Effects of Reduced Connexin43 Function on Mandibular Morphology and Osteogenesis in Mutant Mouse Models of Oculodentodigital Dysplasia

Effects of Reduced Connexin43 Function on Mandibular Morphology and Osteogenesis in Mutant Mouse Models of Oculodentodigital Dysplasia

Mutations in the gene encoding the gap-junctional protein connexin43 (Cx43) is the cause of human disease oculodentodigital dysplasia (ODDD). mandible often affected by this disease, the clinical report describes both the overgrowth of the mandible and vice versa, retrognathia.

Observations were apparently opposed to underline our relative lack of understanding of how ODDD affect the morphology of the lower jaw. Using two mouse models that mimic the mutant phenotype ODDD (I130T / + and G60S / +), we sought to uncover how the altered function of Cx43 can affect the development of the lower jaw.

Specifically, jaw newborn mice were imaged using micro-CT, to allow statistical comparison of forms. network-level comparison of the key areas of the mandible is done by using histomorphology, and we quantified the mRNA expression of some of the cartilage and bone cell differentiation markers. Both G60S / + and I130T / + mice mutant has changed the morphology of the mandibular compared to their wildtype counterparts, and morphological effects are equally locally for both mutants.

In particular, the largest phenotypic differences in mutant mice focused in areas exposed to mechanical forces, such as alveolar bone, muscle attachment sites, and the articular surface. Histological analysis revealed differences intramembranous ossification of the jaw bone both mutant mice compared to their wildtype littermates. However, the organization of chondrocytes in cartilage secondary mandible is not affected in the mutant mice. Overall, our results indicate that morphological differences seen in the jaw G60S / + and I130T / + mouse as delayed ossification and suggested that mechanical forces can exacerbate the effects of ODDD bone.

Effects of Reduced Connexin43 Function on Mandibular Morphology and Osteogenesis in Mutant Mouse Models of Oculodentodigital Dysplasia
Effects of Reduced Connexin43 Function on Mandibular Morphology and Osteogenesis in Mutant Mouse Models of Oculodentodigital Dysplasia

XIAP Protecting retinal ganglion cells in mutant ND4 Rat Model of Leber Hereditary Optic Neuropathy

Objective: Leber hereditary optic neuropathy (LHON) is a genetic form of vision loss that occurs mainly due to a mutation in the nicotinamide adenine dinucleotide dehydrogenase (ND) subunits that make up the complex I of the electron transport chain. LHON mutations resulted in the death of retinal ganglion cell apoptosis. We tested the hypothesis that gene therapy with X-linked inhibitor of apoptosis (XIAP) will prevent retinal ganglion cell apoptosis and reduce disease progression in a mouse model of LHON induced vector that carries a mutation ND4.

Methods: Adeno associated virus (AAV) encoding full-length hemagglutinin-tagged XIAP (AAV2.HA-XIAP) or green fluorescent protein (AAV2.GFP) injected into the vitreous of DBA / 1J mice. Two weeks later, LHON phenotype induced by AAV delivery of mutant ND4 (AAV2.mND4FLAG) into the vitreous. Retinal function was assessed by electroretinography pattern. Optic nerve harvested at 4 months, and XIAP therapeutic effect on the nerve fiber layer and optic nerve integrity was evaluated using immunohistochemistry, transmission electron microscopy and magnetic resonance imaging.

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EUR 995

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EUR 4250

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EUR 995

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EUR 4250

Tissue cDNA, First Strand, Human Diseased (Adult), Hypertension, Heart Ventricle, Left, BioGenomics
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EUR 995

Tissue cDNA, First Strand, Human Diseased (Adult), Hypertension, Heart Ventricle, Left, BioGenomics
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EUR 4250

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EUR 995

Tissue cDNA, First Strand, Human Diseased (Adult), Diabetes, Small Intestine, Duodenum, BioGenomics
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EUR 4250

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MBS652553-40Tests 40Tests
EUR 1195

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MBS652553-5x40Tests 5x40Tests
EUR 5155

Tissue cDNA, First Strand, Human Diseased (Adult), Coronary Artery Atherosclerosis, Heart, BioGenomics
MBS652149-40Tests 40Tests
EUR 1205

Tissue cDNA, First Strand, Human Diseased (Adult), Coronary Artery Atherosclerosis, Heart, BioGenomics
MBS652149-5x40Tests 5x40Tests
EUR 5200

Tissue cDNA, First Strand, Rat Adult Normal, Kidney, BioGenomics
MBS652090-40Tests 40Tests
EUR 680

Tissue cDNA, First Strand, Rat Adult Normal, Kidney, BioGenomics
MBS652090-5x40Tests 5x40Tests
EUR 2835

Tissue cDNA, First Strand, Mouse Adult Normal, Kidney, BioGenomics
MBS652496-40Tests 40Tests
EUR 680

Results: During the development of LHON disease, retinal ganglion cell axons lost. Body core apoptotic cells seen in astrocytes or oligodendrocytes in the optic nerve, and there is thinning of the optic nerve and retinal nerve fiber layer. At 4 months after the onset of illness, XIAP gene therapy protects the nerve fiber layer and optic nerve architecture by maintaining healthy axons. XIAP also decreased nuclear fragmentation in the population of astrocytes or oligodendrocytes and reduce infiltration of glial cells.