<i>Fgf10</i> overexpression during homeostasis changes gastric gland histology but not epithelial proliferation in glandular stomach.

<p>(A–B) Hematoxylin and eosin staining of sections of adult glandular stomach in control littermate (<i>R26^rtTA/+; tet(O)Fgf10/+</i> without dox) (A) and mutant <i>Fgf10</i> overexpressing mice (<i>R26^rtTA/+; tet(O)Fgf10/+</i> with dox) (B). There is a visible decrease in the number of parietal cells and an obvious shift of the mucous neck cells from the luminal side towards the gastric gland base (black arrowheads). (C) qRT-PCR showing a significant increase in Fgf10 expression in the mutants vs controls (*p<0.05). (D-E) PCNA immunostaining of sections of adult glandular stomach in control littermate (<i>R26^rtTA/+; tet(O)Fgf10/+</i> without dox) (D) and mutant <i>Fgf10</i> overexpressing mice (<i>R26^rtTA/+; tet(O)Fgf10/+</i> with dox) (E). (F) Quantification of the percentage of PCNA-positive epithelial cells showed a statistically significant increase in the percentage of PCNA positive epithelial cells indicating increased gastric epithelial proliferation in mutant <i>Fgf10</i> overexpressing mice (<i>R26^rtTA/+; tet(O)Fgf10/+</i> with dox) compared to control littermates (<i>R26^rtTA/+; tet(O)Fgf10/+</i> without dox). Dox was given for 10 days. The scale bar is 50 µm. M = mesenchyme, GE = gastric epithelium, L = lumen.</p

<i>Fgf10</i> overexpression during homeostasis does not cause metaplasia of the gastric epithelium.

<p>(A–C) CDX2, a marker of intestinal metaplasia (IM), immunostaining in adult colon (positive control) (A), control littermate (<i>R26^rtTA/+; tet(O)Fgf10/+</i> without dox) (B) and mutant <i>Fgf10</i> overexpressing mice (<i>R26^rtTA/+; tet(O)Fgf10/+</i> with dox) (C). (D-F) HE4, a marker of spasmolytic polypeptide expressing metaplasia (SPEM), immunostaining in human epididymis (positive control) (D), control littermate (<i>R26^rtTA/+; tet(O)Fgf10/+</i> without dox) (E) and mutant <i>Fgf10</i> overexpressing mice (<i>R26^rtTA/+; tet(O)Fgf10/+</i>) (F). Dox was given for 10 days. The scale bar is 50 µm.</p

Gastric epithelial differentiation is significantly altered by <i>Fgf10</i> overexpression during homeostasis.

<p>Immunostaining for markers of terminally differentiated gastric epithelial cells of sections of adult glandular stomach in control littermate (<i>R26^rtTA/+; tet(O)Fgf10/+</i> without dox) (A,D,G,J) and mutant <i>Fgf10</i> overexpressing mice (<i>R26^rtTA/+; tet(O)Fgf10/+</i> with dox) (B,E,H,K). (A-B) Mucous neck cells are identified by GSII and (C) quantification reveals a significant increase in mutant <i>Fgf10</i> overexpressing mice compared to control littermates (*p<0.05). (D,E) Chief cells are marked by intrinsic factor and (F) quantification shows a significant decrease in chief cell number (*p<0.05). (G,H) Endocrine cells are identified by chromogranin A and (I) quantification demonstrates no significant change in endocrine cell number. (J,K) Parietal cells are visualized with H/K ATPase immunostaining and (L) quantification demonstrates a significant reduction in mutant <i>Fgf10</i> overexpressing mice compared to control littermates (*p<0.05). Dox was given for 10 days. The scale bar is 50 µm. GE = gastric epithelium, L = lumen.</p

FGF10-FGFR2b mediated signaling is not required for normal gastric histology and epithelial proliferation during homeostasis.

<p>Hematoxylin and eosin staining of sections of adult glandular stomach in control littermate (<i>R26^+/+; tet(O)sFgfr2b/+</i> with dox) (A) and mutant mice (<i>R26^rtTA/+; tet(O)sFgfr2b/+</i> with dox) (B) showing normal stomach histology. (C) qRT-PCR confirming robust expression of <i>sFgfr2b</i> in the mutants as compared to controls where the level of <i>sFgfr2b</i> is nearly undetectable. PCNA immunostaining of sections of adult glandular stomach in control littermate (<i>R26^+/+; tet(O)sFgfr2b/+</i> with dox) (D) and mutant mice (<i>R26^rtTA/+; tet(O)sFgfr2b/+</i> with dox) (E) and (F) quantification of the percentage of PCNA-positive epithelial cells showing no significant change in gastric epithelial proliferation in mutant mice compared to control littermates. Dox was given for 1 month. The scale bar is 50 µm. M = mesenchyme, GE = gastric epithelium, L = lumen.</p

FGF10-FGFR2b mediated signaling is not required for gastric epithelial differentiation during homeostasis.

<p>Mucous neck cells are marked by GSII immunostaining of sections of adult glandular stomach in control littermate (<i>R26^+/+; tet(O)sFgfr2b/+</i>with dox) (A) and mutant mice (<i>R26^rtTA/+; tet(O)sFgfr2b/+</i> with dox) (B) and (C) quantification reveals no difference in mucous neck cell number. Chief cells are identified by intrinsic factor immunostaining of sections of adult glandular stomach in control littermate (<i>R26^+/+; tet(O)sFgfr2b/+</i> with dox) (D) and mutant mice (<i>R26^rtTA/+; tet(O)sFgfr2b/+</i> with dox) (E) and (F) quantification reveals no significant change in chief cell number. (G,H) Endocrine cells are identified by chromogranin A and (I) quantification shows no significant change in mutant <i>sFgfr2b</i> overexpressing mice compared to control littermates. Parietal cells are identified by H/K ATPase immunostaining of sections of adult glandular stomach in control littermate (<i>R26^+/+; tet(O)sFgfr2b/+</i>with dox) (J) and mutant mice (<i>R26^rtTA/+; tet(O)sFgfr2b/+</i> with dox) (K) and (L) quantification reveals no significant change in parietal cell number. Dox was given for 1 month. The scale bar is 50 µm. GE = gastric epithelium, L = lumen.</p

Normal expression pattern of <i>Fgf10,</i> its receptors, all other FGFR2b ligands in adult glandular stomach.

<p>(A) PCR of adult glandular stomach and E14.5 wildtype whole embryo (positive control). RT negative controls for both are all negative. (B,E) β-galactosidase staining of adult glandular stomach in <i>Fgf10^LacZ/+</i> (B) and wildtype <i>Fgf10^+/+</i> (E) mice. <i>Fgf10</i> expression occurs only in the mesenchyme. Immunohistochemical analysis of wildtype adult glandular stomach sections stained with anti-FGFR1 (C) or anti-FGFR2 (D). (F,G) Negative control stainings, in which the primary antibody was absent, show minimal to no signal. FGFR1 and FGFR2 staining is strong throughout the gastric epithelium whereas the mesenchymal staining is much weaker. The scale bar is 50 µm. M = mesenchyme, GE = gastric epithelium, L = lumen.</p

FGF10-FGFR2b mediated signaling is not required for parietal cell differentiation during homeostasis.

<p>Hematoxylin and eosin staining of sections of adult glandular stomach in control littermate (<i>R26^+/+; tet(O)sFgfr2b/+</i> with dox) (A) and mutant mice (<i>R26^rtTA/+; tet(O)sFgfr2b/+</i> with dox) (B) showing normal stomach histology. (C) qRT-PCR confirming a significant increase in the expression of <i>sFgfr2b</i> in the mutants as compared to controls (*p<0.05). Parietal cells are identified by H/K ATPase immunostaining of sections of adult glandular stomach in control littermate (<i>R26^+/+; tet(O)sFgfr2b/+</i> with dox) (D) and mutant mice (<i>R26^rtTA/+; tet(O)sFgfr2b/+</i> with dox) (E) and (F) quantification reveals no significant change in parietal cell number. Dox was given for 3 months. The scale bar is 50 µm. M = mesenchyme, GE = gastric epithelium, L = lumen.</p

Bronchial epithelial spheroids: an alternative culture model to investigate epithelium inflammation-mediated COPD-5

<p><b>Copyright information:</b></p><p>Taken from "Bronchial epithelial spheroids: an alternative culture model to investigate epithelium inflammation-mediated COPD"</p><p>http://respiratory-research.com/content/8/1/86</p><p>Respiratory Research 2007;8(1):86-86.</p><p>Published online 26 Nov 2007</p><p>PMCID:PMC2214730.</p><p></p>residual volume (RV) (), and diffusing capacity for monoxide per liter alveolar volume (K) ()

Bronchial epithelial spheroids: an alternative culture model to investigate epithelium inflammation-mediated COPD-2

<p><b>Copyright information:</b></p><p>Taken from "Bronchial epithelial spheroids: an alternative culture model to investigate epithelium inflammation-mediated COPD"</p><p>http://respiratory-research.com/content/8/1/86</p><p>Respiratory Research 2007;8(1):86-86.</p><p>Published online 26 Nov 2007</p><p>PMCID:PMC2214730.</p><p></p>beat frequency was similar in spheroids from both COPD and non-COPD smokers (n = 7) both at basal state (Basal) and after LPS stimulation (10 μg/ml LPS for 24 h) (LPS). () Representative micrographs of untreated (-LPS) and LPS-treated (+LPS) COPD spheroids showing LPS-enhanced expression of IL-8

Bronchial epithelial spheroids: an alternative culture model to investigate epithelium inflammation-mediated COPD-4

<p><b>Copyright information:</b></p><p>Taken from "Bronchial epithelial spheroids: an alternative culture model to investigate epithelium inflammation-mediated COPD"</p><p>http://respiratory-research.com/content/8/1/86</p><p>Respiratory Research 2007;8(1):86-86.</p><p>Published online 26 Nov 2007</p><p>PMCID:PMC2214730.</p><p></p>n COPD and non-COPD BES. Results are expressed as pg of mediators per mg protein of BES. () Levels of IL-8, PGE2 and LTB4 after LPS stimulation (10 μg/ml LPS for 24 h). Results are expressed as fold increase by comparison to untreated conditions. () Correlations between LPS-induced IL-8, PGE2 and LTB4 fold-increase and postbronchodilator FEV. Results are obtained from 16 COPD smokers (filled rhombs) and 13 non-COPD smokers (open rhombs). Mann-Whitney U test for comparisons between groups. Correlations between variables were calculated by means of the Spearman's rank correlation test