ライフサイエンスコーパス: acinar

3 histological features of well-differentiated acinar adenocarcinoma, with strong androgen receptor (AR

4 geneity (Sacin) is thought to be a marker of acinar airway involvement but has not been validated by

5 (CT) densitometry to determine the nature of acinar airway involvement in asthmatic patients.

6 decrease likely caused by relief of an intra-acinar airway obstruction that we propose reflects ampli

7 terations in long-range diffusion within the acinar airways and gas trapping.

8 also led to reduced viability of pancreatic acinar and beta cells.

9 y repeated caerulein injections and isolated acinar and bone marrow cells for ex vivo studies.

10 t, mathematical modeling has been limited to acinar and branching morphogenesis and breast cancer, wi

11 ressed by progenitors that give rise to both acinar and duct cells, genetic ablation of SOX2 results

12 EpiSCs were capable to differentiate into SG acinar and duct cells.

13 M-30-positive (apoptotic) acinar and ductal cell number did not change after SAL o

14 Functions of pancreatic acinar and ductal cells as well as inflammatory cells we

15 the comparative ability of adult pancreatic acinar and ductal cells to respond to oncogenic Kras and

16 MSCs was not required for mSMG cells to form acinar and ductal structures.

17 ling promotes progenitor survival as well as acinar and endocrine specification.

18 In summary, CTSD is expressed in pancreatic acinar and inflammatory cells, undergoes subcellular red

19 -1 had no deleterious effect on functions of acinar and inflammatory cells.

20 nhydrase II(-) (mature ductal), elastase 3a (acinar)(-) , and insulin(-) subpopulations.

21 ct tumor phenotypes in vivo, including solid acinar, and solid nodular malignancies as well as cystic

22 Histologically, MG acinar atrophy was observed with ductal enlargement and

23 ds, blocked progression to CP and pancreatic acinar atrophy.

24 c genes and is essential for the survival of acinar but not ductal cells.

25 tenin is required qualitatively for exocrine acinar but not endocrine development, precisely how this

26 Its deletion or inhibition regulates acinar cell apoptosis but not necrosis in two models of

27 Pancreatic acinar cell carcinoma (ACC) is an aggressive exocrine tu

28 developed various subtypes of PC, including acinar cell carcinoma, ductal adenocarcinoma, sarcomatoi

29 ng proximity of PTF1 and MIST1 in pancreatic acinar cell chromatin implies extensive collaboration, a

30 a was also suppressed in ex vivo cultures of acinar cell clusters isolated from mouse pancreas bearin

31 and thus transforms our understanding of the acinar cell compartment as a pool of equipotent secretor

32 Acinar cell damage and dysfunction cause malnutrition an

33 risk factors, such as chronic pancreatitis, acinar cell damage, and/or defective autophagy increase

34 1, die perinatally due to massive pancreatic acinar cell death, precluding investigation of the effec

35 so activates ER stress pathways that promote acinar cell death.

36 of CTSB affected apoptotic but not necrotic acinar cell death.

37 ownstream of trypsin activation that lead to acinar cell death.

38 is associated with chronic pancreatitis and acinar cell dedifferentiation.

39 Immunohistochemical stains demonstrate an acinar cell defect but normal islet cells.

40 Atg7(Deltapan) mice exhibit severe acinar cell degeneration, leading to pancreatic inflamma

41 Loss of acinar cell differentiation also drives pancreatic cance

42 ression of transcription factors that affect acinar cell differentiation suggested that acinar cells

43 tis, with pathways involved in inflammation, acinar cell differentiation, and cell junctions being sp

44 ption of acinar morphogenesis and incomplete acinar cell differentiation.

45 -regulation of genes that promote the mature acinar cell fate is required to reduce injury associated

46 x of pancreatic acinar cells and critical to acinar cell fate specification and differentiation.

47 lular and molecular mechanisms that maintain acinar cell function and whose dysregulation can lead to

48 pression of proteins critically relevant for acinar cell function.

49 orm crucial functions in food digestion, and acinar cell homeostasis required for secretion of digest

50 The loss of acinar cell homeostasis, differentiation, and identity i

51 works that control pancreatic MPC expansion, acinar cell identity, duct morphogenesis and generation

52 tify a critical role for PDX1 in maintaining acinar cell identity, thus resisting the formation of pa

53 pecialized phenotype of the adult pancreatic acinar cell in vivo Transcriptome sequencing and chromat

54 ce that insulin directly protects pancreatic acinar cell injury induced by bona fide pancreatitis-ind

55 eatitis (AP) suggest a strong association of acinar cell injury with cathepsin B-dependent intracellu

56 FK506 prevented activation of NF-kappaB and acinar cell injury.

57 In conclusion, Hes1 plays a key role in acinar cell integrity and plasticity on cellular insults

58 ses in mouse and human primary acini and the acinar cell line AR42J.

59 Thus, SOX2 is a master regulator of the acinar cell lineage essential to the establishment of a

60 1R signaling in mice reflects an increase in acinar cell mass, without changes in ductal compartments

61 ng with exocrine defects, including impaired acinar cell maturation, the mutant mice exhibited substa

62 addition, Slug attenuated TGF-alpha-induced acinar cell metaplasia to ductal structures and TGF-alph

63 At study end, Ki-67-positive (proliferating) acinar cell number did not change, compared with baselin

64 nnabinoid receptor subtype 2 (CB2R) prevents acinar cell pathogenesis in animal models of acute pancr

65 ying this Ca(2+)-dependent generation of the acinar cell phenotype.

66 f the pancreas and in the maintenance of the acinar cell phenotype.

67 s model, we studied the role of Hes1 in both acinar cell plasticity and pancreatic regeneration after

68 ATA6 and promoting differentiation toward an acinar cell program.

69 Furthermore, oncogenic KRAS did not induce acinar cell proliferation, but did sustain the prolifera

70 delayed recovery of the pancreas and reduced acinar cell proliferation.

71 ppear to be excellent lectins for pancreatic acinar cell purification.

72 We investigated acinar cell replacement during homeostasis, growth, and

73 ing, followed by a chase period, showed that acinar cell replacement is not driven by the differentia

74 oses to PDAC because it induces a process of acinar cell reprogramming known as acinar-to-ductal meta

75 Acinar cell responses to the muscarinic agonist carbacho

76 Perturbation of pancreatic acinar cell state can lead to acinar-to-ductal metaplasi

77 identified the presence of a progenitor-like acinar cell subpopulation.

78 ical role for ATF3 as a key regulator of the acinar cell transcriptional response during injury and m

79 However, in the acinar cell, Munc18c's functions in exocytosis and homeo

80 is only minimal and transient in the early, acinar cell-dependent phase of pancreatitis and much gre

81 Mice with acinar cell-specific expression of Kras(G12D) were cross

82 )) via Cre(ERTM) recombinase regulated by an acinar cell-specific promoter (Ptf1a).

83 ed mice with tamoxifen-inducible, pancreatic acinar cell-specific Sec23b deletion.

84 erentiated phenotype of the adult pancreatic acinar cell.

85 , necrosis, acinar-to-ductal metaplasia, and acinar-cell hypertrophy; this led to tissue atrophy and

86 n PSCs and their better studied neighbouring acinar cells (PACs) and found complete separation of Ca(

87 tested in freshly isolated murine pancreatic acinar cells (PACs) to determine inhibition of toxin-ind

88 mbination strategy in adult mouse pancreatic acinar cells (Yap1fl/fl;Tazfl/fl;Ela1-CreERT2).

89 llular Ca(2+) signals may protect pancreatic acinar cells against Ca(2+) overload, intracellular prot

90 ymogen-containing subcellular compartment of acinar cells and activation of CTSD, CTSB, and trypsinog

91 x transcription factor complex of pancreatic acinar cells and critical to acinar cell fate specificat

92 nisms involved in regulating the function of acinar cells and in the loss of salivary gland function

93 , leading to activation of EGFR signaling in acinar cells and increased ADM.

94 Moreover, Arg-II is mainly expressed in acinar cells and is upregulated with aging, which enhanc

95 scribed in considerable detail in pancreatic acinar cells and oocytes.

96 re to cigarette smoke increased ER stress in acinar cells and sensitized the pancreas to LPS-induced

97 ) that induce saliva secretion from residual acinar cells and the use of saliva substitutes.

98 sed to reflect the proliferative activity of acinar cells and their role in salivary gland homeostasi

99 As a result, Ptf1a-deficient acinar cells are dramatically sensitized to KRAS transfo

100 Despite this requirement, how acinar cells are generated during organogenesis is uncle

101 tion, a loss and abnormal differentiation of acinar cells are observed.

102 Pancreatic acinar cells are reprogrammed to a "ductal-like" state d

103 We further demonstrate that binuclear acinar cells are terminally differentiated acinar cells.

104 ) that induce saliva secretion from residual acinar cells as well as artificial salivary substitutes.

105 This involves not only signalling in acinar cells but also in stellate cells.

106 ally give rise to all endocrine, ductal, and acinar cells but become bipotent by embryonic day 13.5,

107 signals and necrosis in isolated pancreatic acinar cells but the effects of bile acids on stellate c

108 Nicotine induced dedifferentiation of acinar cells by activating AKT-ERK-MYC signaling; this l

109 features of pancreatitis in EtOH-sensitized acinar cells by suppressing the adaptive unfolded protei

110 r TP53(f/f) specifically in adult pancreatic acinar cells by using a full-length pancreatic elastase

111 cells in the pancreas, yet the source of new acinar cells during homeostasis remains unknown.

112 Zymogen secretory granules in pancreatic acinar cells express two vesicle-associated membrane pro

113 EM16A is a significant pathway in pancreatic acinar cells for HCO3 (-) secretion into the lumen.

114 ce KLF5 activity might reduce progression of acinar cells from ADM to PanIN and pancreatic tumorigene

115 Accordingly, conditioned medium of isolated acinar cells from old WT (not Arg-II(-/-)) mice contains

116 I) lectin has been used to label and isolate acinar cells from the pancreas.

117 generation and maintenance of exocrine gland acinar cells have not yet been established.

118 s required for normal function of pancreatic acinar cells in adult mice.

119 lonal expansion of terminally differentiated acinar cells in all major salivary glands.

120 ovel strategy for generating and maintaining acinar cells in culture.

121 s in stellate cells compared to the adjacent acinar cells in pancreatic lobules; whereas taurolithoch

122 genesis, and a lack of differentiated mucous acinar cells in submandibular and sublingual glands.

123 at Lfng is uniquely expressed in a subset of acinar cells in the adult pancreas.

124 gglutinin (PNA) have a specific affinity for acinar cells in the mouse pancreas, with minimal affinit

125 Maintaining the identity of acinar cells in the pancreas could help to prevent the d

126 activation of KRAS in normal, untransformed acinar cells in the pancreatic tissues of mice resulted

127 Addition of NETs and histones to acinar cells induced formation of trypsin and activation

128 cked the irreversible transition of exocrine acinar cells into pancreatic preneoplastic ductal lesion

129 substrate p62/SQSTM1 in stressed Kras(G12D) acinar cells is associated with PDAC development and mai

130 e intracellular Ca(2+) signals in pancreatic acinar cells is largely unknown.

131 ne were also evaluated in primary pancreatic acinar cells isolated from wild-type, nAChR7a(-/-), Trp5

132 t acinar cell differentiation suggested that acinar cells lacking ATF3 maintain a mature cell phenoty

133 Acinar cells make up the majority of all cells in the pa

134 The proliferative capacity of differentiated acinar cells may prove critical in the implementation of

135 tion of Sec23b exclusively in the pancreatic acinar cells of adult mice results in decreased overall

136 in the developing ductal, serous, and mucous acinar cells of salivary glands.

137 secretion of bicarbonate-rich fluid from the acinar cells of the pancreas that accumulates within the

138 directly via G protein-coupled receptors on acinar cells or through inflammatory cells.

139 Epithelial pancreatic acinar cells perform crucial functions in food digestion

140 Acinar cells play an essential role in the secretory fun

141 Pancreatic acinar cells possess very high protein synthetic rates a

142 Acinar cells prepared from the pancreas of rats or mice

143 approaches with acute dissociated pancreatic acinar cells prepared from wild type, CB1R-knockout (KO)

144 xpression, and ectopic expression of KLF4 in acinar cells reduces acinar lineage- and induces ductal

145 Kras activation in Mist1(+) adult acinar cells resulted in brisk PanIN formation, whereas

146 Transcriptome analysis of single acinar cells revealed the existence of a minor populatio

147 not been studied in CP, although pancreatic acinar cells seem to be especially vulnerable to ER dysf

148 dies of this disorder focus on the damage to acinar cells since they are assumed to be the primary ta

149 in rats and in vitro in rat pancreatic AR42J acinar cells stimulated with taurocholate or TNF-alpha.

150 educed caspase-3 activation and apoptosis in acinar cells stimulated with the intestinal hormone chol

151 more extensive necrosis in both stellate and acinar cells than TLC-S alone.

152 pathway; this could be a mechanism by which acinar cells that express activated KRAS become suscepti

153 operties of the ion-transporting pathways in acinar cells that might account for the differences amon

154 The transdifferentiation of pancreatic acinar cells to a ductal phenotype (acinar-to-ductal met

155 ous work demonstrating in vivo conversion of acinar cells to beta-like cells by viral delivery of exo

156 the conversion of terminally differentiated acinar cells to beta-like cells.

157 trast, TGF-beta1 efficiently converted human acinar cells to duct-like cells (AD) in a SMAD-dependent

158 tor Snail (Snai1) can cooperate with Kras in acinar cells to enhance ADM development, the contributio

159 ound shifts in PDX1 chromatin occupancy from acinar cells to PDA.

160 ts that prevent conversion of differentiated acinar cells to proliferative ductal progenitors.

161 lls connect liver hepatocytes and pancreatic acinar cells to the intestine, but the mechanism for the

162 We exposed mouse and human acinar cells to the radiocontrast agent iohexol (Omnipaq

163 in vivo conversion of adult mouse pancreatic acinar cells toward beta cells, we show that induced bet

164 Notably, these effects were recapitulated in acinar cells treated with a pharmacological inhibitor of

165 hat GRP78 could exert a protective effect on acinar cells under stress, as during PDAC development.

166 st-induced Ca(2+) oscillations in pancreatic acinar cells using multiple experimental approaches with

167 transgenic mice expressing Slug and Kras in acinar cells were generated.

168 Moreover, PNA-purified acinar cells were less contaminated with mesenchymal and

169 lasia (ADM), a process that replaces damaged acinar cells with duct-like structures.

170 ncubation of AR42J or primary mouse or human acinar cells with MKC-3946 reduced expression of XBP1s,

171 Better methods for purifying human or mouse acinar cells without the need for genetic modification a

172 y reduced CTSB and trypsinogen activation in acinar cells, and CTSD directly activated CTSB but not t

173 tabolism were measured in pancreatic tissue, acinar cells, and isolated mitochondria.

174 zymes, packaged into the zymogen granules of acinar cells, become activated and cause autodigestion.

175 IER3 expression was discrete in healthy acinar cells, becoming highly prominent in peritumoral a

176 Incubation of mouse and human acinar cells, but not HEK293 or COS7 cells, with iohexol

177 bone marrow chimeras, expression of BCL3 by acinar cells, but not myeloid cells, was required for re

178 ature activation of digestive enzymes within acinar cells, followed by necrosis and inflammation.

179 C-S), known to induce Ca(2+) oscillations in acinar cells, had only minor effects on stellate cells i

180 on, driven by cell-cell interactions between acinar cells, leukocytes, and resident fibroblasts.

181 In acinar cells, our study demonstrates an age-associated A

182 s based predominantly on self-duplication of acinar cells, rather than on differentiation of stem cel

183 salivary glands is due to the impairment of acinar cells, the major glandular cells of protein, salt

184 in the ductal cell layer and/or in surviving acinar cells, to drive transcellular flux of interstitia

185 Since CEL is expressed mainly in pancreatic acinar cells, we asked whether we could find structural

186 ing 3D explant culture of primary pancreatic acinar cells, we show that PKD1 acts downstream of TGFal

187 ajor apical Cl(-) efflux pathway in salivary acinar cells, were significantly greater in PG compared

188 ment of Ca(2+) signaling in mouse pancreatic acinar cells, which suggests a potential cellular mechan

189 ocess involves activation of YAP1 and TAZ in acinar cells, which up-regulate JAK-STAT3 signaling to p

190 r acinar cells are terminally differentiated acinar cells.

191 pathological Ca(2+) signals and necrosis in acinar cells.

192 cholate-induced necrosis in mouse pancreatic acinar cells.

193 elicited simultaneously in the neighbouring acinar cells.

194 2R protein was expressed in mouse pancreatic acinar cells.

195 flammatory cells, compared to UEA-I purified acinar cells.

196 lithocholic acid 3-sulfate primarily affects acinar cells.

197 ed the regenerative potential of pre-labeled acinar cells.

198 trypsin activation were analyzed in isolated acinar cells.

199 SI rapidly accumulates in lumen formed by LG acinar cells.

200 a (PanIN), arise via reprogramming of mature acinar cells.

201 than 2-fold larger in PG and SMG than in SLG acinar cells.

202 16A or TMEM16B as well as from mouse parotid acinar cells.

203 imary basolateral Cl(-) uptake mechanisms in acinar cells.

204 a regeneration of digestive enzyme-producing acinar cells.

205 secretion from primary rabbit lacrimal gland acinar cells.

206 old number of Neurogenin 3 (Ngn3)-expressing acinar cells.

207 a conditional knockout of Atg5, in salivary acinar cells.

208 L, for different downstream responses of the acinar cells.

209 model that involves apoptosis of the central acinar cells.

210 ccelerates disorders of the ER in pancreatic acinar cells.

211 CCK cellular actions directly affected human acinar cells.

212 xygen species generation in mouse pancreatic acinar cells.

213 ges of the developing mouse pancreas: islet, acinar, centroacinar, and ductal.

214 h), indicating an important effect of extra-acinar CTSD on course of the disease.

215 tigates third-phase secretory inhibition and acinar damage caused by the accumulation of prematurely

216 from intracellular trypsin accumulation and acinar damage.

217 ed by persistent inflammation, fibrosis, and acinar dedifferentiation.

218 The acinar defects are due to a combination of fewer MPCs, d

219 of both indexes, consistent with inadequate acinar delivery.

220 Also at the PanIN2 stage, pancreas acinar-derived cells frequently invade along sensory neu

221 oss of GATA6 protein, and subsequent loss of acinar differentiation and hyperactivation of oncogenic

222 lico simulations predict a transient wave of acinar differentiation around E11.5, while endocrine dif

223 perturbed on the deletion of Hes1, terminal acinar differentiation in the adult pancreas is compromi

224 Expression and localization of the acinar differentiation marker MIST1 were altered in Irf6

225 re hypothesized that the master regulator of acinar differentiation, PTF1A, could play a central role

226 e model generates 3D images of the resulting acinar distribution and calculates two global indexes, e

227 peritumoral acini, and particularly high in acinar ductal metaplasia (ADM) and PanIN lesions, where

228 ed, giving rise to three important lineages: acinar, ductal and endocrine.

229 l states to become terminally differentiated acinar, ductal and myoepithelial cells.

230 population that will differentiate into the acinar, ductal or endocrine lineages.

231 Cells in the pancreas that have undergone acinar-ductal metaplasia (ADM) can transform into premal

232 reatic epithelial cells, and augmentation of acinar-ductal metaplasia.

233 In this study, we have explored intra-acinar events downstream of trypsin activation that lead

234 uced expression of ductal markers in ex vivo acinar explant cultures.

235 s, deficient allocation of those MPCs to pre-acinar fate, disruption of acinar morphogenesis and inco

236 e transcription of over a hundred downstream acinar genes.

237 was to describe recruitment/derecruitment at acinar length scales over short-time frames and test the

238 stablished to isolate and support culture of acinar-like cells from the human salivary gland.

239 , these phmSG cells were further promoted to acinar-like cells in vitro, as indicated by an increase

240 ed switch of salivary epithelial cells to an acinar-like phenotype involves remodeling of SOCE and NF

241 ed from salivary gland biopsies, acquired an acinar-like phenotype when the [Ca(2+)] in the serum-fre

242 ns to achieve the maintenance of phmSG in an acinar-like phenotype.

243 Development towards the acinar lineage is paralleled by an increase in GP2 expre

244 and parasympathetic nerves in generating the acinar lineage that has broad implications for epithelia

245 c expression of KLF4 in acinar cells reduces acinar lineage- and induces ductal lineage-related marke

246 H activity can commit to either endocrine or acinar lineages, and can be divided into four sub-popula

247 differentiate into the endocrine, ductal and acinar lineages.

248 ualized by beta-tubulin antibody, lining the acinar lumen in a web-like fashion.

249 SI both targets and transcytoses into the LG acinar lumen, which drains to tear ducts.

250 e UPR, induces cellular injury, and provokes acinar metaplasia.

251 res of glandular epithelium in vivo, such as acinar morphogenesis and apical expression patterns of E

252 those MPCs to pre-acinar fate, disruption of acinar morphogenesis and incomplete acinar cell differen

253 as a monolayer, implying that lrECM-induced acinar morphogenesis is essential in EcSOD-gene activati

254 SF6) decreases reflected preacinar and intra-acinar obstruction relief, respectively.

255 ages promoted lineage-specific generation of acinar or endocrine cells.

256 rn group (micropapillary or solid v lepidic, acinar, or papillary) was a significant prognostic facto

257 tion of Ca(2+) signalling between pancreatic acinar (PACs) and stellate cells (PSCs).

258 nd exocrine pancreas, whereas hepatocyte and acinar pancreas development is not affected.

259 Induction of acinar pancreatitis by supramaximal cholecystokinin (CCK

260 ntage of each histologic component (lepidic, acinar, papillary, micropapillary, and solid) was record

261 Because data on these human acinar preparations are sparse, we assessed their functi

262 anscription factors are devoted to promoting acinar redifferentiation after injury.

263 rmore, inactivation of mkk4/mkk7 compromised acinar regeneration following acute inflammatory stress

264 ation is functionally imperative in mice for acinar reprogramming by oncogenic KRAS.

265 r islet endocrine subtypes can be derived by acinar reprogramming.

266 1a(EDD) changed radically towards unipotent, acinar-restricted conversion.

267 Acinar Sec23b deletion results in induction of ER stress

268 ch isoform, exon-9-included CASC4, increased acinar size and proliferation, and decreased apoptosis,

269 Furthermore, we show that SOX2 targets acinar-specific genes and is essential for the survival

270 ell markers (keratin 5 and nanog) as well as acinar-specific markers-namely, alpha-amylase, cystatin

271 Importantly, AQP5, an acinar-specific protein critical for function, is up-reg

272 stologically more aggressive, with a loss of acinar structures and low/absent AR and PSA expression.

273 pression of EcSOD when HMEC formed polarized acinar structures in a 3D-culture condition.

274 fies a functionally and molecularly distinct acinar subpopulation and thus transforms our understandi

275 develop into disorganized masses resembling acinar to ductal metaplasia and chronic pancreatitis.

276 reatic epithelial cells, led to formation of acinar to ductal metaplasia, and induced focal inflammat

277 ling halt their differentiation and leads to acinar to ductal metaplasia.

278 accompanied by strong pancreatic atrophy and acinar-to-adipocyte differentiation, which was also refl

279 pecific study of certain mechanisms, such as acinar-to-beta-cell reprogramming and pancreatitis.

280 transcription factors, our approach achieves acinar-to-beta-cell reprogramming through transient cyto

281 ry but, at later time points, showed reduced acinar-to-duct cell metaplasia.

282 Acinar-to-ductal metaplasia (ADM) has been identified as

283 al studies suggest that pancreatitis-induced acinar-to-ductal metaplasia (ADM) is a key event for pan

284 of pancreatic acinar cell state can lead to acinar-to-ductal metaplasia (ADM), a precursor lesion to

285 bution of the microenvironment to pancreatic acinar-to-ductal metaplasia (ADM), a preneoplastic trans

286 ion of regenerative mechanisms that initiate acinar-to-ductal metaplasia (ADM), a process that replac

287 OX9) is required for oncogenic Kras-mediated acinar-to-ductal metaplasia (ADM), pancreatic intraepith

288 rocess of acinar cell reprogramming known as acinar-to-ductal metaplasia (ADM)-a precursor of pancrea

289 in smoke-exposed floxed mice that facilitate acinar-to-ductal metaplasia (ADM).

290 s in mice that express KrasG12D by promoting acinar-to-ductal metaplasia (ADM).

291 well-known mediator of pancreatitis, during acinar-to-ductal metaplasia and in early pancreatic intr

292 Importantly, acinar-to-ductal metaplasia, a crucial step for initiati

293 ncreatic acinar cells to a ductal phenotype (acinar-to-ductal metaplasia, ADM) occurs after injury or

294 nt mice had signs of inflammation, necrosis, acinar-to-ductal metaplasia, and acinar-cell hypertrophy

295 d secretory phenotype (SASP) that attenuates acinar-to-ductal metaplasia, pancreatic intraepithelial

296 Loss of Ptf1a alone is sufficient to induce acinar-to-ductal metaplasia, potentiate inflammation, an

297 KLF4 is upregulated in and required for acinar-to-ductal metaplasia.

298 HDAC activity and led to the persistence of acinar-to-ductal metaplastic complexes, with prolonged S

299 multiple-breath inert gas washout parameter acinar ventilation heterogeneity (Sacin) is thought to b

300 rway opening, to a greater extent than overt acinar wall destruction.