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1 ndoparvovirus, AAV2, in differentiated human airway epithelia.
2 r 1 (TfR1), are expressed in polarized human airway epithelia.
3 efects in a fraction of cilia covering mouse airway epithelia.
4 rrent in H441 epithelia and in human primary airway epithelia.
5 ither basolateral or apical interaction with airway epithelia.
6 mal tidal breathing, regulates ASL volume in airway epithelia.
7 elimination from the apical surface of human airway epithelia.
8 rimary cultures of well-differentiated human airway epithelia.
9 stored transepithelial Cl(-) transport to CF airway epithelia.
10 ADA1 (not ADA2) mRNA was detected in human airway epithelia.
11 adenosine regulate mucociliary clearance in airway epithelia.
12 1 to establish persistent infection of human airway epithelia.
13 d biofilms on the apical surface of cultured airway epithelia.
14 vector, AAV2/9, across murine nasal and lung airway epithelia.
15 al than the basolateral surface of polarized airway epithelia.
16 rs to efficiently and persistently transduce airway epithelia.
17 ion proteins could prove to be less toxic to airway epithelia.
18 2)-R-dependent Ca(2+)(i) signals in CF human airway epithelia.
19 m to the apical surface of differentiated CF airway epithelia.
20 try into polarized primary cultures of human airway epithelia.
21 ell-differentiated cultures of primary human airway epithelia.
22 arly modulate tight junction permeability in airway epithelia.
23 e increased in CF compared with normal human airway epithelia.
24 ted from newborn piglets and ASL on cultured airway epithelia.
25 e role of NADPH oxidase in H(+) secretion by airway epithelia.
26 demonstration of regulated ATP release from airway epithelia.
27 s underlie cAMP-regulated Na(+) transport in airway epithelia.
28 ithelial cells and well differentiated human airway epithelia.
29 nd electrolyte transport assays in polarized airway epithelia.
30 D was identified as the major PDE species in airway epithelia.
31 possess the capacity of differentiating into airway epithelia.
32 absolutely required for apical expression in airway epithelia.
33 lycoprotein-pseudotyped FIV-based vectors in airway epithelia.
34 in the transitional zone of motile cilia in airway epithelia.
35 tors following apical infection of polarized airway epithelia.
36 of adenosine on the mucosal surface of human airway epithelia.
37 esponse to bacterial components in the human airway epithelia.
38 ctors that demonstrate increased tropism for airway epithelia.
39 AV-2/5 and rAAV-2 from the apical surface of airway epithelia.
40 ith vectors applied to the apical surface of airway epithelia.
41 ha was observed in primary cultures of human airway epithelia.
42 plays a role in the expression of RANTES in airway epithelia.
43 ms that resolve these changes to form normal airway epithelia.
44 d them in well-differentiated cultures of CF airway epithelia.
45 d by in situ hybridization, are expressed in airway epithelia.
46 rimary cultures of well-differentiated human airway epithelia.
47 ding and entry through the apical surface of airway epithelia.
48 teases that serve similar functions in human airway epithelia.
49 ateral membrane of well differentiated human airway epithelia.
50 nd normal human lung tissue localized DSP to airway epithelia.
51 N) localized mainly to the apical surface of airway epithelia.
52 in primary cultures of human cystic fibrosis airway epithelia.
53 cused on correcting electrolyte transport in airway epithelia.
54 elivering genes and other pharmaceuticals to airway epithelia.
55 most important barriers to gene transfer in airway epithelia.
56 tigated as a vector to transfer CFTR cDNA to airway epithelia.
57 for the osmotic water permeability (P(f)) of airway epithelia.
58 binding and endocytosis of vectors by human airway epithelia.
59 cy of other AAV serotypes at infecting human airway epithelia.
60 R-dependent anion secretion in primary human airway epithelia.
61 derived cytokines on the function of CD40 in airway epithelia.
62 prove the outlook for gene delivery to human airway epithelia.
63 membrane conductance regulator gene to human airway epithelia.
64 lactosidase transduced 1-14% of adult rabbit airway epithelia.
65 ascular endothelia and aquaporin-4 (AQP4) in airway epithelia.
66 y of other adenovirus serotypes at infecting airway epithelia.
67 model of well differentiated, ciliated human airway epithelia.
68 transmembrane conductance regulator cDNA to airway epithelia.
69 stic fibrosis (CF) Cl(-) transport defect in airway epithelia.
70 f gene transfer to well-differentiated human airway epithelia.
71 e highly efficient in gene delivery to human airway epithelia.
72 mportant for normal CFTR channel function in airway epithelia.
73 MV infection in primary cultures of porcine airway epithelia.
74 2+) release from the ER, and apoptosis in CF airway epithelia.
75 unction in well differentiated primary human airway epithelia.
76 sed at the apical membrane of intestinal and airway epithelia.
77 d Klebsiella pneumoniae biofilm formation on airway epithelia.
78 d fluid absorption across colon, kidney, and airway epithelia.
79 ECs, which differentiate in situ within lung airway epithelia.
80 various cell types and by stretch/strain in airway epithelia.
81 restored Cl(-) transport to cystic fibrosis airway epithelia.
82 rom asthmatic patients versus that in normal airway epithelia.
83 ic strategy to reduce the inflammation of CF airway epithelia.
84 hloride currents in both CF human and ferret airway epithelia.
85 clinical specimens using reconstituted human airway epithelia.
86 lls as well as human and ferret CF polarized airway epithelia.
87 Na(+) conductances were altered in human CF airway epithelia.
88 rain into pannexin 1-mediated ATP release in airway epithelia.
89 n disrupts the barrier function of polarized airway epithelia.
90 retion in normal compared to cystic fibrosis airway epithelia.
91 is transmembrane regulator (CFTR)-expressing airway epithelia.
92 regulation of transcellular ion transport in airway epithelia.
93 an (rich in 2,3N-linked sialic acid) and pig airway epithelia (2,6N-linked sialic acid), significantl
97 rmacologic disruption of barrier function in airway epithelia allowed responses to apical application
98 cantly reduced transepithelial resistance in airway epithelia and altered tight junction permeability
99 cted in cell culture (A549 and primary human airway epithelia and alveolar macrophages) using chemica
100 sed primary cultures of differentiated human airway epithelia and assessed expression of claudins, th
101 ptional response across all subjects in both airway epithelia and BAL cells, with strong association
102 ological processes such as the secretions of airway epithelia and exocrine glands, the contraction of
103 complexes that may degrade DeltaF508-CFTR in airway epithelia and identifies a new role for NEDD8 in
105 ery that is advantageous for growth in human airway epithelia and in vivo confers susceptibility to p
106 n vitro human cystic fibrosis (CF) polarized airway epithelia and in vivo human CF bronchial xenograf
108 allergic asthma, transcriptional changes in airway epithelia and inflammatory cells are influenced b
110 65 is concentrated at the apical membrane in airway epithelia and interacts with EBP50 in cells.
111 iates ATP release from hypotonically swollen airway epithelia and investigated mechanisms regulating
112 n the lung, HBD-2 is an inducible product of airway epithelia and may play a role in innate mucosal d
114 the potentially deleterious effects of CS on airway epithelia and outline a hitherto unrecognized sig
115 A subunits localize to the apical surface of airway epithelia and PP2A phosphatase activity co-purifi
116 cs that enables on-chip engineering of human airway epithelia and precise reproduction of physiologic
117 opulation of smooth muscle cells surrounding airway epithelia and promote airway differentiation of e
118 nterferon gamma (IFN-gamma), and IL-1beta in airway epithelia and secretions from cystic fibrosis (CF
119 jor adrenergic receptor isoform expressed in airway epithelia and that it colocalizes with CFTR at th
120 to mediate effective gene transfer to human airway epithelia and that the cytoplasmic domain of CAR
121 n complement the CF defect in differentiated airway epithelia and thereby further the development of
122 CFTR reciprocally regulates AMPK function in airway epithelia and whether such regulation is involved
123 (AQP1) in microvascular endothelia, AQP4 in airway epithelia, and AQP5 at the apical plasma membrane
124 found that BBS genes were expressed in human airway epithelia, and BBS2 and BBS4 localized to cellula
125 f CD103 (Itgae), were mislocalized away from airway epithelia, and demonstrated an impaired ability t
126 failure of vectors to attach and enter into airway epithelia, and may require redirecting vectors to
128 ompetitively inhibited bacterial adhesion to airway epithelia, and MUC1-ED immunodepletion completely
129 ional cellular complex with AMPK and CFTR in airway epithelia, and NDPK-A catalytic function is requi
130 of sodium absorption is a function of human airway epithelia, and prostasin is a likely candidate fo
131 nscellular pathway for Cl and HCO in porcine airway epithelia, and reduced anion permeability may ini
132 an important determinant of CFTR activity in airway epithelia, and support the use of PDE4 inhibitors
133 nd mediate gene transfer to human and murine airway epithelia, and the tropism of AAV5 may be useful
134 pH were identified in the apical membrane of airway epithelia, and their activities were measured.
135 bility in non-cystic fibrosis (non-CF) or CF airway epithelia, AQP-transfected Fisher rat thyroid cel
136 at, when polarized/well-differentiated human airway epithelia are infected with HBoV1 in vitro, they
141 However, earlier work has shown that human airway epithelia are resistant to infection by Ad2 and A
143 e apical surface of the differentiated human airway epithelia as well as in human tracheal tissue sec
144 predominant basolateral location in cultured airway epithelia as well as in normal human airway tissu
145 lay a critical role in retinol metabolism in airway epithelia as well as in other epithelia of colon,
148 st study investigating the effect of AMPs on airway-epithelia associated genes upon administration to
149 AAV2.5T binds to the apical surface of human airway epithelia at higher levels and has more receptors
150 ) is inefficient at infecting differentiated airway epithelia because of a lack of receptors at the a
152 producing isotonic volume responses in human airway epithelia but were typically short acting and les
155 These results indicate that transduction of airway epithelia by AAV vectors is limited by entry and
158 n from the apical surface of human polarized airway epithelia by modulating the intracellular traffic
159 The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the
161 a predominant gel-forming mucin secreted by airway epithelia, can be induced by various inflammatory
162 moter-LUC was transfected into primary human airway epithelia cells (EC), the luciferase activity was
165 ) are relatively high for both normal and CF airway epithelia, consistent with an isosmotic ASL.
168 in contrast to AAV2, the apical membrane of airway epithelia contains abundant high affinity recepto
169 ane conductance regulator to cystic fibrosis airway epithelia, correcting the Cl(-) transport defect.
170 rate that AAV1 transduction biology in human airway epithelia differs from that of AAV2 and AAV5 by v
171 ally or basolaterally to primary cultures of airway epithelia, discrete foci of eGFP expression appea
172 When expressed in well differentiated CF airway epithelia, each construct localized predominantly
176 data indicate for the first time that human airway epithelia express catalytically active NEU1 siali
177 part by sialidase activity, we asked whether airway epithelia express catalytically active sialidase(
180 Here we show that the apical membrane of airway epithelia express the urokinase plasminogen activ
184 We found that following infection, human airway epithelia first released adenovirus to the basola
185 te surface proteins for migrating across the airway epithelia for Ag and pathogen capture, transport,
186 ctively used to augment rAAV transduction in airway epithelia for gene therapy of cystic fibrosis.
187 Cl(-) transport defect in differentiated CF airway epithelia for the life of the culture (>3 months)
189 imilar differences were observed in cultured airway epithelia from CF and non-CF pigs exposed to the
190 ER density was morphometrically analyzed in airway epithelia from normal subjects, DeltaF508 homozyg
191 t explain their altered ability to transduce airway epithelia from the apical membrane, we examined t
192 d viruses (AAVs) such as AAV5 that transduce airway epithelia from the apical surface are attractive
197 olayers but failed to migrate across primary airway epithelia grown at the air-liquid interface.
198 ivity in an in vitro model of human ciliated airway epithelia (HAE) derived from nasal and tracheobro
199 at infects well-differentiated primary human airway epithelia (HAE) in vitro In human embryonic kidne
202 ssing CFTR and increased Na(+) absorption in airway epithelia has remained elusive, although substant
207 Here we show that in differentiated human airway epithelia, heregulin-alpha is present exclusively
209 ilized Ca(2+)(i), which were investigated in airway epithelia in a long term culture in the absence o
210 the lung exhibit two general functions: (1) airway epithelia in all regions 'defend' the lung agains
211 important for ciliogenesis in multiciliated airway epithelia in mice, and antagonizes canonical Wnt
213 ainst infectious and noxious agents; and (2) airway epithelia in the proximal regions replenish water
215 proved gene transfer to differentiated human airway epithelia in vitro and to the mouse lung in vivo.
221 This is the first report of pyroptosis in airway epithelia infected by a respiratory virus.IMPORTA
222 ell-differentiated primary cultures of human airway epithelia, infection primarily occurred from the
223 w report, however, that differentiated human airway epithelia internalize rAAV type-2 virus efficient
225 elicited by apical P2Y(2)-R activation in CF airway epithelia is an expansion of the apical ER Ca(2+)
226 dy shows that adenosine elimination on human airway epithelia is mediated by ADA1, CNT2, and CNT3, wh
228 k has shown that the apical surface of human airway epithelia is resistant to infection by AAV2, pres
229 ltured cells show that the apical surface of airway epithelia is resistant to transduction by AAV2 ve
230 ured CFTR(-/-) and CFTR(DeltaF508/DeltaF508) airway epithelia lacked anion conductance, and they did
233 targeting apical receptors in differentiated airway epithelia may be sufficient for gene transfer in
235 revious reports suggest that cystic fibrosis airway epithelia may respond to injury by increasing pro
237 nhibitable aquaporin (AQP) water channels in airway epithelia modulate airway surface liquid volume.
239 mples] and 80.0 +/- 3.5 [n = 6 samples]) and airway epithelia (mV, mean +/- SEM CFTR-mediated Cl(-) c
241 omatically acquired molecular alterations in airway epithelia of lung cancer patients has remained un
242 yk expression increased significantly in the airway epithelia of OVA-sensitized and OVA-challenged (O
247 ltured cystic fibrosis (DeltaF508/DeltaF508) airway epithelia partially restored DeltaF508-cystic fib
250 tic) culture conditions revealed that normal airway epithelia possess an adenosine-regulated pathway
252 th increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, fin
255 ncreased in IPF lung and concentrated in the airway epithelia, suggesting a potential role for DSP in
258 inked sialic acid residues on the surface of airway epithelia that mediate rapid internalization and
259 cultures of normal and cystic fibrosis (CF) airway epithelia that, like the native tissue, contain c
262 raction between the virus and differentiated airway epithelia; the virus preferentially enters the ce
264 me height in normal and cystic fibrosis (CF) airway epithelia through extracellular ATP- and adenosin
265 m cells maintain secretory daughter cells in airway epithelia through forward regulation, suggesting
266 tions, ranging from electrolyte secretion in airway epithelia to cellular excitability in sensory neu
267 previously used directed evolution in human airway epithelia to create adeno-associated virus 2.5T (
268 These data suggest that the ability of human airway epithelia to inactivate quorum-sensing signal mol
269 We investigated the ability of non-CF and CF airway epithelia to kill bacteria through the generation
270 fect this pathway by reducing the ability of airway epithelia to respond appropriately to nucleotides
271 Exposure of 30-40-day-old cultures of normal airway epithelia to supernatant from mucopurulent materi
272 nt deleting residues 708-759 complemented CF airway epithelia to the same extent as wild-type CFTR an
275 y of NTHi to form biofilms and its impact on airway epithelia using in vivo and in vitro analyses.
276 and rAAV2/5 transduction in polarized human airway epithelia using viruses purified by a newly devel
278 AV2/1 apical transduction of human polarized airway epithelia was 10-fold lower than that for rAAV2/2
279 Furthermore, binding and gene transfer to airway epithelia was competed by lectins that specifical
280 ria multivorans by well-differentiated human airway epithelia was investigated by immunohistology and
282 tion to the apical surface of differentiated airway epithelia we found that a recombinant AAV5 bound
284 apical gene transfer to differentiated human airway epithelia, we expressed CAR in which the transmem
285 e apically confined ER Ca(2+) stores, normal airway epithelia were chronically exposed to supernatant
286 The present study investigated whether CF airway epithelia were hyperinflammatory and, if so, whet
287 luminal mechanical stimulation in polarized airway epithelia were initiated by the release of the 5'
288 rimary cultures of well-differentiated human airway epithelia were transduced when filovirus GP-pseud
289 uced fully differentiated, nondividing human airway epithelia when applied to the apical surface.
290 ghly expressed in multiple tissues including airway epithelia, where it acts as an apical conduit for
291 e-limiting step for sodium absorption across airway epithelia, which in turn regulates airway surface
293 rmed adherent biofilms on the apical surface airway epithelia with decreased susceptibility to antibi
296 monstrated that apical transduction of human airway epithelia with rAAV2/1 was 100-fold more efficien
299 vate levels of CSTA expression in lung small airway epithelia, with still further upregulation in squ
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