Distribution of microtubules and microfilaments in exocrine (Ventral prostatic epithelial cells and pancreatic exocrine cells) and endocrine cells (Cells of the adenohypophysis and islets of Langerhans)

1987 ◽  
Vol 87 (3) ◽  
pp. 223-227 ◽  
Author(s):  
H. Kurihara ◽  
K. Uchida
1994 ◽  
Vol 3 (4) ◽  
pp. 307-313 ◽  
Author(s):  
Fred Levine ◽  
Gillian M. Beattie ◽  
Alberto Hayek

We have studied the expression of the β1 family of integrins in fetal and adult human pancreas. Immunohistochemical staining with a monoclonal anti-β1 antibody revealed that the epithelial cells of the human fetal pancreas express high amounts of β1 integrin, while the pancreatic stromal cells express substantially lower amounts. Islets of Langerhans from human adult pancreas also expressed high amounts of β1 integrin. Taking advantage of the extremely high affinity binding between the invasin protein of Yersinia pseudotuberculosis and many β1 integrins, we have been able to isolate highly enriched populations of fetal pancreatic epithelial cells. Epithelial-enriched cell populations retain the ability to differentiate into mature endocrine cells following transplantation into nude mice.


2000 ◽  
Vol 116 (4) ◽  
pp. 507-520 ◽  
Author(s):  
Duk-Su Koh ◽  
Mark W. Moody ◽  
Toan D. Nguyen ◽  
Bertil Hille

We asked if the mechanisms of exocytosis and its regulation in epithelial cells share features with those in excitable cells. Cultured dog pancreatic duct epithelial cells were loaded with an oxidizable neurotransmitter, dopamine or serotonin, and the subsequent release of these exogenous molecules during exocytosis was detected by carbon-fiber amperometry. Loaded cells displayed spontaneous exocytosis that may represent constitutive membrane transport. The quantal amperometric events induced by fusion of single vesicles had a rapid onset and decay, resembling those in adrenal chromaffin cells and serotonin-secreting leech neurons. Quantal events were frequently preceded by a “foot,” assumed to be leak of transmitters through a transient fusion pore, suggesting that those cell types share a common fusion mechanism. As in neurons and endocrine cells, exocytosis in the epithelial cells could be evoked by elevating cytoplasmic Ca2+ using ionomycin. Unlike in neurons, hyperosmotic solutions decreased exocytosis in the epithelial cells, and giant amperometric events composed of many concurrent quantal events were observed occasionally. Agents known to increase intracellular cAMP in the cells, such as forskolin, epinephrine, vasoactive intestinal peptide, or 8-Br-cAMP, increased the rate of exocytosis. The forskolin effect was inhibited by the Rp-isomer of cAMPS, a specific antagonist of protein kinase A, whereas the Sp-isomer, a specific agonist of PKA, evoked exocytosis. Thus, PKA is a downstream effector of cAMP. Finally, activation of protein kinase C by phorbol-12-myristate-13-acetate also increased exocytosis. The PMA effect was not mimicked by the inactive analogue, 4α-phorbol-12,13-didecanoate, and it was blocked by the PKC antagonist, bisindolylmaleimide I. Elevation of intracellular Ca2+ was not needed for the actions of forskolin or PMA. In summary, exocytosis in epithelial cells can be stimulated directly by Ca2+, PKA, or PKC, and is mediated by physical mechanisms similar to those in neurons and endocrine cells.


Sign in / Sign up

Export Citation Format

Share Document