Epithelial Sodium Channel (ENaC) Activity In Type I Cells Differs From Type II Cells Following B-Adrenergic Stimulation

Author(s):  
Charles A. Downs ◽  
Lisa H. Kriener ◽  
Ling Yu ◽  
Douglas C. Eaton ◽  
Lucky Jain ◽  
...  
1966 ◽  
Vol 30 (3) ◽  
pp. 563-578 ◽  
Author(s):  
T. J. Biscoe ◽  
W. E. Stehbens

An electron microscope investigation was made of the carotid body in the cat and the rabbit. In thin-walled blood vessels the endothelium was fenestrated. Larger vessels were surrounded by a layer of smooth muscle fibers. Among the numerous blood vessels lay groups of cells of two types covered by basement membranes. Aggregates of Type I cells were invested by Type II cells, though occasionally cytoplasmic extensions were covered by basement membrane only. Type I cells contained many electron-opaque cored vesicles (350 to 1900 A in diameter) resembling those in endocrine secretory cells. Type II cells covered nerve endings terminating on Type I cells and enclosed nerve fibers in much the same manner as Schwann cells. The nerve endings contained numerous microvesicles (∼500 A in diameter), mitochondria, glycogen granules, and a few electron-opaque cored vesicles. Junctions between nerve endings and Type I cells were associated with regions of increased density in both intercellular spaces and the adjoining cytoplasm. Cilia of the 9 + 0 fibril pattern were observed in Type I and Type II cells and pericytes. Nonmyelinated nerve fibers, often containing microvesicles, mitochondria, and a few electron-opaque cored vesicles (650 to 1000 A in diameter) were present in Schwann cells, many of which were situated close to blood vessels Ganglion cells near the periphery of the gland, fibrocytes, and segments of unidentified cells were also seen. It was concluded that, according to present concepts of the structure of nerve endings, those endings related to Type I cells could be efferent or afferent.


2002 ◽  
Vol 282 (3) ◽  
pp. L431-L439 ◽  
Author(s):  
Joseph A. Kitterman ◽  
Cheryl J. Chapin ◽  
Jeff N. Vanderbilt ◽  
Nicolas F. M. Porta ◽  
Louis M. Scavo ◽  
...  

Oligohydramnios (OH) retards fetal lung growth by producing less lung distension than normal. To examine effects of decreased distension on fetal lung development, we produced OH in rats by puncture of uterus and fetal membranes at 16 days of gestation; fetuses were delivered at 21 or 22 days of gestation. Controls were position-matched littermates in the opposite uterine horn. OH lungs had lower weights and less DNA, protein, and water, but no differences in saturated phosphatidylcholine, surfactant proteins (SP)-A and -B, and mRNA for SP-A, -B, -C, and -D. To evaluate effects on epithelial differentiation, we used RTI40 and RTII70, proteins specific in lung to luminal surfaces of alveolar type I and II cells, respectively. At 22 days of gestation, OH lungs had less RTI40 mRNA ( P < 0.05) and protein ( P < 0.001), but RTII70 did not differ from controls. With OH, type I cells (in proportion to type II cells) covered less distal air space perimeter ( P < 0.01). We conclude that OH, which retards lung growth, has little effect on surfactant and impedes formation of type I cells relative to type II cells.


1951 ◽  
Vol s3-92 (17) ◽  
pp. 55-77
Author(s):  
MARGARET GUNN

1. The extrinsic nerve-supply to the gut in the frog (Rana temporaria) is contained in the vagus and splanchnic nerves--both of which appear to contain parasympathetic and sympathetic fibres. 2. The vagus supplies the gut from the proximal part of the oesophagus to the most proximal part of the intestine. The splanchnic nerves supply the gut from the oesophagus to the rectum. 3. No vagal fibres accompany the splanchnic nerves. 4. A possible explanation is given for the variable effects produced on stimulation of the extrinsic nerves supplying the gut. 5. A plexus of nerve-fibres is present i n the submucosa which probably corresponds to Meissner's plexus of mammals, but no nerve-cells are present. 6. In the myenteric plexus the nerve-cells are commonly grouped int o ganglia in the oesophagus and stomach, but in theintestine the nerve-cells are fairly evenly distributed, distinct ganglia not being present. 7. Cells of three types have been found corresponding to Dogiel's three types. Type I cells are of two varieties: (a) large, strongly argyrophi l cells which are multi-polar possessing numerous short dendrites and a very prominent axon; (b)smaller cells having a prominent axon and often unipolar. Type I cells are enclosed in capsules. Type II cells are small multipolar cells with long dendrites. Type III cells are small multipolar cells with shorter dendrites and an axon bearing no collaterals. 8. Cells in the oesophagus and stomach are entirely of Type I. In the intestine these cells are present in fairly large numbers at the most proximal end, but throughout the rest of the intestine they only occur commonly close to the attachment of the mesentery, where they are found singly and fairly evenly spaced. 9. Cells of Types II and III occur only in the myenteric plexus of the intestine, where they are distributed fairly evenly, not forming distinct ganglia. 10. It is suggested that the Type II and III cells formed the original autonomic nerve plexus of the gut, the Type II cells being motor and the Type III sensory. The Type I cells are the post-ganglionic cells of the parasympathetic system and are an additional motor contribution to the plexus. 11. The endings of th e pre-ganglionic parasympathetic fibres on the ganglion cells may take any of three forms: (a) pericellular varicose endings which occur on the large variety of Typ e I cell; (b) pericapsular varicose endings which are borne by the smaller variety of Type I cell; and(c) club-shaped endings occurring on the larger Type I cells. 12. The type of synapse formed by the processes of cells of Types II and III consists of the simple endings of their processes on the cell bodies or dendrites of other cells, or the passing contact of their processes with the bodies of other cells. 13. Fine varicose fibrils have been observed on the surface of muscle-cells. These are presumably the distal ends of the cell processes and sympathetic fibres which form the motor endings. 14. The types of sensory endings which have been found are: (a) typical sensory varicose endings spread out in the submucosa of the oesophagus and rectum; those in the oesophagus originating from vagal fibres; and (b) Pacinian corpuscle in the sub-mucosa of the intestine. 15. The ‘interstitial cells of Cajal’ form an apparently anastomosing network in the gut-wall which appears to be distinct from the anastomosing Schwann plasmodium which covers the nerve-fibres.


2009 ◽  
Vol 297 (3) ◽  
pp. L439-L454 ◽  
Author(s):  
Chuanxiu Yang ◽  
Lijing Su ◽  
Yang Wang ◽  
Lin Liu

UTP is known to regulate alveolar fluid clearance. However, the relative contribution of alveolar type I cells and type II cells to this process is unknown. In this study, we investigated the effects of UTP on ion transport in type I-like cell (AEC I) and type II-like cell (AEC II) monolayers. Luminal treatment of cell monolayers with UTP increased short-circuit current ( Isc) of AEC II but decreased Isc of AEC I. The Cl− channel blockers NPPB and DIDS inhibited the UTP-induced changes in Isc (Δ Isc) in both types of cells. Amiloride, an inhibitor of epithelial Na+ channels (ENaC), abolished the UTP-induced Δ Isc in AEC I, but not in AEC II. The general blocker of K+ channels, BaCl2, eliminated the UTP-induced Δ Isc in AEC II, but not in AEC I. The intermediate conductance (IKCa) blocker, clofilium, also blocked the UTP effect in AEC II. The signal transduction pathways mediated by UTP were the same in AEC I and AEC II. Furthermore, UTP increased Cl− secretion in AEC II and Cl− absorption in AEC I. Our results suggest that UTP induces opposite changes in Isc in AEC I and AEC II, likely due to the reversed Cl− flux and different contributions of ENaC and IKCa. Our results further imply a new concept that type II cells contribute to UTP-induced fluid secretion and type I cells contribute to UTP-induced fluid absorption in alveoli.


1997 ◽  
Vol 273 (1) ◽  
pp. F67-F75 ◽  
Author(s):  
J. P. Lavelle ◽  
H. O. Negrete ◽  
P. A. Poland ◽  
C. L. Kinlough ◽  
S. D. Meyers ◽  
...  

Barrier epithelia such as the renal collecting duct (in the absence of antidiuretic hormone) and thick ascending limb, as well as the stomach and mammalian bladder, exhibit extremely low permeabilities to water and small nonelectrolytes. A cell culture model of such epithelia is needed to determine how the structure of barrier apical membranes reduce permeability and how such membranes may be generated and maintained. In the present studies, the transepithelial electrical resistance and isotopic water and urea fluxes were measured for Madin-Darby canine kidney (MDCK) type I and type II cells, as well as type I cells expressing the mucin protein, MUC1, in their apical membranes. Although earlier studies had found the unstirred layer effects too great to permit measurement of transepithelial permeabilities, use of ultrathin semipermeable supports in this study overcame this difficulty. Apical membrane diffusive water permeabilities were 1.8 +/- 0.4 x 10(-4) cm/s and 3.5 +/- 0.5 x 10(-4) cm/s in MDCK type I and type II cells, respectively, at 20 degrees C. Urea permeability in type I cells at the same temperature was 6.0 +/- 0.9 x 10(-6) cm/s. These values resemble those of other barrier epithelial apical membranes, either isolated or in intact epithelia, and the water permeability values are far below those of other epithelial cells in culture. Transfection of MDCK type I cells with the major human urinary epithelial mucin, MUC1, led to abundant expression of the fully glycosylated form of the protein on immunoblots, and flow cytometry revealed that virtually all the cells expressed the protein. However, MUC1 had no effect on water or urea permeabilities. In conclusion, MDCK cells grown on semipermeable supports form a model barrier epithelium. Abundant expression of mucins does not alter the permeability properties of these cells.


2017 ◽  
Vol 313 (1) ◽  
pp. L41-L51 ◽  
Author(s):  
Qian Chen ◽  
Varsha Suresh Kumar ◽  
Johanna Finn ◽  
Dianhua Jiang ◽  
Jiurong Liang ◽  
...  

The alveolar epithelium is composed of type I cells covering most of the gas-blood exchange surface and type II cells secreting surfactant that lowers surface tension of alveoli to prevent alveolar collapse. Here, we have identified a subgroup of type II cells expressing a higher level of cell surface molecule CD44 (CD44high type II cells) that composed ~3% of total type II cells in 5–10-wk-old mice. These cells were preferentially apposed to lung capillaries. They displayed a higher proliferation rate and augmented differentiation capacity into type I cells and the ability to form alveolar organoids compared with CD44low type II cells. Moreover, in aged mice, 18–24 mo old, the percentage of CD44high type II cells among all type II cells was increased, but these cells showed decreased progenitor properties. Thus CD44high type II cells likely represent a type II cell subpopulation important for constitutive regulation of alveolar homeostasis.


2006 ◽  
Vol 291 (5) ◽  
pp. L1101-L1111 ◽  
Author(s):  
Min Yee ◽  
Peter F. Vitiello ◽  
Jason M. Roper ◽  
Rhonda J. Staversky ◽  
Terry W. Wright ◽  
...  

Type II epithelial cells are essential for lung development and remodeling, as they are precursors for type I cells and can produce vascular mitogens. Although type II cell proliferation takes place after hyperoxia, it is unclear why alveolar remodeling occurs normally in adults whereas it is permanently disrupted in newborns. Using a line of transgenic mice whose type II cells could be identified by their expression of enhanced green fluorescent protein and endogenous expression of surfactant proteins, we investigated the age-dependent effects of hyperoxia on type II cell proliferation and alveolar repair. In adult mice, type II cell proliferation was low during room air and hyperoxia exposure but increased during recovery in room air and then declined to control levels by day 7. Eight weeks later, type II cell number and alveolar compliance were indistinguishable from those in room air controls. In newborn mice, type II cell proliferation markedly increased between birth and postnatal day 7 before declining by postnatal day 14. Exposure to hyperoxia between postnatal days 1 and 4 inhibited type II cell proliferation, which resumed during recovery and was aberrantly elevated on postnatal day 14. Eight weeks later, recovered mice had 70% fewer type II cells and 30% increased lung compliance compared with control animals. Recovered mice also had higher levels of T1α, a protein expressed by type I cells, with minimal changes detected in genes expressed by vascular cells. These data suggest that perinatal hyperoxia adversely affects alveolar development by disrupting the proper timing of type II cell proliferation and differentiation into type I cells.


2008 ◽  
Vol 413 (3) ◽  
pp. e11-e12 ◽  
Author(s):  
Roland Reinehr ◽  
Dieter Häussinger

Whereas ligation of the CD95 death receptor in the plasma membrane of so-called type I cells leads to a direct caspase 8-dependent activation of downstream effector caspases, mitochondrial amplification of caspase 8-derived signals is required in so-called type II cells in order to execute apoptotic cell death. In type I cells CD95L (CD95 ligand) binding to CD95 results in a ceramide-dependent formation of the DISC (death-inducing signalling complex) and caspase 8-dependent CD95 clustering in the plasma membrane, followed by an internalization of these multimeric-receptor–DISC complexes. In contrast, in the hepatocyte, a type II cell, the bulk of CD95 is stored intracellularly under resting conditions and only a few ‘sentinel’ CD95 receptors are present in the plasma membrane. However, their activation by CD95L is sufficient to trigger a caspase 8-dependent endosomal acidification and a ceramide-dependent trafficking of intracellularly stored CD95 to the plasma membrane, thereby amplifying CD95 activation. Thus, in both type I and type II cells, ceramide and CD95 receptor endo- and exo-cytosis are involved in CD95-mediated apoptosis, but apparently in different ways. This, however, is not the only effect of CD95 ligation on intracellular membrane flow in type II cells, and evidence has been presented that soon after CD95 ligation Golgi elements intermix caspase-dependently with mitochondria. In this issue of the Biochemical Journal, Matarrese et al. report another aspect on endocytosis in response to CD95 ligation in type II cells, namely a caspase-independent endocytosis with vesicle translocation to the mitochondrial compartment, suggestive of an interplay between both organelles in the sense of an ‘organelle scrambling’. Thus early effects of CD95 activation on intracellular membrane flow may be much more complex than previously thought, but much has still to be learned about signalling mechanisms and the role they play in apoptosis.


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