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131.
Maintenance of highly contractile tissue-cultured avian skeletal myotubes in collagen gel 总被引:2,自引:0,他引:2
Herman H. Vandenburgh Patricia Karlisch Lynne Farr 《In vitro cellular & developmental biology. Plant》1988,24(3):166-174
Summary Highly contractile skeletal myotubes differentiated in tissue culture are normally difficult to maintain on collagen-coated
tissue culture dishes for extended periods because of their propensity to detach as a sheet of cells from their substratum.
This detachment results in the release of mechanical tension in the growing cell “sheet” and, consequently, loss of cellular
protein. We developed a simple method of culturing high density contractile primary avian myotubes embedded in a collagen
gel matrix (collagel) attached to either a stainless steel mesh or nylon support structure. With this system the cells are
maintained in a highly contractile state for extended periods in vitro under tension. Structural integrity of the myotubes
can be maintained for up to 10 d in basal medium without serum or embryo extract. Total cellular protein and myosin heavy
chain accumulation in the cells can be maintained for weeks at levels which are two to three times those found in timematched
controls that are under little tension. Morphologically, the myotubes are well differentiated with structural characteristics
of neonatal myofibers. This new collagel culture system should prove useful in the analysis of in vitro gene expression during
myotube to myofiber differentiation and its regulation by various environmental factors such as medium growth factors, innervation,
and mechanical activity.
This work was supported by grant AM 36266 from the National Institutes of Health, Bethesda, MD, and grant NAG2-414 from the
National Aeronautics and Space Administration, Washington, D.C.
Parts of this work have appeared in abstract form, In Vitro 23:24a; 1987. 相似文献
132.
133.
Membrane-depleted nuclei from Ehrlich ascites tumor (EAT) cells isolated at low ionic strength in the presence of EDTA exhibit highly decondensed chromatin fibers and a loss of morphologically identifiable nucleoli. Treatment of these nuclei with nucleases and 2 M NaCl followed by low-speed centrifugation permitted the facile isolation of the nuclear lamina layer. Under the same conditions, but after heat-shock treatment of the living cells, the chromatin appears in a more condensed state, the nucleoli are well-defined, and the nuclear lamina layer was destabilized in concert with the appearance of an internal nuclear matrix and nucleolar skeleton. Furthermore, we also found both an increase in the protein mass as well as the appearance of a relatively large number of new proteins in this fraction, which are phosphorylated. The major proteins of the nuclear lamina, the lamins, and the residual vimentin remained insoluble. These heat-shock-induced changes were also accompanied by a dephosphorylation of lamins A and C but not of lamin B. 相似文献
134.
Epithelial CaSR deficiency alters intestinal integrity and promotes proinflammatory immune responses
Sam X. Cheng Yaíma L. Lightfoot Tao Yang Mojgan Zadeh Lieqi Tang Bikash Sahay Gary P. Wang Jennifer L. Owen Mansour Mohamadzadeh 《FEBS letters》2014
The intestinal epithelium is equipped with sensing receptor mechanisms that interact with luminal microorganisms and nutrients to regulate barrier function and gut immune responses, thereby maintaining intestinal homeostasis. Herein, we clarify the role of the extracellular calcium-sensing receptor (CaSR) using intestinal epithelium-specific Casr−/− mice. Epithelial CaSR deficiency diminished intestinal barrier function, altered microbiota composition, and skewed immune responses towards proinflammatory. Consequently, Casr−/− mice were significantly more prone to chemically induced intestinal inflammation resulting in colitis. Accordingly, CaSR represents a potential therapeutic target for autoinflammatory disorders, including inflammatory bowel diseases. 相似文献
135.
Lacy J. Barton Shameika R. Wilmington Melinda J. Martin Hannah M. Skopec Kaylee E. Lovander Belinda S. Pinto Pamela K. Geyer 《Genetics》2014,197(2):653-665
The nuclear lamina is an extensive protein network that contributes to nuclear structure and function. LEM domain (LAP2, emerin, MAN1 domain, LEM-D) proteins are components of the nuclear lamina, identified by a shared ∼45-amino-acid motif that binds Barrier-to-autointegration factor (BAF), a chromatin-interacting protein. Drosophila melanogaster has three nuclear lamina LEM-D proteins, named Otefin (Ote), Bocksbeutel (Bocks), and dMAN1. Although these LEM-D proteins are globally expressed, loss of either Ote or dMAN1 causes tissue-specific defects in adult flies that differ from each other. The reason for such distinct tissue-restricted defects is unknown. Here, we generated null alleles of bocks, finding that loss of Bocks causes no overt adult phenotypes. Next, we defined phenotypes associated with lem-d double mutants. Although the absence of individual LEM-D proteins does not affect viability, loss of any two proteins causes lethality. Mutant phenotypes displayed by lem-d double mutants differ from baf mutants, suggesting that BAF function is retained in animals with a single nuclear lamina LEM-D protein. Interestingly, lem-d double mutants displayed distinct developmental and cellular mutant phenotypes, suggesting that Drosophila LEM-D proteins have developmental functions that are differentially shared with other LEM-D family members. This conclusion is supported by studies showing that ectopically produced LEM-D proteins have distinct capacities to rescue the tissue-specific phenotypes found in single lem-d mutants. Our findings predict that cell-specific mutant phenotypes caused by loss of LEM-D proteins reflect both the constellation of LEM-D proteins within the nuclear lamina and the capacity of functional compensation of the remaining LEM-D proteins. 相似文献
136.
Rob J. Van Geest Jan Willem Leeuwis Amélie Dendooven Frederick Pfister Klazien Bosch Kees A. Hoeben Ilse M.C. Vogels Dionne M. Van der Giezen Nadine Dietrich Hans-Peter Hammes Roel Goldschmeding Ingeborg Klaassen Cornelis J.F. Van Noorden Reinier O. Schlingemann 《The journal of histochemistry and cytochemistry》2014,62(2):109-118
Early retinal vascular changes in the development of diabetic retinopathy (DR) include capillary basal lamina (BL) thickening, pericyte loss and the development of acellular capillaries. Expression of the CCN (connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed) family member CCN2 or connective tissue growth factor (CTGF), a potent inducer of the expression of BL components, is upregulated early in diabetes. Diabetic mice lacking one functional CTGF allele (CTGF+/−) do not show this BL thickening. As early events in DR may be interrelated, we hypothesized that CTGF plays a role in the pathological changes of retinal capillaries other than BL thickening. We studied the effects of long-term (6-8 months) streptozotocin-induced diabetes on retinal capillary BL thickness, numbers of pericytes and the development of acellular capillaries in wild type and CTGF+/− mice. Our results show that an absence of BL thickening of retinal capillaries in long-term diabetic CTGF+/− mice is associated with reduced pericyte dropout and reduced formation of acellular capillaries. We conclude that CTGF is involved in structural retinal vascular changes in diabetic rodents. Inhibition of CTGF in the eye may therefore be protective against the development of DR. 相似文献
137.
《Cytokine & growth factor reviews》2014,25(1):45-55
Transforming growth factor (TGF)-β, a pleiotropic cytokine released by both immune and non-immune cells in the gut, exerts an important tolerogenic action by promoting regulatory T cell differentiation. TGF-β also enhances enterocyte migration and regulates extracellular matrix turnover, thereby playing a crucial role in tissue remodeling in the gut. In this review we describe the mechanisms by which abnormal TGF-β signaling impairs intestinal immune tolerance and tissue repair, thus predisposing to the onset of immune-mediated bowel disorders, such as inflammatory bowel disease and celiac disease. Additionally, we will discuss potential therapeutic strategies aiming at restoring physiologic TGF-β signaling in chronic intestinal diseases. 相似文献
138.
Luciana R. Podgaiski Camila da Silva Goldas Claire P. R. Ferrando Fernanda S. Silveira Fernando Joner Gerhard E. Overbeck Milton de Souza Mendonça Jr Valério D. Pillar 《Austral ecology》2014,39(6):686-695
Disturbances are primary forces creating spatial heterogeneity in ecosystems, and inducing changes on biological communities, abiotic characteristics and ecological processes. Here we focus on the effects of fire disturbance in the decomposition process at subtropical Campos grasslands in South Brazil, where burns are traditionally used to reduce shrub encroachment, and improve forage quality. We experimentally investigated how burns and the changes they produce in grassland habitat conditions affect soil fauna detritivory and surface leaf‐litter decaying patterns over one year. Previously to fire, we found significant correlation of litter decay with plant evenness and detritivory rates in non‐disturbed grasslands. One month after fire grassland patches presented reduced soil fauna densities and surface feeding activity possible because of the mortality caused directly by heating, and/or due to harsh microenvironmental filters to fauna colonization and permanency (e.g. decreased humidity). At 6–7 months after fire however these features did not differ any more from the paired unburned plots. On the other hand, canopy openness accelerated the decaying of leaf‐litter in burned patches by allowing increased action of abiotic factors as solar radiation potentially triggering photodegradation. These effects seemed to last less than one year. Overall, our results bring insights regarding drivers of soil ecological processes at local scales in subtropical grasslands, and suggest that detritivory and litter decay processes are sensitive to fire, but resilient following grassland recovering. 相似文献
139.
Nishioku T Dohgu S Takata F Eto T Ishikawa N Kodama KB Nakagawa S Yamauchi A Kataoka Y 《Cellular and molecular neurobiology》2009,29(3):309-316
The blood–brain barrier (BBB) is highly restrictive of the transport of substances between blood and the central nervous system.
Brain pericytes are one of the important cellular constituents of the BBB and are multifunctional, polymorphic cells that
lie within the microvessel basal lamina. The present study aimed to evaluate the role of pericytes in the mediation of BBB
disruption using a lipopolysaccharide (LPS)-induced model of septic encephalopathy in mice. ICR mice were injected intraperitoneally
with LPS or saline and were sacrificed at 1, 3, 6, and 24 h after injection. Sodium fluorescein accumulated with time in the
hippocampus after LPS injection; this hyperpermeability was supported by detecting the extravasation of fibrinogen. Microglia
were activated and the number of microglia increased with time after LPS injection. LPS-treated mice exhibited a broken basal
lamina and pericyte detachment from the basal lamina at 6–24 h after LPS injection. The disorganization in the pericyte and
basal lamina unit was well correlated with increased microglial activation and increased cerebrovascular permeability in LPS-treated
mice. These findings suggest that pericyte detachment and microglial activation may be involved in the mediation of BBB disruption
due to inflammatory responses in the damaged brain. 相似文献
140.