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959 results on '"Willecke, Klaus"'

52. Loss of connexin 26 in mammary epithelium during early but not during late pregnancy results in unscheduled apoptosis and impaired development

Author

Bry, Celine, Maass, Karen, Miyoshi, Keiko, Willecke, Klaus, Ott, Thomas, Robinson, Gertraud W., and Hennighausen, Lothar

Subjects
Apoptosis -- Research, Biological sciences
Abstract

Gap junctions are intercellular channels that are formed by the protein family of connexins (Cxs). In mammary tissue, Cx26 and Cx32 are present in the secretory epithelium and Cx43 is localized in the myoepithelium. The expression of Cx26 and Cx32 is induced during pregnancy and lactation, respectively, thus suggesting unique roles for them in the functional development of the gland. The requirement for these connexins was explored using several strains of genetically altered mice: mice with an inactivated Cx32 gene, mice in which the Cx43 gene had been replaced with the Cx32 gene (Cx43KI32 mice) and mice in which the Cx26 gene was specifically ablated in mammary epithelium at different stages of development using Cre-loxP-based recombination. Normal mammary development was obtained in Cx32-null mice and in Cx43KI32 mammary tissue. In contrast, loss of Cx26 in mammary epithelium before puberty resulted in abrogated lobuloalveolar development and increased cell death during pregnancy, which was accompanied by impaired lactation. Loss of Cx26 in mammary epithelium during the later part of pregnancy did not adversely interfere with functional mammary development. These results demonstrate that the presence of Cx26 is critical during early stages but not during the end of pregnancy when the tissue has completed functional differentiation. Cx26 is considered a tumor suppressor gene and Cx26-null mammary tissue was evaluated after five pregnancies. No hyperproliferation or hyperplasia was observed, suggesting that Cx26 does not function as a tumor suppressor. Keywords: Connexins; Gap junction; Mammary gland; Apoptosis; Alveolar development; Differentiation

Published
2004

60. Role of gap junctions in fluid secretion of lacrimal glands

Author

Walcott, Benjamin, Moore, Leon C., Birzgalis, Aija, Claros, Nidia, Valiunas, Virginijus, Ott, Thomas, Willecke, Klaus, and Brink, Peter R.

Subjects
Liver -- Physiological aspects, Pancreas -- Secretions, Immunocytochemistry -- Analysis, Lacrimal organs -- Physiological aspects, Biological sciences
Abstract

In glands such as the liver and pancreas, gap junctions containing connexin 26 and 32 (Cx26 and Cx32, respectively) couple the secretory cells. Uncoupling these junctions compromises the secretory function of these glands. Lacrimal glands also contain extensive arrays of gap junctions consisting of Cx26 and Cx32. We wanted to determine the role of these junctions in fluid secretion. In Cx32-deficient mice, immunocytochemistry showed that, in the male lacrimal gland, the remaining Cx26 was found evenly distributed in the membrane whereas there was little in the membranes of female glands. Western blot analysis of Cx26 showed that female Cx32-deficient mice expressed Cx26. Patch-clamp analyses of acinar cell coupling showed that the cell pairs from male glands were coupled whereas those from female glands were not. Stimulated fluid production by the glands from Cx32-deficient mice was abnormally low in female glands compared with controls at low topical doses of carbachol. The protein secretory response to different doses of carbachol was the same in all animals. These data suggest that gap junctions are essential for optimal fluid secretion in lacrimal glands. connexin 26; connexin 32; mouse; tears

Published
2002

99. Loss of connexin36 channels alters [beta]-cell coupling, islet synchronization of glucose-induced [Ca.sup.2+] and insulin oscillations, and basal insulin release

Author

Ravier, Magalie A., Guldenagel, Martin, Charollais, Anne, Gjinovci, Asllan, Caille, Dorothee, Sohl, Goran, Wollheim, Claes B., Willecke, Klaus, Henquin, Jean-Claude, and Meda, Paolo

Subjects
Secretion, Pancreatic diseases, Insulin, Diabetes, Health
Abstract

Normal insulin secretion requires the coordinated functioning of [beta]-cells within pancreatic islets. This coordination depends on a communications network that involves the interaction of [beta]-cells with extracellular signals and neighboring cells. In particular, adjacent [beta]-cells are coupled via channels made of connexin36 (Cx36). To assess the function of this protein, we investigated islets of transgenic mice in which the Cx36 gene was disrupted by homologous recombination. We observed that compared with wild-type and heterozygous littermates that expressed Cx36 and behaved as nontransgenic controls, mice homozygous for the Cx36 deletion (Cx3[6.sup.-/-]) featured [beta]-cells devoid of gap junctions and failing to exchange microinjected Lucifer yellow. During glucose stimulation, islets of Cx3[6.sup.-/-] mice did not display the regular oscillations of intracellular calcium concentrations ([[Ca.sup.2+].sub.i]) seen in controls due to the loss of cell-to-cell synchronization of [[Ca.sup.2+].sub.i] changes. The same islets did not release insulin in a pulsatile fashion, even though the overall output of the hormone in response to glucose stimulation was normal. However, under nonstimulatory conditions, islets lacking Cx36 showed increased basal release of insulin. These data show that Cx36-dependent signaling is essential for the proper functioning of [beta]-cells, particularly for the pulsatility of [[Ca.sup.2+].sub.i] and insulin secretion during glucose stimulation., Normal insulin secretion requires the coordinated functioning of [beta]-cells within pancreatic islets. This coordination is achieved through extracellular signals and ligands of the connective matrix as well as through the [...]

Published
2005

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