scholarly journals CD44high alveolar type II cells show stem cell properties during steady-state alveolar homeostasis

2017 ◽  
Vol 313 (1) ◽  
pp. L41-L51 ◽  
Author(s):  
Qian Chen ◽  
Varsha Suresh Kumar ◽  
Johanna Finn ◽  
Dianhua Jiang ◽  
Jiurong Liang ◽  
...  
Keyword(s):  
Alveolar Epithelium ◽  
Cell Subpopulation ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Cell Surface Molecule ◽  
Type I Cells ◽  
Blood Exchange ◽  
I Cells

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.

Effects of oligohydramnios on lung growth and maturation in the fetal rat

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 ◽  
...  
Keyword(s):  
Fetal Lung ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Lung Growth ◽  
Type I Cells ◽  
Fetal Lung Development ◽  
Fetal Rat ◽  
I Cells

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.

scholarly journals UTP regulation of ion transport in alveolar epithelial cells involves distinct mechanisms

2009 ◽  
Vol 297 (3) ◽  
pp. L439-L454 ◽  
Author(s):  
Chuanxiu Yang ◽  
Lijing Su ◽  
Yang Wang ◽  
Lin Liu
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Alveolar Epithelial Cells ◽  
Alveolar Type ◽  
Channel Blockers ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
I Cells

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.

Expression ofN-deacetylase/sulfotransferase and 3-O-sulfotransferase in rat alveolar type II cells

2000 ◽  
Vol 279 (2) ◽  
pp. L292-L301 ◽  
Author(s):  
Zhong-Yuan Li ◽  
Kazunori Hirayoshi ◽  
Yasuhiro Suzuki
Keyword(s):  
Heparan Sulfate ◽  
Protein A ◽  
Sodium Chlorate ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Basal laminae beneath alveolar type I cells are suggested to contain highly sulfated heparan sulfate-containing proteoglycans (PGs), and cultured type II cells accumulate highly sulfated matrices. To characterize the regulation of PG synthesis during the transition from type II cells to type I cells, we examined mRNA expression of N-deacetylase/sulfotransferase (NST) and 3- O-sulfotransferase (3-OST), two enzymes specific for heparan sulfate synthesis. We found that both freshly isolated and cultured type II cells expressed NST and 3-OST as shown by in situ hybridization. Expression of surfactant-associated protein A, B, and C mRNAs, determined by semiquantitative PCR, decreased during culture. Expression of type I cell marker T1α mRNA increased except in cells cultured on an Engelbrecht-Holm-Swarm gel. Expression of NST was dependent on cell density and matrix and was intense in conditions where cells spread fully, whereas 3-OST expression was unchanged in the conditions examined. The PG sulfation inhibitor sodium chlorate significantly inhibited cultured type II cell spreading, and this inhibition was reversed by sodium sulfate. These results suggest that highly sulfated PGs modified by NST are necessary for the spreading of cells during transdifferentiation of type II cells to mature type I cells.

scholarly journals Characteristics of Cl− uptake in rat alveolar type I cells

2009 ◽  
Vol 297 (5) ◽  
pp. L816-L827 ◽  
Author(s):  
Meshell Johnson ◽  
Lennell Allen ◽  
Leland Dobbs
Keyword(s):  
Fetal Lung ◽  
Fluid Secretion ◽  
Normal Lung ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Adult Lung ◽  
Type I Cells ◽  
I Cells

Although Cl− transport in fetal lung is important for fluid secretion and normal lung development, the role of Cl− transport in adult lung is not well understood. In physiological studies, the cystic fibrosis transmembrane regulator (CFTR) plays a role in fluid absorption in the distal air spaces of adult lung, and alveolar type II cells cultured for 5 days have the capacity to transport Cl−. Although both alveolar type I and type II cells express CFTR, it has previously not been known whether type I cells transport Cl−. We studied Cl− uptake in isolated type I cells directly, using either radioisotopic tracers or halide-sensitive fluorescent indicators. By both methods, type I cells take up Cl−. In the presence of β-adrenergic agonist stimulation, Cl− uptake can be inhibited by CFTR antagonists. Type I cells express both the Cl−/HCO3− anion exchanger AE2 and the voltage-gated Cl− channels CLC5 and CLC2. Inhibitors of AE2 also block Cl− uptake in type I cells. Together, these results demonstrate that type I cells are capable of Cl− uptake and suggest that the effects seen in whole lung studies establishing the importance of Cl− movement in alveolar fluid clearance may be, in part, the result of Cl− transport across type I cells.

scholarly journals FoxM1 mediates the progenitor function of type II epithelial cells in repairing alveolar injury induced by Pseudomonas aeruginosa

2011 ◽  
Vol 208 (7) ◽  
pp. 1473-1484 ◽  
Author(s):  
Yuru Liu ◽  
Ruxana T. Sadikot ◽  
Guy R. Adami ◽  
Vladimir V. Kalinichenko ◽  
Srikanth Pendyala ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Intratracheal Instillation ◽  
Alveolar Epithelium ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Forkhead Transcription Factor ◽  
Type I Cells ◽  
Barrier Repair ◽  
I Cells

The alveolar epithelium is composed of the flat type I cells comprising 95% of the gas-exchange surface area and cuboidal type II cells comprising the rest. Type II cells are described as facultative progenitor cells based on their ability to proliferate and trans-differentiate into type I cells. In this study, we observed that pneumonia induced by intratracheal instillation of Pseudomonas aeruginosa (PA) in mice increased the expression of the forkhead transcription factor FoxM1 in type II cells coincidentally with the induction of alveolar epithelial barrier repair. FoxM1 was preferentially expressed in the Sca-1+ subpopulation of progenitor type II cells. In mice lacking FoxM1 specifically in type II cells, type II cells showed decreased proliferation and impaired trans-differentiation into type I cells. Lungs of these mice also displayed defective alveolar barrier repair after injury. Expression of FoxM1 in the knockout mouse lungs partially rescued the defective trans-differentiation phenotype. Thus, expression of FoxM1 in type II cells is essential for their proliferation and transition into type I cells and for restoring alveolar barrier homeostasis after PA-induced lung injury.

scholarly journals Thoughts on the alveolar phase of COVID-19

2020 ◽  
Vol 319 (1) ◽  
pp. L115-L120 ◽  
Author(s):  
Robert J. Mason
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Severe Disease ◽  
Innate Immune ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
I Cells

COVID-19 can be divided into three clinical stages, and one can speculate that these stages correlate with where the infection resides. For the asymptomatic phase, the infection mostly resides in the nose, where it elicits a minimal innate immune response. For the mildly symptomatic phase, the infection is mostly in the pseudostratified epithelium of the larger airways and is accompanied by a more vigorous innate immune response. In the conducting airways, the epithelium can recover from the infection, because the keratin 5 basal cells are spared and they are the progenitor cells for the bronchial epithelium. There may be more severe disease in the bronchioles, where the club cells are likely infected. The devastating third phase is in the gas exchange units of the lung, where ACE2-expressing alveolar type II cells and perhaps type I cells are infected. The loss of type II cells results in respiratory insufficiency due to the loss of pulmonary surfactant, alveolar flooding, and possible loss of normal repair, since type II cells are the progenitors of type I cells. The loss of type I and type II cells will also block normal active resorption of alveolar fluid. Subsequent endothelial damage leads to transudation of plasma proteins, formation of hyaline membranes, and an inflammatory exudate, characteristic of ARDS. Repair might be normal, but if the type II cells are severely damaged alternative pathways for epithelial repair may be activated, which would result in some residual lung disease.

scholarly journals Mechanical stretch activates piezo1 in caveolae of alveolar type I cells to trigger ATP release and paracrine stimulation of surfactant secretion from alveolar type II cells

2020 ◽  
Vol 34 (9) ◽  
pp. 12785-12804 ◽  
Author(s):  
Kathrin Diem ◽  
Michael Fauler ◽  
Giorgio Fois ◽  
Andreas Hellmann ◽  
Natalie Winokurow ◽  
...  
Keyword(s):  
Atp Release ◽  
Mechanical Stretch ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Surfactant Secretion ◽  
I Cells ◽  
Stimulation Of
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