ライフサイエンスコーパス: goblet cell

1 ells, and Mtg16(-/-) mice have a decrease in goblet cells.

2 and [Ca(2+)]i, and activated ERK1/2 in human goblet cells.

3 evere colitis associated with loss of mature goblet cells.

4 nule decondensation and exocytosis in the CF goblet cells.

5 ng effector gli-1) or maintenance (RREB2) of goblet cells.

6 which accumulates in colonic enterocytes and goblet cells.

7 exhibit morphological defects in Paneth and goblet cells.

8 hereas nongoblet cell metaplasia (NGM) lacks goblet cells.

9 ontrol mucin granule accumulation in colonic goblet cells.

10 deposition, and loss of colon epithelial and goblet cells.

11 inducing Muc2 production from proximal colon goblet cells.

12 io-lateral axis, especially among intestinal goblet cells.

13 elium lining of the esophagus is replaced by goblet cells.

14 )] and stimulate secretion from conjunctival goblet cells.

15 f ciliated, nonciliated, and mucin-secretory goblet cells.

16 hagus in terms of the presence of intestinal goblet cells.

17 -18 is specifically required for homeostatic goblet cell AMP production.

18 ivation rescued the Shp2 phenotype, promoted goblet cell and inhibited paneth cell generation.

19 is study, we used human colonoids comprising goblet cells and a thick mucin barrier as an intestinal

20 6 deficiency leads to defective autophagy in goblet cells and abrogated mucus secretion into the larg

21 tion of IRE1alpha in IECs results in loss of goblet cells and failure of intestinal epithelial barrie

22 cytokine induced by IL-33, markedly induces goblet cells and gene expression consistent with goblet

23 n, increased spontaneous degranulation in WT goblet cells and improved exocytotic dynamics in CF gobl

24 Furthermore, the numbers of mucus-producing goblet cells and inflammatory cell infiltrates were redu

25 e also observed lower numbers of PAS-stained goblet cells and less Muc2 in germfree mice.

26 eriodic acid-Schiff (PAS)-stained intestinal goblet cells and less mucin (Muc2) in Nod1 and Nod2 doub

27 nists enhanced the production of PAS-stained goblet cells and Muc2 in germfree mice.

28 ultaneously increased numbers of PAS-stained goblet cells and Muc2-expressing cells, whereas treatmen

29 age differentiation into mature enterocytes, goblet cells and Paneth cells.

30 Mucus is thus secreted attached to the goblet cells and requires an enzyme, meprin beta in the

31 gy, including hyperplasia of mucus-secreting goblet cells and smooth muscle hypercontractility.

32 ase molecule that we find to be expressed by goblet cells and that inhibits bacterial growth.

33 ultrastructurally to detect the presence of goblet cells and to compare the findings with those in f

34 RgCBM40 binds to mucus produced by goblet cells and to purified mucins, providing direct ev

35 e into intestinal-like epithelium (including goblet cells) and thereby reproduce Barrett's metaplasia

36 culture characteristics such as ciliated and goblet cells, and ion channel function.

37 ges in expression of markers of enterocytes, goblet cells, and proliferative cells were detected.

38 ansforms cultured airway epithelial cells to goblet cells, and this is not inhibited by corticosteroi

39 Goblet cells are a specialized cell type of IEC that sec

40 Mucins secreted by intestinal goblet cells are considered an important component of in

41 Goblet cells are important secretory cell components of

42 Goblet cells are the principal cell type involved in exo

43 that contain abundant submucosal glands and goblet cells are uncertain.

44 FF) and mucins (Muc) - primarily produced by goblet cells - are thought to play a major role in provi

45 signaling to autophagy and highlighting the goblet cell as a critical innate immune player in the co

46 In contrast, MUC5AC emerged from goblet cells as wispy threads and sometimes formed mucin

47 s in stem, Paneth, enteroendocrine, tuft and goblet cells, as well as enterocytes.

48 was associated with the formation of colonic goblet cell-associated antigen passages (GAPs), which tr

49 33 stimulated apical CXCL8/IL-8 release from goblet cells, but not from normally differentiated cells

50 e and helminth infection, induces intestinal goblet cells, but the mechanism remains unclear.

51 Under physiologic conditions, conjunctival goblet cells (CGCs) secrete mucins into the tear film to

52 ein expression on the apical side surface of goblet cells compared with normally differentiated cells

53 The goblet cells constituted approximately 2% of the normal

54 ewer histological signs of damage and higher goblet cells count when compared with samples without LP

55 ime points regarding preservation injury and goblet cells count.

56 h RvE1 and RvD1 on LTB4-induced responses of goblet cells cultured from rat conjunctiva.

57 Geldanamycin did not induce goblet cell death, nor did it solely block mucin synthes

58 ogenesis and its role in the pathogenesis of goblet cell deficiency-associated keratoconjunctivitis s

59 Goblet Cell Density (GCD) was measured in 71 current or

60 The main outcomes were: goblet cell density (GCD), limbal dendritic cell density

61 g have significant negative correlation with goblet cell density (r = -0.174, P = 0.036) and tear MUC

62 icant positive correlation with conjunctival goblet cell density (r = 0.181, P = 0.03).

63 ion of BE to EAC was associated with reduced goblet cell density and increased levels of Notch expres

64 We measured goblet cell density and levels of Notch messenger RNAs i

65 ts; there was an inverse correlation between goblet cell density and levels of NOTCH3 and JAG2 messen

66 X3 preserved tear secretion and conjunctival goblet cell density and mitigated inflammation and scarr

67 In current smokers, Schirmer I test value, goblet cell density and tear MUC5AC concentration were s

68 that smoking might decrease tear secretion, goblet cell density and tear MUC5AC concentration.

69 ds and significantly increasing conjunctival goblet cell density compared with a standard diet.

70 s associated with a significant reduction in goblet cell density comparing nondysplastic regions of t

71 on, MUC5AC concentration in tears depends on goblet cell density in the conjunctiva among office work

72 Adjustment for goblet cell density revealed slightly less marked, yet s

73 enzyme-linked immunoassay, and conjunctival goblet cell density was counted after Periodic-acid Schi

74 Goblet cell density was significantly lower in ABX treat

75 to evaluate the correlations of conjunctival goblet cell density with tear MUC5AC concentration and o

76 er cigarette smoking affects tear secretion, goblet cell density, and tear MUC5AC concentration.

77 a number of outcomes such as tear clearance, goblet cells density and corneal epithelial integrity, s

78 Goblet cells develop in the outer layer while multicilia

79 ting the transcriptional program instructing goblet cell development.

80 4 or 5 (Klf4 or Klf5) which in turn controls goblet cell differentiation and activates mucin 5/ac syn

81 Runx2, a novel regulator for goblet cell differentiation and asthma development.

82 The effect of IL-33 on goblet cell differentiation and cytokine secretion has n

83 own regarding the transcriptional control of goblet cell differentiation and mucus hyperproduction.

84 the conducting airways, where they regulate goblet cell differentiation and mucus production.

85 SPDEF was required for goblet cell differentiation and pulmonary Th2 inflammati

86 Airway goblet cell differentiation and related mucus overproduc

87 ther, our results indicate that SPDEF causes goblet cell differentiation and Th2 inflammation during

88 cKO mice, suggesting that TGFbeta restricted goblet cell differentiation directly by repressing Spdef

89 h signaling has been known to associate with goblet cell differentiation in intestinal and respirator

90 e report that IL-33 does not directly induce goblet cell differentiation in murine enteroids; however

91 njunctiva; however, mechanisms that regulate goblet cell differentiation in the conjunctiva are not w

92 ignaling and increased the expression of the goblet cell differentiation marker mucin 2 (MUC2).

93 es demonstrate that IL-33 induces intestinal goblet cell differentiation not through direct action on

94 p-regulated by 6.4-fold during IL-13-induced goblet cell differentiation of human bronchial epithelia

95 Runx2 inhibited the house dust mite-induced goblet cell differentiation with a 75% reduction in mucu

96 To induce goblet cell differentiation, indole acts via the xenobio

97 Ets-like factor (SPDEF), a known factor for goblet cell differentiation, resulting in an activation

98 oliferation of epithelial cells and promotes goblet cell differentiation, reversing an effect of agin

99 way epithelial cells in neonatal mice caused goblet cell differentiation, spontaneous eosinophilic in

100 on factor 2 (Runx2) as a novel regulator for goblet cell differentiation.

101 l mechanistic role for TGFbeta in regulating goblet cell differentiation.

102 intestinal epithelial development to repress goblet cell differentiation.

103 et cells and gene expression consistent with goblet cell differentiation.

104 anism through which IL-33 affects intestinal goblet cell differentiation.

105 and enteroid gene expression consistent with goblet cell differentiation.

106 However, the effects of indoles on goblet cells do not depend on type I IFN or on IL-22 sig

107 Conjunctival goblet cell dysfunction and death are promoted by the T

108 Together, these findings indicate that goblet cell dysfunction is an epithelial-autonomous defe

109 These results inform on the mechanism of goblet cell dysfunction that underlies the pathology of

110 e including inflammatory gene expression and goblet cell dysfunction, which were associated with exce

111 mize their secretory functions, by employing goblet cell enrichment, air-lifting culture, and 3D sphe

112 TRMP5 abrogates the expansion of tuft cells, goblet cells, eosinophils, and type 2 innate lymphoid ce

113 such as aqueous tear secretion, conjunctival goblet cells, epithelial corneal integrity, and reduce t

114 Some CF goblet cells exhibited an ectopic granule location and d

115 facilitated by epithelial cell extrusion and goblet cell exocytosis; however, LAP-induced cell juncti

116 face epithelial hyperplasia and conjunctival goblet cell expansion that invaginates into the subconju

117 perly, but young mice displayed conjunctival goblet cell expansion, demonstrating that TGFbeta signal

118 We report that isolated colonic goblet cells express components of several inflammasomes

119 ing determines the choice between paneth and goblet cell fates and also affects stem cells, which exp

120 FOXA3 was highly expressed in airway goblet cells from patients with asthma and chronic obstr

121 Goblet cells from rat bulbar and forniceal conjunctiva w

122 We also observed a loss of goblet cells from the colon and Paneth cells from the sm

123 mice, which had normal survival, growth and goblet cell function as compared to wild-type (WT) mice.

124 orptive enterocytes and secretory Paneth and goblet cell function while negatively regulating chromog

125 l Tear Neurostimulator (ITN) on conjunctival goblet cell (GC) degranulation.

126 This study aimed at investigating whether goblet cell (GC) metaplasia and mucus production are dif

127 To compare goblet cell (GC) number and area in the covered superior

128 Goblet cells (GCs) are specialized secretory cells that

129 e secretory phospholipase A2 (sPLA2) and the goblet cell glycoprotein mucin2 (MUC2).

130 in WT goblet cells, mucin granules within CF goblet cells had an alkaline pH, which may adversely aff

131 from a CF mouse model, we determined that CF goblet cells have altered exocytotic dynamics, which inv

132 cells and improved exocytotic dynamics in CF goblet cells; however, there was still an apparent incoo

133 active smoking have all been associated with goblet cell hyperplasia (GCH) in small studies.

134 also induces an ILC2-driven, IL-13-dependent goblet cell hyperplasia and increased production of muci

135 6-deficient asthmatic mice exhibited reduced goblet cell hyperplasia and increased TGF-beta productio

136 and veins; lung remodeling (mucin-producing goblet cell hyperplasia and metaplasia and smooth muscle

137 ns modulate the lung immune response, induce goblet cell hyperplasia and metaplasia, and mucus hypers

138 ing anti-major basic protein immunostaining, goblet cell hyperplasia by using periodic acid-Schiff st

139 romoted eosinophilic airway inflammation and goblet cell hyperplasia driven by adoptively transferred

140 is known about the pathophysiology of CB and goblet cell hyperplasia in COPD, and treatment options a

141 eosinophilia, bronchial hyperreactivity, and goblet cell hyperplasia in the airways.

142 A caused AHR, eosinophilic inflammation, and goblet cell hyperplasia in wild-type (WT) mice.

143 osal type 2 responses to helminth infection; goblet cell hyperplasia is abrogated and worm expulsion

144 In vivo, IL-33-induced intestinal goblet cell hyperplasia is dependent on IL-13.

145 Histologically, the mean goblet cell hyperplasia score was reduced by a statistic

146 imulated with interleukin (IL)-13 to promote goblet cell hyperplasia showed increased OPN production

147 However, in ROCK2(+/-) mice, goblet cell hyperplasia was reduced in medium but not la

148 epithelial shedding, barrier integrity, and goblet cell hyperplasia were found in the large intestin

149 ing interleukins (IL) IL-4 and IL-13, induce goblet cell hyperplasia with mucus production, ultimatel

150 c airway disease, such as lung eosinophilia, goblet cell hyperplasia, Ag-specific Th2 responses, and

151 to alleviate allergen-induced Th2 cytokines, goblet cell hyperplasia, and airway inflammation.

152 reased lung inflammatory cells infiltration, goblet cell hyperplasia, and higher levels of Th2 and Th

153 llenge, including reductions in eosinophils, goblet cell hyperplasia, and IL-5 levels.

154 sulting in anti-Pneumocystis IgE production, goblet cell hyperplasia, and increased airway resistance

155 ecruited CD4+ T cells enhanced eosinophilia, goblet cell hyperplasia, and overall inflammation within

156 eated mice were protected from eosinophilia, goblet cell hyperplasia, and T(H)2 cell infiltration.

157 s show that SEA-induced airway inflammation, goblet cell hyperplasia, and Th2 cytokine production wer

158 ignificant reduction in airway inflammation, goblet cell hyperplasia, and Th2 cytokine production, in

159 Goblet cell hyperplasia, as indicated by PAS staining, w

160 and is characterized by epithelial shedding, goblet cell hyperplasia, basement membrane thickening, s

161 Furthermore, goblet cell hyperplasia, collagen deposition, and airway

162 to interleukin-13 (IL-13) reconstituted the goblet cell hyperplasia, cytokine hypersecretion and dec

163 as demonstrated by an influx of eosinophils, goblet cell hyperplasia, elevated serum Igs, and inducti

164 nt of eosinophils and basophils to the lung, goblet cell hyperplasia, expression of Muc5ac, Clca3, an

165 nd OVA-induced airway hyperresponsiveness or goblet cell hyperplasia, irrespective of the presence or

166 Moreover, histological staining exhibited goblet cell hyperplasia, lung inflammation, thickening o

167 okines (IL-4, IL-5, and IL-13) and decreased goblet cell hyperplasia.

168 in defective recruitment of eosinophils and goblet cell hyperplasia.

169 t not ROCK1 plays a role in allergen-induced goblet cell hyperplasia.

170 ncreased Th2 cytokine expression, and airway goblet cell hyperplasia.

171 novel mucous ciliated cell state, as well as goblet cell hyperplasia.

172 ition of HDM-induced airway inflammation and goblet cell hyperplasia.

173 S transcription factor, which contributes to goblet cell hyperplasia.

174 inophilia; smooth muscle cell, collagen, and goblet cell hyperplasia; hyper IgE syndrome; mucus plugg

175 ent on a protective mucus layer generated by goblet cells, impairment of which is a hallmark of the i

176 promoted differentiation of mucin-producing goblet cells in intestinal organoid cultures.

177 into the airway submucosa; proliferation of goblet cells in the airway epithelium; and the productio

178 tle is known about the exocytotic process of goblet cells in the CF intestine.

179 ly, RELMbeta, expressed predominantly in the goblet cells in the colon, is released both apically and

180 nges, resulting in a decreased proportion of goblet cells in the colon.

181 Allergan ITN can stimulate degranulation of goblet cells in the conjunctiva, which is a promising ne

182 ithelia resulted in the ectopic formation of goblet cells in the eyelid and peripheral cornea in adul

183 S, or GPR99 have reduced baseline numbers of goblet cells, indicating an additional function in regul

184 However, the regulatory pathways involved in goblet cell-induced mucus secretion remain largely unkno

185 Here, we show that mucus secretion by goblet cells is altered in the colon of TMF(-/-) mice, r

186 Regulation of the intestinal mucus layer by goblet cells is important for preventing inflammation an

187 itors to promote differentiation of tuft and goblet cells, leading to increased frequencies of both.

188 uman gene products in a human colonic cancer goblet cell line (HT29-18N2) revealed new proteins, incl

189 ation in vitro, generating both ciliated and goblet cell lineages.

190 Colitis and goblet cell loss were rescued in Il18bp(-/-);Il18r(Delta

191 y, luminal bleeding, loss of mucin-producing goblet cells, loss of defined crypt architecture and the

192 ocyte markers, but reduced expression of the goblet cell marker Mucin2 and fewer Paneth cells.

193 IL-18 inhibited goblet cell maturation by regulating the transcriptional

194 the relationship between Notch signaling and goblet cell maturation, a feature of BE, during EAC path

195 The presence of lacrimal gland goblet cells may have physiologic implications for the p

196 ion of a gut-resident pathogen by inhibiting goblet cell-mediated bacterial translocation.

197 Bronchial epithelial goblet cell metaplasia (GCM) with hyperplasia is a promi

198 Goblet cell metaplasia accompanies common pulmonary diso

199 d with persistent pulmonary inflammation and goblet cell metaplasia and contribute to significant mor

200 Foxa3 induced goblet cell metaplasia and enhanced expression of a netw

201 uscle, as well as a significant depletion of goblet cell metaplasia and mucus secretion markers after

202 ng postnatal development and is required for goblet cell metaplasia and normal Th2 inflammatory respo

203 transcription factor FOXA3 in regulation of goblet cell metaplasia and pulmonary innate immunity.

204 Mechanisms regulating both goblet cell metaplasia and susceptibility to viral infec

205 2xPten(+/-) mice also demonstrated increased goblet cell metaplasia compared with Pten(+/-) mice.

206 s, ROCK1 and ROCK2, to AHR, inflammation and goblet cell metaplasia in a mast cell-dependent model of

207 Jagged inhibition also reversed goblet cell metaplasia in a preclinical asthma model, pr

208 ed airway hyperreactivity, eosinophilia, and goblet cell metaplasia in allergen-sensitized mice.

209 sponsiveness, IL-4 and IL-13 production, and goblet cell metaplasia in an Aspergillus fumigatus-induc

210 minated foci of emphysema and large areas of goblet cell metaplasia in bronchial and bronchiolar epit

211 FOXA3 induces goblet cell metaplasia in response to infection or Th2 s

212 ging-associated increase in the incidence of goblet cell metaplasia in the prostate epithelium.

213 her HSP90 inhibitors prevented IL-13-induced goblet cell metaplasia in vitro and in vivo.

214 therapeutic option for airway diseases with goblet cell metaplasia of unknown mechanism.

215 Our findings suggest that persistent airway goblet cell metaplasia requires HSP90 activity and that

216 ge as well as airway hyperresponsiveness and goblet cell metaplasia were evaluated.

217 r inflammation, smooth muscle thickening and goblet cell metaplasia without changes in IgE and Th1, T

218 Goblet cell metaplasia, a disabling hallmark of chronic

219 geldanamycin would also revert IL-17-induced goblet cell metaplasia, a prediction confirmed by our ex

220 racterized by increased airway eosinophilia, goblet cell metaplasia, accumulation of ILC2s and TH2 ce

221 ma-like pathology characterized by increased goblet cell metaplasia, airway hyperresponsiveness, and

222 airway eosinophilia, type 2 cytokine levels, goblet cell metaplasia, and airway hyperresponsiveness.

223 gnificantly exacerbated airway inflammation, goblet cell metaplasia, and airway remodeling, but all o

224 way neutrophilia, elevated mucin expression, goblet cell metaplasia, and distal airspace enlargement,

225 f inflammatory cells, submucosal thickening, goblet cell metaplasia, and increased collagen content.

226 ay inflammation with increased eosinophilia, goblet cell metaplasia, and TH2 cytokine production in W

227 tivity and that HSP90 inhibitors will revert goblet cell metaplasia, despite active upstream inflamma

228 lium or myeloid inflammatory cells decreased goblet cell metaplasia, reduced lung inflammation, and d

229 concomitant epithelial mucus hypersecretion, goblet cell metaplasia, subepithelial fibrosis and enhan

230 o PVs correlated with the severity of airway goblet cell metaplasia, suggesting that PVs can influenc

231 To identify novel therapeutic targets for goblet cell metaplasia, we studied the transcriptional r

232 velopment of airway hyperresponsiveness, and goblet cell metaplasia, without any synergistic effects.

233 ssion pathways associated with IL-13-induced goblet cell metaplasia.

234 elopment and decreased along with increasing goblet cell metaplasia.

235 nce IL-13-driven effects on lung function or goblet cell metaplasia.

236 veness (AHR), eosinophilic inflammation, and goblet cell metaplasia.

237 ay inflammation in the asthmatic airway with goblet cell metaplasia.

238 hronic lung disorders accompanied by chronic goblet cell metaplasia.

239 osinophilia, OVA-specific IgE production and goblet cell metaplasia.

240 e DC compartment alleviates inflammation and goblet cell metaplasia.

241 hronic peribronchial airway inflammation and goblet cell metaplasia.

242 Geldanamycin also reverted established goblet cell metaplasia.

243 pression of Muc5ac and Gob5 mRNA, markers of goblet cell metaplasia/hyperplasia.

244 cian Blue, and GCD was measured as number of goblet cells/mm basement membrane.

245 tinal luminal spaces, and restored villi and goblet cell morphology.

246 including basal stem cells, mucus-secreting goblet cells, motile ciliated cells, cystic fibrosis tra

247 syndrome patients with dry eye and decreased goblet cell mucin expression.

248 distribution, is a critical orchestrator of goblet cell mucin granule exocytosis.

249 tions of LXA4 on cultured human conjunctival goblet cell mucin secretion and increase in intracellula

250 Compared with those within WT goblet cells, mucin granules within CF goblet cells had

251 d normal lacrimal glands for the presence of goblet cells (mucocytes).

252 n innate immune regulatory pathway governing goblet cell mucus secretion, linking nonhematopoietic in

253 injection causes Paneth loss and release of goblet cell mucus.

254 ing is thought to regulate IML formation via goblet cell Nlrp6 inflammasome activity that controls se

255 Moreover, goblet cell number was increased at E16.5.

256 Goblet cell numbers and resistin-like molecule beta (REL

257 HDM inhalation markedly increased airway goblet cell numbers and thickness of the epithelium and

258 of the proliferative zone and an increase in goblet cell numbers in the colon crypts of Zfp36(DeltaIE

259 exclusive to the respiratory epithelium and goblet cells of bronchial structures.

260 of C2GnT-M and KRT1 was also detected in the goblet cells of human colon epithelial tissue and primar

261 Mucus production by goblet cells of the large intestine serves as a crucial

262 Mucin 5AC (MUC5AC) is secreted by goblet cells of the respiratory tract and, surprisingly,

263 ence on the relative numbers of enterocytes, goblet cells or Paneth cells.

264 No goblet cells or subepithelial inflammation were present.

265 d IL-33-stimulated CXCL8/IL-8 secretion from goblet cells (P < 0.001).

266 -33-induced apical CXCL8/IL-8 secretion from goblet cells (P < 0.02).

267 IL-33 increased ERK 1/2 phosphorylation in goblet cells (P < 0.05), and PD98059, a MAPK/ERK kinase

268 tion (ss-tubulin IV+ ciliated cells, MUC5AC+ goblet cells, p63 + basal cells).

269 iated intestinal cell lineages (enterocytes, goblet cells, Paneth cells, tuft cells and enteroendocri

270 we identify CD69(+)CD274(+) cells as related goblet cell precursors.

271 ine submucosal glands produce MUC5B, whereas goblet cells produce predominantly MUC5AC plus some MUC5

272 roportion of intraepithelial lymphocytes and goblet cells reduced, and the enteroendocrine cells incr

273 nd inflammasome signaling mediates efficient goblet cell release of mucus containing granules.

274 cretory cell lineages, we show that although goblet cells resist E11 infection, enteroendocrine cells

275 We conclude that conjunctival goblet cells respond to LXA4 through the ALX/FPR2 recept

276 l information on the role of Nod proteins in goblet cell response and Muc2 production in relation to

277 of Nod proteins in regulation of intestinal goblet cell response in naive mice and mice infected wit

278 intestinal stem cells as well as Paneth and Goblet cells, resulting in enlarged intestinal crypts.

279 Goblet cells secrete CXCL8/IL-8, and this is increased b

280 eness of the ITN application on conjunctival goblet cell secretory response.

281 contributes to ileal villus maintenance and goblet cell size.

282 infects actively secreting small intestinal goblet cells, specialized epithelial cells that maintain

283 gh the expressions of enterocyte-, tuft- and goblet-cell specific markers are largely not affected.

284 Conjunctival goblet cells synthesize and secrete mucins which play an

285 IBD, we observe a positional remodelling of goblet cells that coincides with downregulation of WFDC2

286 the lacrimal gland is the presence of acinar goblet cells that had been long overlooked; they are inc

287 NLRP6 is highly expressed by epithelial and goblet cells to regulate epithelial renewal and mucus pr

288 ed pseudostratified columnar epithelium with goblet cells, trans-epithelial electrical resistance (TE

289 aried from 0.669 for signet cell to 0.75 for goblet cell tumors.

290 tanding the mechanisms of MUC2 production by goblet cells upon amebic infection, regulation of antimi

291 ce to suggest that ciliated cells can become goblet cells using immunoelectron microscopy.

292 secretion into the apical (air) side of the goblet cells was greater than from normally differentiat

293 Goblet cells were cultured from rat conjunctiva.

294 Enterocytes were lost, and goblet cells were increased.

295 etaplasia (IM) is defined by the presence of goblet cells whereas nongoblet cell metaplasia (NGM) lac

296 verproduction and hypersecretion of mucus by goblet cells, which leads to worsening airflow obstructi

297 O) by intestinal epithelial cells, including goblet cells, which secrete the enzyme into the lumen.

298 ced MAPK signaling and led to a reduction of goblet cells while promoting paneth cell development.

299 adients of progenitor cells, colonocytes and goblet cells within intestinal crypts.

300 naling is required for normal restriction of goblet cells within the conjunctiva.