lacks delta-sarcoglycan. The absence of delta-sarcoglycan produces microinfarcts in heart and skeletal muscle that should recruit regenerative ...

Conocido por Skeletal Muscle |  stem cell |  situ hybridization |  transplantation hematopoietic |  donor derived
KOL Index score: 10455

The protein product of the c-fps/fes (c-fes) proto-oncogene has been implicated in the normal development of myeloid cells (macrophages and neutrophils). mRNA for c-fes has been detected exclusively in myeloid cells and vascular endothelial cells in adult mammals. Although a 13-kilobase-pair (kb) human c-fes transgene exhibits high levels of expression in mice, the sequences that confer myeloid-cell-specific expression of the human c-fes gene have not been defined. Transient-transfection ...

Conocido por Fes Promoter |  myeloid cells |  sp1 transcription factor |  proto oncogene |  cell specific
KOL Index score: 10400

RATIONALE: S100A12 is a small calcium binding protein that is a ligand of RAGE (receptor for advanced glycation end products). RAGE has been extensively implicated in inflammatory states such as atherosclerosis, but the role of S100A12 as its ligand is less clear.

OBJECTIVE: To test the role of S100A12 in vascular inflammation, we generated and analyzed mice expressing human S100A12 in vascular smooth muscle under control of the smooth muscle 22alpha promoter because S100A12 is not ...

Conocido por Aortic Aneurysm |  s100a12 mice |  transgenic muscle |  vascular smooth |  ligand rage
KOL Index score: 10029

Over the past decade different stem cell (SC) based approaches were tested to treat Duchenne Muscular Dystrophy (DMD), a lethal X-linked disorder caused by mutations in dystrophin gene. Despite research efforts, there is no curative therapy for DMD. Allogeneic SC therapies aim to restore dystrophin in the affected muscles; however, they are challenged by rejection and limited engraftment. Thus, there is a need to develop new more efficacious SC therapies. Chimeric Cells (CC), created via ...

Conocido por Dystrophin Expressing |  chimeric cells |  duchenne muscular dystrophy |  stem cell |  myoblast origin
KOL Index score: 9984

Most single-gene diseases, including muscular dystrophy, display a nonuniform phenotype. Phenotypic variability arises, in part, due to the presence of genetic modifiers that enhance or suppress the disease process. We employed an unbiased mapping approach to search for genes that modify muscular dystrophy in mice. In a genome-wide scan, we identified a single strong locus on chromosome 7 that influenced two pathological features of muscular dystrophy, muscle membrane permeability and ...

Conocido por Muscular Dystrophy |  latent tgf |  knockout mice |  binding protein |  muscle fibrosis
KOL Index score: 9317

Loss-of-function mutations in the genes encoding dystrophin and the associated membrane proteins, the sarcoglycans, produce muscular dystrophy and cardiomyopathy. The dystrophin complex provides stability to the plasma membrane of striated muscle during muscle contraction. Increased SMAD signaling due to activation of the transforming growth factor-β (TGFβ) pathway has been described in muscular dystrophy; however, it is not known whether this canonical TGFβ signaling is pathogenic in ...

Conocido por Muscular Dystrophy |  smad signaling |  muscle dysfunction |  drosophila model |  heart function
KOL Index score: 9200

Duchenne Muscular Dystrophy (DMD) is a progressive and lethal disease caused by mutations of the dystrophin gene. Currently no cure exists. Stem cell therapies targeting DMD are challenged by limited engraftment and rejection despite the use of immunosuppression. There is an urgent need to introduce new stem cell-based therapies that exhibit low allogenic profiles and improved cell engraftment. In this proof-of-concept study, we develop and test a new human stem cell-based approach to ...

Conocido por Duchenne Muscular Dystrophy |  dystrophin expressing chimeric |  human cells |  dec dmd |  flow cytometry
KOL Index score: 8880

Estrogen has profound effects on bone metabolism, yet its precise mechanism of action remains unknown. Several recent investigations have located the estrogen receptor (ER) on osteoblast-like cells, suggesting a potential direct action of estrogen via its own receptor on bone cells. The protective role of estrogen on bone in osteoporosis is well known; however, neither the existence nor the mechanism of an estrogenic role in tracture healing has been well studied. In this investigation ...

Conocido por Fracture Healing |  estrogen receptor |  messenger rats |  mrna expression |  bone metabolism
KOL Index score: 8804

Many monogenic disorders, including the muscular dystrophies, display phenotypic variability despite the same disease-causing mutation. To identify genetic modifiers of muscular dystrophy and its associated cardiomyopathy, we used quantitative trait locus mapping and whole genome sequencing in a mouse model. This approach uncovered a modifier locus on chromosome 11 associated with sarcolemmal membrane damage and heart mass. Whole genome and RNA sequencing identified Anxa6, encoding ...

Conocido por Muscular Dystrophy |  annexin a6 |  sarcolemmal repair |  genetic modifiers |  mouse model
KOL Index score: 8633

Although transforming growth factors-beta and bone morphogenetic proteins are both capable of inducing bone formation in vivo, the target cells of their osteoinductive actions may be different. To evaluate periosteal cells as potential targets of the actions of transforming growth factor-beta and bone morphogenetic protein, we investigated the ability of three members of the transforming growth factor-beta superfamily to modulate expression of the gene encoding the alpha 1(II) chain of ...

Conocido por Transforming Growth |  collagen gene |  factor beta |  derived cells |  bone formation
KOL Index score: 7606

Duchenne Muscular Dystrophy (DMD) is a progressive lethal disease caused by X-linked mutations of the dystrophin gene. Dystrophin deficiency clinically manifests as skeletal and cardiac muscle weakness, leading to muscle wasting and premature death due to cardiac and respiratory failure. Currently, no cure exists. Since heart disease is becoming a leading cause of death in DMD patients, there is an urgent need to develop new more effective therapeutic strategies for protection and ...

Conocido por Duchenne Muscular Dystrophy |  dystrophin expressing |  dec cells |  mesenchymal stem |  mdx mouse
KOL Index score: 7065

BACKGROUND: The calcium-binding protein S100A12 is highly up-regulated in the serum and sputum of patients with allergic asthma and is suggested to be a biomarker and pathologic mediator of asthma.

OBJECTIVE: To test the role of S100A12 in mediating airway inflammation in a mouse model of allergic lung inflammation.

METHODS: Transgenic (TG) mice that express human S100A12 and wild-type (WT) littermates were sensitized and challenged with ovalbumin (OVA) and assessed for inflammation, ...

Conocido por Airway Inflammation |  transgenic expression |  smooth muscle |  human s100a12 |  s100 proteins
KOL Index score: 6663

Retinoic acid has been identified as a key morphogen governing pattern formation in the developing cartilaginous skeleton. Retinoids have also been implicated in the premature closure of the cartilage growth plate following vitamin A intoxication or administration of retinoids for dermatologic conditions. Previous studies of the mechanism of action of retinoids in non-chondrogenic cells have concluded that retinoic acid is a negative regulator of AP-1 responsive metalloprotease genes. We ...

Conocido por Retinoic Acid |  chondrocyte phenotype |  gene expression |  messenger rats |  cartilage matrix

Gente clave para Muscular Dystrophy

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Ahlke Heydemann:Impacto experto

Conceptos para los cualesAhlke Heydemanntiene influencia directa:Muscular dystrophy,  Skeletal muscle,  Duchenne muscular dystrophy,  Vascular spasm,  Mouse models,  Annexin a6,  Retinoic acid,  Dystrophin expressing.

Ahlke Heydemann:Impacto de Kol

Conceptos relacionados con el trabajo de otros autores para los cualesfor which Ahlke Heydemann tiene influencia:Muscular dystrophy,  Growth factor,  Skeletal muscle,  Fracture healing,  Stem cells,  Articular cartilage,  Mdx mice.



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Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612, USA | Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois, USA | Department of Physiology and Biophysics, University o