High levels of filamentous actin and apoptosis correlate with mast cell refractoriness under alloxan-evoked diabetes
Mast cell number and reactivity were shown to be down-regulated under diabetic conditions. Since the balance between globular and filamentous actin plays a pivotal role in the activity of secretory cells, we investigated whether an imbalance in that system could underlie the hyporesponsiveness of ma...
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| Published in: | Life sciences (1973) Vol. 79; no. 12; pp. 1194 - 1202 |
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| Abstract | Mast cell number and reactivity were shown to be down-regulated under diabetic conditions. Since the balance between globular and filamentous actin plays a pivotal role in the activity of secretory cells, we investigated whether an imbalance in that system could underlie the hyporesponsiveness of mast cells in diabetes. The apoptotic state was also evaluated. By means of rhodamine/phalloidine staining of F-actin, we noted that diabetic mast cells exhibited an increase in fluorescence intensity and reduction in cellular size, when compared with cells from normal animals, in parallel with elevation in the percentage of cells developing apoptosis. The levels of Bax, a pro-apoptotic member of Bcl-2 family, appeared increased at baseline in mast cells from diabetic rats compared with normal cells. These phenomena correlated with reduction in histamine and PGD
2 release following antigen challenge in vitro. The steroid antagonist RU 486 abolished the reduction of histamine secretion from diabetic mast cells. We conclude that hyporesponsiveness of mast cells noted in diabetes may be accounted for by reduction in actin filament plasticity, in clear association with the rise in the percentage of cells undergoing apoptosis. In addition, the refractoriness of diabetic mast cells to antigen in vitro seems to be dependent on glucocorticoids. |
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| AbstractList | Mast cell number and reactivity were shown to be down-regulated under diabetic conditions. Since the balance between globular and filamentous actin plays a pivotal role in the activity of secretory cells, we investigated whether an imbalance in that system could underlie the hyporesponsiveness of mast cells in diabetes. The apoptotic state was also evaluated. By means of rhodamine/phalloidine staining of F-actin, we noted that diabetic mast cells exhibited an increase in fluorescence intensity and reduction in cellular size, when compared with cells from normal animals, in parallel with elevation in the percentage of cells developing apoptosis. The levels of Bax, a pro-apoptotic member of Bcl-2 family, appeared increased at baseline in mast cells from diabetic rats compared with normal cells. These phenomena correlated with reduction in histamine and PGD2 release following antigen challenge in vitro. The steroid antagonist RU 486 abolished the reduction of histamine secretion from diabetic mast cells. We conclude that hyporesponsiveness of mast cells noted in diabetes may be accounted for by reduction in actin filament plasticity, in clear association with the rise in the percentage of cells undergoing apoptosis. In addition, the refractoriness of diabetic mast cells to antigen in vitro seems to be dependent on glucocorticoids. Mast cell number and reactivity were shown to be down-regulated under diabetic conditions. Since the balance between globular and filamentous actin plays a pivotal role in the activity of secretory cells, we investigated whether an imbalance in that system could underlie the hyporesponsiveness of mast cells in diabetes. The apoptotic state was also evaluated. By means of rhodamine/phalloidine staining of F-actin, we noted that diabetic mast cells exhibited an increase in fluorescence intensity and reduction in cellular size, when compared with cells from normal animals, in parallel with elevation in the percentage of cells developing apoptosis. The levels of Bax, a pro-apoptotic member of Bcl-2 family, appeared increased at baseline in mast cells from diabetic rats compared with normal cells. These phenomena correlated with reduction in histamine and PGD 2 release following antigen challenge in vitro. The steroid antagonist RU 486 abolished the reduction of histamine secretion from diabetic mast cells. We conclude that hyporesponsiveness of mast cells noted in diabetes may be accounted for by reduction in actin filament plasticity, in clear association with the rise in the percentage of cells undergoing apoptosis. In addition, the refractoriness of diabetic mast cells to antigen in vitro seems to be dependent on glucocorticoids. |
| Author | Barja-Fidalgo, Thereza C. Barreto, Emiliano O. Carvalho, Vinícius F. Martins, Marco A. Oliveira, Michelle S. Bertho, Álvaro L. Cordeiro, Renato S.B. e Silva, Patrícia M.R. |
| Author_xml | – sequence: 1 givenname: Emiliano O. surname: Barreto fullname: Barreto, Emiliano O. organization: Laboratory of Inflammation, Department of Physiology and Pharmacodynamics, Brazil – sequence: 2 givenname: Vinícius F. surname: Carvalho fullname: Carvalho, Vinícius F. organization: Laboratory of Inflammation, Department of Physiology and Pharmacodynamics, Brazil – sequence: 3 givenname: Michelle S. surname: Oliveira fullname: Oliveira, Michelle S. organization: Laboratory of Inflammation, Department of Physiology and Pharmacodynamics, Brazil – sequence: 4 givenname: Álvaro L. surname: Bertho fullname: Bertho, Álvaro L. organization: Laboratory of Immunoparasitology, Department of Immunology, Oswaldo Cruz Institute/FIOCRUZ, Av. Brazil, no 4365, Manguinhos, CEP 21045-900, Brazil – sequence: 5 givenname: Thereza C. surname: Barja-Fidalgo fullname: Barja-Fidalgo, Thereza C. organization: Department of Pharmacology, State University of Rio de Janeiro, Rio de Janeiro, Brazil – sequence: 6 givenname: Renato S.B. surname: Cordeiro fullname: Cordeiro, Renato S.B. organization: Laboratory of Inflammation, Department of Physiology and Pharmacodynamics, Brazil – sequence: 7 givenname: Marco A. surname: Martins fullname: Martins, Marco A. organization: Laboratory of Inflammation, Department of Physiology and Pharmacodynamics, Brazil – sequence: 8 givenname: Patrícia M.R. surname: e Silva fullname: e Silva, Patrícia M.R. email: patmar@ioc.fiocruz.br organization: Laboratory of Inflammation, Department of Physiology and Pharmacodynamics, Brazil |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16647092$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_ejphar_2011_08_004 crossref_primary_10_1016_j_ejphar_2012_06_010 crossref_primary_10_1016_j_ejphar_2006_08_037 crossref_primary_10_1152_ajpendo_00439_2007 crossref_primary_10_1111_j_1365_2613_2008_00620_x crossref_primary_10_1016_j_tice_2008_02_006 crossref_primary_10_1002_JLB_3A0917_364RR |
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| SubjectTerms | Abortifacient Agents - pharmacology Actin microfilament Actins - metabolism Actins - ultrastructure Adrenalectomy Animals Antineoplastic Agents - pharmacology Apoptosis Apoptosis - physiology bcl-2-Associated X Protein - metabolism Blood Glucose - metabolism Blotting, Western Body Weight - drug effects Cell Separation Depsipeptides - pharmacology Diabetes Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Flow Cytometry Glucocorticoids Glucocorticoids - physiology Histamine Release - drug effects Male Mast cells Mast Cells - physiology Microscopy, Fluorescence Mifepristone - pharmacology Prostaglandin D2 - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Rats, Wistar |
| Title | High levels of filamentous actin and apoptosis correlate with mast cell refractoriness under alloxan-evoked diabetes |
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