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Biomedical subjects

A Mauger

Publications and source records attributed to A Mauger.

At least 55 records · Page 3Linked to original sources

Immunofluorescent localization of extracellular matrix components during muscle morphogenesis. II. In chick embryos with hereditary muscular dysgenesis (cn/cn).

The immunofluorescent distribution of types I and III collagen, fibronectin, and laminin during muscle morphogenesis of the crooked neck dwarf mutant chick embryo differs from that of the normal chick. The drastic difference is related to the inability of the mutant embryo to maintain a harmonious muscle pattern. The first sign of the defect is the disaggregation of type I collagen fibers of the tendons and the disorganization of the intermuscular spaces. The organization of the connective tissue never proceeds beyond the appearance of an epimysial envelope, rich in types I and III collagen, which becomes disorganized shortly after. No perimysial envelopes displaying types I and III collagen fibers and fibronectin, nor endomysial sheaths develop. Only large spaces filled with types I and III collagen fibers subdivide groups of muscle cells irregularly. On the whole, type III collagen is less abundant than type I collagen. Fibronectin disappears from the periphery of the muscle cell. Laminin is more thickly deposited in the basal lamina around irregularly sized muscle cells than around the normal muscle cell. The results are discussed in terms of morphogenetic interactions between connective tissue cells and muscle cells, and in terms of fibrosis, which characterizes some muscle diseases.

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Effect of hydrocortisone on skin development in the chick embryo: ultrastructural, immunohistological, and biochemical analysis.

The effect of hydrocortisone on the development of dorsal skin was analyzed in the chick embryo by (1) transmission electron microscopy, (2) indirect immunofluorescence histology of extracellular matrix components (collagen types I, III, and IV; fibronectin; and laminin), and (3) quantitative determination of collagen content and proline incorporation, between administration of the drug at 6 or 6.5 days and final retrieval of skin pieces at 11 days of incubation. Treatment caused the formation of featherless skin areas which exhibited an early maturation of the epidermis, a uniform distribution of interstitial collagen and rarefaction of fibronectin in the dermal extracellular matrix, and a significant increase of collagen content and proline incorporation in collagen noncollagen proteins, characterized by an increased hydroxyproline-to-proline ratio. The distribution of type IV collagen and of laminin was unchanged. The absence of feather formation in hydrocortisone-induced apteria is interpreted as resulting primarily from an early extinction of epidermal morphogenetic competence, and secondarily from modifications in the amount and distribution of extracellular matrix components in the dermis.

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Tissue interactions in the organization and maintenance of the muscle pattern in the chick limb.

Recent investigations on a hereditary muscular dysgenesis (cn/cn) in the chicken (Kieny, Mauger, Hedayat & Goetinck, 1983) have suggested that limb muscle pattern development and subsequent maintenance are two independent steps in the formation of the musculature. The respective activities or muscle cells and connective tissue cells in the ontogeny of the musculature have been investigated in avian embryos 1) by in ovo administration of drugs interfering with collagen biosynthesis, and 2) by heterogenetic somite-exchange experiments between normal and mutant embryos. None of the drugs administered to the chick embryo caused any disturbance of muscle pattern formation or maintenance whether treatment occurred before (5 days) or after (7.5 days) the muscle splitting period. Heterogenetic implantations were performed at 2 days of incubation either at the leg or at the wing level. Somitic mesoderm from non-mutant quail embryo was grafted to replace a piece of somitic mesoderm in putative mutant (cn/cn) chick embryos. The introduction of normal myogenic cells into a mutant leg or wing led to a normally patterned musculature, which demonstrates that the muscular dysgenesis cn/cn results from a defect of the somitic myogenic cell line.

2,2'-Dipyridyl↗

Ontogeny of the leg muscle tissue in the crooked neck dwarf mutant (cn/cn) chick embryo.

The crooked neck dwarfism (cn/cn) is characterized, among other anomalies, by a muscular hypoplasia, particularly conspicuous in the tibiotarsal segment. Histological observations were performed between day 6 and day 12.5 of incubation. They show, in the tibiotarsal segment, that the hereditary muscular hypoplasia is not caused by a defect of the normal muscular splitting pattern. Indeed, in the mutant, the splitting of muscle masses proceeds normally up to the last partition (day 7-7.5), but is followed by the secondary fusion of individuated muscles into an unpatterned muscle tissue. Thus the mutant phenotype is the result of an inability of the muscle pattern to become stabilized into definitive structures.

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Origin of satellite cells in avian skeletal muscles.

The study of the embryonic origin of the striated satellite cells is based 1) on a comparison of the specific morphology of the nuclei in satellite cells and in myofibers, in late embryonic and postnatal chick and quail muscles; 2) on a species-identification of the satellite cell nuclei in hetero-specific muscle tissues where myofibers derive from implanted quail somite and connective tissue fibroblasts from the chick host somatopleura. Observations clearly demonstrate that myofibers and satellite cells are of the same somitic origin. It is concluded that satellite cells represent a portion of the myogenic cell lineage.

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[Distribution of collagen, fibronectin, and laminin during morphogenesis of skin and cutaneous appendages in the chick embryo (author's transl)].

In the dermis of inter-appendage and glabrous skin, interstitial collagen types I, III, and V are abundant, while fibronectin is scarce. Conversely, in the morphogenetically active foci of cutaneous appendages, interstitial collagen is scarce or absent, whereas fibronectin is abundant. Type IV collagen and laminin are localized at the dermal-epidermal junction and distributed evenly.

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The dermal-epidermal junction during the development of skin and cutaneous appendages in the chick embryo.

The ultrastructure of the junction zone between dermis and epidermis was examined in the chick embryo during the development of feather-forming, scale-forming and glabrous skin. Direct contacts between dermal and epidermal cells were extremely rare and seen sporadically in feather-forming skin only, in connection with anchor filaments. Everywhere else, the basement membrane (BM) comprised an uninterrupted lamina densa. In feather-forming skin, zones of close parallel apposition (CPA) of dermal cell processes against the BM lamina densa were frequent at the margin of feather buds and at the base of feather filaments, and scarce in interplumar skin. In scale-forming skin, the density of CPA was lower, at 10 days, in the interplacode region than within the scale primordium, and, at 11 and 12 days, at the apex of the scale than at its base. At 11 days, dermal cells in scale primordia were equipped with long and thin tubular processes oriented predominantly at right angle with respect to the basal-apical axis of the scale. In the midventral apterium, CPA of dermal cell processes against the BM was very rare at 12 days, and non-existent at later stages, when a complex collagenous matrix was laid down in orthogonal ply-wood fashion underneath the BM lamina densa. Thus, it appeared that the heterogeneity of the distribution of dermal cell processes beneath the basement membrane might represent part of the morphogenetic message that the dermis is known to transmit to the epidermis during the formation of the appendages.

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