ライフサイエンスコーパス: goblet cell

1 d in the regulated secretory granulae of the goblet cell.

2 evere colitis associated with loss of mature goblet cells.

3 nule decondensation and exocytosis in the CF goblet cells.

4 which accumulates in colonic enterocytes and goblet cells.

5 exhibit morphological defects in Paneth and goblet cells.

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

7 ontrol mucin granule accumulation in colonic goblet cells.

8 hibitor tunicamycin in cultured human LS174T goblet cells.

9 tear production and had normal conjunctival goblet cells.

10 se showed sparse and scattered TFF2 positive goblet cells.

11 were present in rat conjunctiva and cultured goblet cells.

12 lls and occasional nonciliated cells but not goblet cells.

13 helial cells, including enterochromaffin and goblet cells.

14 ealed the cellular source of this Ang4 to be goblet cells.

15 ocytotic core has not been defined in airway goblet cells.

16 t cell cultures prevented differentiation of goblet cells.

17 cells and harbored structures presumed to be goblet cells.

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

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

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

21 features of allergic asthma, including IgE, goblet cells, airway hyperreactivity (AHR), inflammatory

22 ficant downregulation of a similar subset of goblet cell and colonocyte genes, and GATA6 was found to

23 he colon following T. muris infection is the goblet cell and expression is under the control of IL-13

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

25 6 deficiency leads to defective autophagy in goblet cells and abrogated mucus secretion into the larg

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

27 ER stress by maintaining mucin production in goblet cells and helps the intestine preserve the mucus

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

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

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

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

32 Microscopically, in all dacryops specimens goblet cells and luminal pseudoapocrine apical cytoplasm

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

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

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

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

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

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

39 both rapamycin and dexamethasone suppressed goblet cells and total CD4(+) T cells including activate

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

41 microscopy indicated deficient maturation of goblet cells, and coimmunofluorescence demonstrated alte

42 neutrophil infiltration, loss of mucin from goblet cells, and increase in mast cell numbers.

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

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

45 Because goblet cells are characteristic for the midintestine in

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

47 Goblet cells are important secretory cell components of

48 Goblet cells are the principal cell type involved in exo

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

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

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

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

53 noglobulin A responses, antigen delivered by goblet cell-associated antigen passages contributes to p

54 Similarly, goblet cell-associated RELM-beta in lung and intestinal

55 33 stimulated apical CXCL8/IL-8 release from goblet cells, but not from normally differentiated cells

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

57 One of these, the goblet cells, contained a distinct cKit/CD117(+) crypt b

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

59 on of 5-HT(4)Rs evoked mucosal 5-HT release, goblet cell degranulation, and Cl(-) secretion.

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

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

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

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

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

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

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

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

68 Goblet cell density was significantly lower in ABX treat

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

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

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

72 Goblet cells develop in the outer layer while multicilia

73 Bile acids might initiate goblet cell development.

74 ting the transcriptional program instructing goblet cell development.

75 4 or 5 (Klf4 or Klf5) which in turn controls goblet cell differentiation and activates mucin 5/ac syn

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

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

78 rate that Spdef is required for conjunctival goblet cell differentiation and down-regulation of SPDEF

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

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

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

82 Airway goblet cell differentiation and related mucus overproduc

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

84 ined that Spdef is required for conjunctival goblet cell differentiation and that Spdef(-/-) mice, wh

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

86 pithelia resulted in complete suppression of goblet cell differentiation during and subsequent to dev

87 al role in the initiation and maintenance of goblet cell differentiation for normal ocular surface mo

88 Factors regulating goblet cell differentiation in conjunctival epithelium a

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

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

91 ranscription factor (Spdef) is essential for goblet cell differentiation in tracheobronchial and gast

92 ment with PMA/Io increased expression of the goblet cell differentiation marker MUC2; these changes w

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

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 TLR4 prevents goblet cell differentiation, independently of the microb

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

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

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

100 intestinal epithelial development to repress goblet cell differentiation.

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

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

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

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

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

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

107 inophil ratio in BALF was 3%, hyperplasia of goblet cell, eosinophilic invasion to bronchial epitheli

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

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

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

111 e (5-HT) and prostaglandin E2 (PGE2) induced goblet cell exocytosis followed by normal mucin discharg

112 ecretion also demonstrated apparently normal goblet cell exocytosis, but in contrast, this was not fo

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

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

115 eptor alpha deficient mice demonstrated that goblet cell expression of Ang4 is controlled either dire

116 ression of Agr2 is sufficient to promote the goblet cell fate in the developing airway epithelium.

117 pithelium leads to ectopic activation of the goblet cell fate program, in part, through de-repression

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

119 Ngn3(+) cells, Notch favored enterocyte and goblet cell fates, while selecting against endocrine and

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

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

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

126 Goblet cells (GCs) are specialized secretory cells that

127 ow that in the steady state, small intestine goblet cells (GCs) function as passages delivering low m

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

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

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

131 hat Spdef(-/-) mice, which lack conjunctival goblet cells, have significantly increased corneal surfa

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

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

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

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

136 rent understanding of the pathophysiology of goblet cell hyperplasia in COPD, and current therapies f

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

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

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

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

141 erbated AHR and airway inflammation, whereas goblet cell hyperplasia was not modified.

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

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

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

145 hanges consistent with asthma (eosinophilia, goblet cell hyperplasia), but with the unexpected findin

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

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

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

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

150 -associated effects (pulmonary eosinophilia, goblet cell hyperplasia, and increased IL-4 and IL-5), y

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

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

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

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

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

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

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

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

159 T1/ST2 deficiency also diminished goblet cell hyperplasia, mucus hypersecretion, bronchoal

160 phenotypes, including basal cell (BC) and/or goblet cell hyperplasia, squamous metaplasia, structural

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

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

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

164 minal mucus plugging or airways inflammation/goblet cell hyperplasia.

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

166 in defective recruitment of eosinophils and goblet cell hyperplasia.

167 elial cells, occasional syncytium formation, goblet cell hyperplasia/metaplasia, and mucus hypersecre

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

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

170 2 and 3 showed that TFF1 and 3 localized to goblet cells in both normal colon tissue and in tissue f

171 TLR4 also regulates differentiation of goblet cells in intestinal organoid and enterocyte cell

172 No staining for TFF2 was seen in goblet cells in normal colon tissue whereas the majority

173 contrast, conventional IC staining detected goblet cells in only 17 of 47 (36.2%) samples; these wer

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

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

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

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

178 The presence of goblet cells in the cornea was determined by PAS-hematox

179 Goblet cells in the corneal epithelium were detected by

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

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

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

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

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

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

186 and regeneration by directly restricting the goblet cell lineage program.

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

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

189 he extent of colonic epithelial hyperplasia, goblet cell loss, diarrhea, and pathogen colonization.

190 SPDEF may play a role in human dry eye with goblet cell loss.

191 bers of cells that expressed both Paneth and goblet cell markers.

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

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

194 Goblet cell metaplasia accompanies common pulmonary diso

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

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

197 ed in accumulation of inflammatory cells and goblet cell metaplasia and increased levels of Pim1 kina

198 FOXM1 induced goblet cell metaplasia and Muc5AC expression through the

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

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

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

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

203 2xPten(+/-) mice also demonstrated increased goblet cell metaplasia compared with Pten(+/-) mice.

204 nflammation, airway hyperresponsiveness, and goblet cell metaplasia in 2 asthma models.

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

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

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

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

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

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

211 us insults induce airway mucus secretion and goblet cell metaplasia to preserve airway sterility and

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

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

214 ed sustained lung neutrophilic inflammation, goblet cell metaplasia, airway hyperresponsiveness, and

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

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

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

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

219 challenge, peribronchovascular inflammation, goblet cell metaplasia, and fibrotic remodeling of the a

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

221 y response is characterized by eosinophilia, goblet cell metaplasia, and T helper T(H)2 cytokine prod

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

223 ion in the bronchioles, causing squamous and goblet cell metaplasia, and the loss of Clara and ciliat

224 However, goblet cell metaplasia, mucus hypersecretion, and airway

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

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

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

228 , lung inflammation, airway hyperreactivity, goblet cell metaplasia, Th2/Th17 cytokines, dendritic ce

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

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

231 hronic lung disorders accompanied by chronic goblet cell metaplasia.

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

233 elopment and decreased along with increasing goblet cell metaplasia.

234 l for allergen-induced lung inflammation and goblet cell metaplasia.

235 cell infiltration, collagen deposition, and goblet cell metaplasia.

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

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

238 tein response (UPR), substantially restoring goblet cell Muc2 production.

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

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

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

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

243 d activates ERK1/2 to stimulate conjunctival goblet cell mucous secretion, and that activation of all

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

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

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

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

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

249 Goblet cell numbers decrease within the conjunctival epi

250 Mucin expression and goblet cell numbers were similar in the two eosinophil g

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

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

253 ns, predominantly mucin (Muc) 2, secreted by goblet cells of the intestine.

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

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

256 accumulation of misfolded Muc2 in the ER of goblet cells of Winnie mice and increased T-cell product

257 No goblet cells or subepithelial inflammation were present.

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

259 -33-induced apical CXCL8/IL-8 secretion from goblet cells (P < 0.02).

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

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

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

263 mucosa lining, expansion of mucin-secreting goblet cell populations and raised levels of vascular en

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

265 Conjunctival goblet cells primarily synthesize mucins to lubricate th

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

267 by OVA+SEB, such as bronchial eosinophilia, goblet cell proliferation, production of OVA-specific Ig

268 We found that in colonic goblet cells, proteins involved in initiation and elonga

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

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

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

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

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

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

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

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

277 In the intestine, goblet cells secrete mucus that is required for homeosta

278 Goblet cell secretion of high molecular weight glycoconj

279 Histamine-stimulated conjunctival goblet cell secretion of high molecular weight glycoprot

280 used by histamine to stimulate conjunctival goblet cell secretion.

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

282 contributes to ileal villus maintenance and goblet cell size.

283 Spdef(-/-) mice revealed down-regulation of goblet cell-specific genes (Muc5ac, Tff1, Gcnt3).

284 Conjunctival goblet cells synthesize and secrete mucins which play an

285 estinal Paneth cells and a subset of colonic goblet cells that are regulated by Notch signaling and s

286 th an enzyme-linked lectin assay on cultured goblet cells that were serum-starved for 2 hours before

287 After release from goblet cells, the unfolded full-length MUC2 formed strat

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

289 In conclusion, in cultured rat conjunctival goblet cells, VPAC1 and 2 receptors are functional.

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

291 ed from NEC; epithelial differentiation into goblet cells was increased via suppressed Notch signalin

292 Enterocytes were lost, and goblet cells were increased.

293 In the colon, cKit(+) goblet cells were interdigitated with Lgr5(+) stem cells

294 lar microbial profiles; increased numbers of goblet cells were observed in mice given antibiotics.

295 mples from patients with NEC, and numbers of goblet cells were reduced.

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

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

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

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

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