Calcium and wound healing in Xenopus early embryos

Development ◽  
1982 ◽  
Vol 67 (1) ◽  
pp. 195-205
Author(s):  
Martin Stanisstreet
Keyword(s):  
Wound Healing ◽  
Divalent Cations ◽  
Local Application ◽  
Ionophore A23187 ◽  
Excess Calcium ◽  
Early Embryos ◽  
Cell Shapes ◽  
Healing Of Wounds ◽  
Made In

The role of calcium in the healing of wounds made in the ectoderm of Xenopus neurulae has been studied. Embryos have been wounded in the presence of calcium inhibitors, and the effects on wound healing observed by scanning electron microscopy. In addition, unwounded embryos have been exposed to a local application of ionophore A23187 to simulate the possible calcium fluxes following wounding. Lanthanum, which competes for calcium channels, inhibits wound healing. EDTA, which binds divalent cations, also inhibits wound healing, but its effect can be reversed by the addition of excess calcium. Local application of ionophore A23187, which promotes transport of calcium across biological membranes, results in a local change in cell shapes. These observations lend support to the hypothesis that wound healing in amphibian early embryos, which is effected by changes in cell shapes similar to those seen in certain examples of normal morphogenesis, is initiated by a local influx of calcium into cells.

scholarly journals The role of divalent cations in the regulation of microtubule assembly. In vivo studies on microtubules of the heliozoan axopodium using the ionophore A23187.

1976 ◽  
Vol 70 (3) ◽  
pp. 527-540 ◽  
Author(s):  
M Schliwa
Keyword(s):  
Divalent Cations ◽  
Light And Electron Microscopy ◽  
Microtubule Assembly ◽  
In Vivo Studies ◽  
Ionophore A23187 ◽  
Low Concentrations ◽  
Microtubule Formation

Low concentrations of calcium and magnesium ions have been shown to influence microtubule assembly in vitro. To test whether these cations also have an effect on microtubules in vivo, specimens of Actinosphaerium eichhorni were exposed to different concentrations of Ca++ and Mg++ and the divalent cation ionophore A23187. Experimental degradation and reformation of axopodia were studied by light and electron microscopy. In the presence of Ca++ and the ionophore axopodia gradually shorten, the rate of shortening depending on the concentrations of Ca++ and the ionophore used. Retraction of axopodia was observed with a concentration of Ca++ as low as 0.01 mM. After transfer to a Ca++-free solution containing EGTA, axopodia re-extend; the initial length is reached after about 2 h. Likewise, reformation of axopodia of cold-treated organisms is observed only in solutions of EGTA or Mg++, whereas it is completely inhibited in a Ca++ solution. Electron microscope studies demonstrate degradation of the axonemal microtubular array in organisms treated with Ca++ and A23187. No alteration was observed in organisms treated with Mg++ or EGTA plus ionophore. The results suggest that, in the presence of the ionophore, formation of axonemal microtubules can be regulated by varying the Ca++ concentration in the medium. Since A23187 tends to equilibrate the concentrations of divalent cations between external medium and cell interior, it is likely that microtubule formation invivo is influenced by micromolar concentrations of Ca++. These concentrations are low enough to be of physiological significance for a role in the regulation of microtubule assembly in vivo.

Mast cells in health and disease

2011 ◽  
Vol 120 (11) ◽  
pp. 473-484 ◽  
Author(s):  
Charlotte L. Weller ◽  
Sarah J. Collington ◽  
Tim Williams ◽  
Jonathan R. Lamb
Keyword(s):  
Wound Healing ◽  
Mast Cells ◽  
Allergic Disease ◽  
Effector Functions ◽  
Health And Disease ◽  
Developing Area ◽  
Deficient Mice ◽  
Made In

Although MCs (mast cells) were discovered over 100 years ago, for the majority of this time their function was linked almost exclusively to allergy and allergic disease with few other roles in health and disease. The engineering of MC-deficient mice and engraftment of these mice with MCs deficient in receptors or mediators has advanced our knowledge of the role of MCs in vivo. It is now known that MCs have very broad and varied roles in both physiology and disease which will be reviewed here with a focus on some of the most recent discoveries over the last year. MCs can aid in maintaining a healthy physiology by secreting mediators that promote wound healing and homoeostasis as well as interacting with neurons. Major developments have been made in understanding MC function in defence against pathogens, in recognition of pathogens as well as direct effector functions. Probably the most quickly developing area of understanding is the involvement and contribution MCs make in the progression of a variety of diseases from some of the most common diseases to the more obscure.

scholarly journals Regulation of macrophage lysosomal enzyme secretion: role of arachidonate metabolites, divalent cations and cyclic AMP

1980 ◽  
Vol 44 (1) ◽  
pp. 299-315
Author(s):  
R.M. McMillan ◽  
D.E. Macintyre ◽  
J.E. Beesley ◽  
J.L. Gordon
Keyword(s):  
Cyclic Amp ◽  
Lysosomal Enzyme ◽  
Lysosomal Enzymes ◽  
Divalent Cations ◽  
Cell Types ◽  
Enzyme Secretion ◽  
Ionophore A23187 ◽  
Enzyme Release ◽  
Arachidonate Metabolites

We have investigated the role in macrophage lysosomal enzyme release of arachidonate metabolites, extracellular divalent cations and cyclic AMP (cAMP) which modulate secretion in other cell types. Lysosomal enzyme secretion induced by zymosan was accompanied by release of malondialdehyde (MDA), which is derived from arachidonic acid via prostaglandin synthase. Blockade of MDA formation, by aspirin or indomethacin, was associated with only a small inhibitory effect on lysosomal enzyme release by zymosan: arachidonate metabolites thus play only a minor role in mediating macrophage lysosomal enzyme release. Zymosan-induced secretion of lysosomal enzymes from macrophages did not require extracellular magnesium or calcium although release was enhanced by magnesium and inhibited by calcium. These effects may be related to an influence of the ions on phagocytosis. Elevation of intracellular divalent cation concentrations, by ionophore A23187, induced release of lysosomal enzymes but this was a result of cell lysis. Adenylate cyclase stimulants and dibutyryl cAMP produced slight inhibition of zymosan-induced lysosomal enzyme release. Aminophylline and papaverine caused more marked inhibition but their effects may be due to actions independent of phosphodiesterase inhibition. Our data indicate that arachidonate metabolites and cAMP do not play a major role in regulating zymosan-induced enzyme release from macrophages. Extracellular calcium and magnesium may modulate secretion but the role of intracellular divalent cations remains to be established. We conclude that macrophage lysosomal enzyme secretion is controlled by regulatory mechanisms different from those which control similar degranulation processes in other cell types.

Macrophage recruitment during limb development and wound healing in the embryonic and foetal mouse

1994 ◽  
Vol 107 (5) ◽  
pp. 1159-1167 ◽  
Author(s):  
J. Hopkinson-Woolley ◽  
D. Hughes ◽  
S. Gordon ◽  
P. Martin
Keyword(s):  
Wound Healing ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Limb Development ◽  
Close Association ◽  
Active Role ◽  
Tissue Remodelling ◽  
Fibroblastic Cells ◽  
Made In

Macrophages play a pivotal role in the adult inflammatory response to wounding. They are directly responsible for cellular debridement and, by providing a source of growth factors and cytokines, they recruit other inflammatory and fibroblastic cells and influence cell proliferation and tissue remodelling. In this paper we investigate the role of macrophages in clearing areas of programmed cell death in the developing embryo and also their role in embryonic and foetal wound healing. Immunocytochemistry using the monocyte/macrophage-specific monoclonal antibody, F4/80, reveals a close association between areas of programmed cell death in the remodelling interdigital regions of the mouse footplate and of F4/80-positive cells, suggesting that monocyte-derived macrophages, and not locally recruited fibroblastic cells, as previously believed, are responsible for phagocytosing and clearing areas of interdigital apoptosis. Our studies of wound healing reveal that macrophages are not recruited to, and therefore cannot be playing an active role in the healing of, excisional wounds made in the mouse embryo at any stage up until E14.5. Beyond this transition stage we see a significant recruitment of macrophages within 12 hours of wounding. We find that macrophages can be attracted to wounds in earlier embryos if the wound results in significant cell death such as after burning.

scholarly journals Role of calcium ions in the control of embryogenesis of Xenopus. Changes in the subcellular distribution of calcium in early cleavage embryos after treatment with the ionophore A23187.

1979 ◽  
Vol 80 (3) ◽  
pp. 589-604 ◽  
Author(s):  
J C Osborn ◽  
C J Duncan ◽  
J L Smith
Keyword(s):  
Divalent Cations ◽  
Subsequent Development ◽  
Abnormal Development ◽  
Ionophore A23187 ◽  
Early Cleavage ◽  
Amphibian Embryo ◽  
High Incidence ◽  
Intracellular Action

Treatment of stage 5 Xenopus embryos with the ionophore A23187 for only 10 min, in the absence of extracellular Mg2+ and Ca2+, causes cortical contractions and a high incidence of abnormal embryos during subsequent development. Cation analysis shows that divalent ions are not lost from the embryos, but that Ca2+ is redistributed within the subcellular fractions. Ca2+ is probably released from yolk platelets and/or pigment granules by the action of A23187, [Ca2+] rises in the cytosol, and the mitochondria attempt to take up this free Ca2+. The mitochondria concomitantly undergo characteristic ultrastructural transformations, changing towards energized-twisted and energized-zigzag conformations. A23187 allows these changes to be demonstrated in situ. Extracellular divalent cations (10(-4) M) interfere with this intracellular action of A23187. Intracellular accumulation of Na+ (by treatment with ouabain) or Li+ also causes abnormal development, probably by promoting a release of Ca2+ from the mitochondria. It is suggested (a) that all these treatments cause a rise in [Ca2+]i which interferes with normal, integrated cell division, so causing, in turn, abnormal embryogenesis, (b) that levels of [Ca2+]i are of importance in regulating cleavage, (c) that the mitochondria could well have a function in regulating [Ca2+]i during embryogenesis in Xenopus, and (d) that vegetalizing agents may well act by promoting a rise in [Ca2+]i in specific cells in the amphibian embryo.

scholarly journals Role of Kshara Sootra in complicated cases of Arsha (interno-externo haemorrhoids) -A case series

2020 ◽  
Vol 1 (1) ◽  
pp. 68-71
Author(s):  
Manisha Kapadiya ◽  
T.S. Dudhamal
Keyword(s):  
Wound Healing ◽  
Spinal Anaesthesia ◽  
Case Series ◽  
Local Application ◽  
Sitz Bath ◽  
Ancient Time ◽  
Anal Stricture ◽  
Complete Wound Healing

Kasharasutra is being practiced in Indian system of medicine since ancient time in various ano-rectal disorders. In this case series, 2 patients of arsha (internal external haemorrhoids) underwent ksharasutra trans fixation at 3,7,11 o’ clock under spinal anaesthesia. Ksharasutra prepared as per the ayurvedic pharmacopeia of India (API). Ligated pile mass sloughed out on 5th post-operative day. Wound healed within 30 days. Panchavalkal kwatha for sitz bath, jatyadi taila for local application, gud haritaki were used as adjuvant drugs. Follow up after 4 weeks, no recurrence was observed, sphincter tone was normal and there was no evidence of anal stricture after complete wound healing. 

scholarly journals Evidence for a role of glycoprotein IIb-IIIa, distinct from its ability to support aggregation, in platelet activation by ionophores in the presence of extracellular divalent cations

Blood ◽  
1994 ◽  
Vol 83 (9) ◽  
pp. 2549-2559 ◽  
Author(s):  
B Lages ◽  
HJ Weiss
Keyword(s):  
Monoclonal Antibodies ◽  
Platelet Activation ◽  
Platelet Rich Plasma ◽  
Divalent Cations ◽  
Ionophore A23187 ◽  
Myristate Acetate ◽  
Serotonin Secretion ◽  
Occupied State ◽  
Induced Aggregation

Abstract Ionophore A23187-induced 14C-serotonin secretion and thromboxane B2(TxB2) formation were found to be absent in citrated platelet-rich plasma (PRP) from thrombasthenic subjects and in normal PRP treated with glycoprotein (GP) IIb-IIIa complex-specific monoclonal antibodies. Both responses were restored to normal levels when 5 mmol/L EDTA was present, indicating that their absence was not caused by the absence of aggregation per se. In gel-filtered platelets (GFP) incubated with various additions, the blockade or absence of GPIIb-IIIa resulted in reduced A23187-induced secretion and TxB2 formation in media containing 1 mmol/L Ca2+ with or without fibrinogen and 1 mmol/L Mg2+ plus fibrinogen, but not when Ca, Mg-free buffer alone, 1 mmol/L EDTA, or fibrinogen alone were present. In contrast, no such dependence or GPIIb- IIIa was seen in GFP stimulated with thrombin or phorbol myristate acetate in the presence of 1 mmol/L Ca2+, 1 mmol/L EDTA, or buffer alone. The inhibition of ionophore-induced responses seen in both normal GFP treated with antibodies and thrombasthenic GFP was not associated with any significant alteration of the ionophore-mediated [Ca2+]i increase, as measured in both aequorin-loaded GFP stimulated with A23187 and fura-2-loaded GFP stimulated with ionomycin. Incubation of normal GFP with either the monoclonal antibodies or the ligand binding site peptide RGDS in the presence of 1 mmol/L Ca2+ caused virtually complete inhibition of A23187-induced aggregation, measured as the loss of single platelets, but RGDS, in contrast to the antibodies, did not inhibit secretion or TxB2 formation. We conclude that platelet activation induced by ionophores in the presence, but not in the absence, of extracellular divalent cations involves a GPIIb-IIIa- dependent process that most likely involves a property of the ligand- occupied form of the complex distinct from its ability to support aggregation. This could represent another example of an aggregation- independent activity of the receptor-occupied state of the GPIIb-IIIa complex in signal transduction.

Scanning electron microscopy of wound healing in rat embryos

Development ◽  
1984 ◽  
Vol 83 (1) ◽  
pp. 109-117
Author(s):  
Martin J. Smedley ◽  
Martin Stanisstreet
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Wound Healing ◽  
Wound Closure ◽  
Free Calcium ◽  
Cellular Mechanisms ◽  
Amphibian Embryos ◽  
Early Embryos ◽  
Healing Of Wounds ◽  
Scanning Electron

Wound healing in rat early embryos has been studied by scanning electron microscopy. Initially the wound gapes slightly and cells peripheral to the wound assume a cobble-stone appearance. Wound closure is quite rapid; some small wounds are almost closed within 10 min of incision. Wound closure is accompanied by the appearance of some elongated cells at the wound edge. These features are similar to, although less pronounced than, those which have been observed to accompany wound closure in amphibian and avian embryos. Healing of wounds made in the amnion is also accompanied by changes in the shapes of cells at the wound margins. Wound healing in embryos cultured in Hank's saline is similar to wound healing in embryos cultured in serum, suggesting that the macromolecular components of serum are not essential to wound healing. Cytochalasin B, which inhibits wound closure in amphibian embryos, does not inhibit wound healing in rat early embryos unless used at a concentration high enough to cause cell dissociation. Similarly chelation of the free calcium in the medium, which also prevents wound closure in amphibian embryos, does not inhibit wound closure unless the embryo is dissociating. Removal of free calcium does however cause collapse of the elevated neural folds. These observations suggest that the cellular mechanisms involved in wound healing are different in mammalian and amphibian embryos.

Calcium regulation of flagellation in Naegleria gruberi

1983 ◽  
Vol 63 (1) ◽  
pp. 311-326
Author(s):  
F.L. Schuster ◽  
R. Twomey
Keyword(s):  
Plasma Membrane ◽  
Calcium Uptake ◽  
Regulatory Protein ◽  
Ultrastructural Localization ◽  
Calcium Flux ◽  
Ionophore A23187 ◽  
Direct Inhibition ◽  
Excess Calcium ◽  
Naegleria Gruberi

The amoeba-to-flagellate transformation of Naegleria gruberi was studied, exploring the role of calcium in control of this pattern of morphogenesis. A direct and an indirect role for calcium are postulated based on experimental results. Direct inhibition in the presence of calcium is caused by ionophore A23187, substances with ionophore-like activity (amphotericin) and the hormone calcitonin, which facilitate calcium uptake into the cytosol. The indirect role is difficult to assess, but is believed to be related to calcium regulatory protein and its control of cyclic nucleotide levels in the cell, based on inhibition by trifluoperazine. Calcium flux was studied by addition of 45Ca2+ to cell cultures, and tracing its movement during the transformation period. Ultrastructural localization of calcium was attempted in amoeboid and flagellate stages, as well as in reverting flagellates. Deposits that might represent calcium were observed under the plasma membrane and, in calcium-induced reversion, in electron-dense spheres seen in the cytoplasm and at sub-membrane locations, suggesting expulsion of excess calcium.

scholarly journals Evidence for a role of glycoprotein IIb-IIIa, distinct from its ability to support aggregation, in platelet activation by ionophores in the presence of extracellular divalent cations

Blood ◽  
1994 ◽  
Vol 83 (9) ◽  
pp. 2549-2559 ◽  
Author(s):  
B Lages ◽  
HJ Weiss
Keyword(s):  
Monoclonal Antibodies ◽  
Platelet Activation ◽  
Platelet Rich Plasma ◽  
Divalent Cations ◽  
Ionophore A23187 ◽  
Myristate Acetate ◽  
Serotonin Secretion ◽  
Occupied State ◽  
Induced Aggregation

Ionophore A23187-induced 14C-serotonin secretion and thromboxane B2(TxB2) formation were found to be absent in citrated platelet-rich plasma (PRP) from thrombasthenic subjects and in normal PRP treated with glycoprotein (GP) IIb-IIIa complex-specific monoclonal antibodies. Both responses were restored to normal levels when 5 mmol/L EDTA was present, indicating that their absence was not caused by the absence of aggregation per se. In gel-filtered platelets (GFP) incubated with various additions, the blockade or absence of GPIIb-IIIa resulted in reduced A23187-induced secretion and TxB2 formation in media containing 1 mmol/L Ca2+ with or without fibrinogen and 1 mmol/L Mg2+ plus fibrinogen, but not when Ca, Mg-free buffer alone, 1 mmol/L EDTA, or fibrinogen alone were present. In contrast, no such dependence or GPIIb- IIIa was seen in GFP stimulated with thrombin or phorbol myristate acetate in the presence of 1 mmol/L Ca2+, 1 mmol/L EDTA, or buffer alone. The inhibition of ionophore-induced responses seen in both normal GFP treated with antibodies and thrombasthenic GFP was not associated with any significant alteration of the ionophore-mediated [Ca2+]i increase, as measured in both aequorin-loaded GFP stimulated with A23187 and fura-2-loaded GFP stimulated with ionomycin. Incubation of normal GFP with either the monoclonal antibodies or the ligand binding site peptide RGDS in the presence of 1 mmol/L Ca2+ caused virtually complete inhibition of A23187-induced aggregation, measured as the loss of single platelets, but RGDS, in contrast to the antibodies, did not inhibit secretion or TxB2 formation. We conclude that platelet activation induced by ionophores in the presence, but not in the absence, of extracellular divalent cations involves a GPIIb-IIIa- dependent process that most likely involves a property of the ligand- occupied form of the complex distinct from its ability to support aggregation. This could represent another example of an aggregation- independent activity of the receptor-occupied state of the GPIIb-IIIa complex in signal transduction.

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