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Biomedical subjects

B H Lipton

Publications and source records attributed to B H Lipton.

9 recordsLinked to original sources
PubMed1992

Histamine-modulated transdifferentiation of dermal microvascular endothelial cells.

Homeostatic and inflammatory functions of skin microvessels are tightly regulated by vasoactive amines. Following stimulation with histamine, dermal microvascular endothelial cells (MEC) undergo a rapid change in phenotype (transdifferentiation) and subsequently exhibit an enhanced rate of growth. To elucidate mechanisms regulating MEC transdifferentiation, this study investigated the functional relationships among vimentin, Ca2+, and protein kinase C (PKC) in histamine-modulated dermal MEC in vitro. Distribution of vimentin and PKC in foreskin-derived MEC cultivated in a modified Iscove's medium was assessed with immunocytochemistry. Calcium ion kinetics in histamine-treated MEC were analyzed using the Ca2+ probe Fluo-3 in conjunction with interactive laser cytometry. Histamine, acting through H-1 receptors, produces a rapid (less than 100 ms) and differential elevation of free calcium in each of three cytological compartments defined by the vimentin cytoskeleton in epithelial MEC. A distinctive compartmentalized and nonuniform distribution of PKC precisely coincides with that observed for free-Ca2+ released in response to histamine. The studies reveal that histamine modulation of the MEC phenotype is associated with a rapid patterned reorganization of the vimentin skeleton. It is hypothesized that histamine induces vimentin post-translational modifications by activating a spatially localized interaction among cytoplasmic free Ca2+, PKC, and the vimentin matrix. The results further suggest that vimentin, in addition to its structural role, may participate in signal transduction and gene regulation processes in effecting MEC transdifferentiation.

Calcium↗
PubMed1991

Microvessel endothelial cell transdifferentiation: phenotypic characterization.

Human dermal microvessel endothelial cells (MEC) have two basic functions: maintenance of tissue homeostasis and facilitation of inflammatory responses. The former requires that the endothelium expresses traits of an epithelium, while inflammatory reactions are associated with intimal disruption. Acute inflammation transiently alters endothelium, whereas chronic inflammation may result in vessel reorganization and MEC mesenchymalization. Foreskin MEC in vitro undergo a similar epithelial-mesenchymal modulation. In the presence of cAMP, cultivated dermal MEC exhibit the structural and functional characteristics of an epithelium. MEC grown in cAMP-deficient medium initially have a "transitional" configuration and are subsequently transformed into mesenchymal cells. If cAMP is replaced by histamine, MEC maintain a stable intermediate transitional configuration. Transitional MEC refed cAMP-supplemented medium revert to an epithelial phenotype, whereas parallel cultures fed cAMP-deficient medium are transformed into mesenchymal cells. Phenotypic modulation can be induced without cell division and thus provides a unique example of direct transdifferentiation. Our data furthermore suggest that this transdifferentiation results in the acquisition of properties usually attributed to cells of the reticuloendothelial system.

Cell Differentiation↗
PubMed1979

Developmental fate of skeletal muscle satellite cells.

Radioisotopically labeled satellite cells from clonal cultures were implanted into normal muscle of the original donor. Implanted cells invariably retained their myogenic potential by participating in the regeneration of damaged myofibers or in the development of existing fibers.

Animals↗
PubMed1978

The effect of Marcaine on muscle and non-muscle cells in vitro.

The effect of the local anaesthetic Marcaine on muscle and non-muscle cell types was examined using an in vitro assay. Each of the cell types examined (myotubes, myoblasts, fibroblasts and liver parenchyma) expressed morphological alterations when incubated in Marcaine-medium. Myotubes were the most sensitive of the cells studied and exhibited several pronounced membrane structural changes after short incubation periods in Marcaine-medium. The toxic effects of Marcaine were irreversible and the myotubes continued to degenerate despite being placed in fresh medium. Myoblasts and non-muscle cells, however, demonstrated a rapid recovery when removed from the Marcaine-medium. Since Marcaine is thought to complete with Ca++ for specific sites on cell membranes, it is proposed that the differential effects which were observed are dependent upon the level of calcium related activities being carried out by the cells.

Animals↗
PubMed1977

An ultrastructural study of peripheral neurons and associated non-neural structures in the bivalve mollusc, Spisula solidissima.

The ultrastructural morphology of peripheral neurons and associated structures in the bivalve mollusc. Spisula solidissima have been studied in an effort to describe the synaptic topography and to provide anatomical correlates of previous physiological observations. The somata of the peripheral neurons are located within the perineurium at branch points of the siphonal nerves. There are many fiber-fiber synaptic contacts which are characterized by isolated sites of contact with membrane specialization and unilateral accumulation of synaptic vesicles. There are also synaptic contacts involving the somata, both axo-somatic and somato-axonic, the two being distinguishable on the basis of the polarity of vesicle accumulation. All of the observed synaptic profiles were similar in appearance regardless of the neuron loci involved. Much of the non-synaptic soma surface is covered with processes of glial cells. Likewise, in many cases, individual fibers and groups of fibers are encases with glial processes. Unique clusters of membrane bound, pigment containing glial like cells occur throughout the nervous system of Spisula. The heterogenous appearance of the inclusions and the presence of lysosome-like bodies in the cytoplasm of these cells suggest a possible phagocytic role.

Axons↗