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Cellular basis of urothelial squamous metaplasia: roles of lineage heterogeneity and cell replacement.

Liang FX, Bosland MC, Huang H, Romih R, Baptiste S, Deng FM, Wu XR, Shapiro E, Sun TT - J. Cell Biol. (2005)

Bottom Line: Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency.During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium.These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia.

View Article: PubMed Central - PubMed

Affiliation: Epithelial Biology Unit, The Ronald O. Perelman Department of Dermatology.

ABSTRACT
Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency. Moreover, these cells remain phenotypically distinct even after they have been serially passaged under identical culture conditions, thus ruling out local mesenchymal influence as the sole cause of their in vivo differences. During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium. These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia.

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The initial formation of keratinized foci in the mouse bladder urothelium during vitamin A deficiency. Serial sections of the urinary tracts of female mice that had been kept on vitamin A–deficient diets for 8–56 wk (a–f, 8 wk; g and h, 12 wk; and i–l, 16 wk) were stained with hematoxylin and eosin (a, b, and i), AU1 mouse monoclonal antibody to UP IIIa (c, d, and g), a rabbit antiserum to keratin K1 (e, f, and h), and a mouse monoclonal antibody to PCNA (j–l). Panels a, c, and e; b, d, and f; g and h; and I and j were serial sections. Bracket in panel i indicates an area of normal urothelium. Note the formation of small keratinized foci that contained K1-positive and UP-negative suprabasal cells (asterisks in a–h). Also note that the PCNA-positive cells were present in all cell layers in the nonkeratinized epithelium (k) but were mainly restricted to the basal layer in keratinized epithelium (l). L, lumen; asterisks denote keratinized regions in all panels. Bars (i and j), 200 μm; (a–h, k, and l) 100 μm.
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fig5: The initial formation of keratinized foci in the mouse bladder urothelium during vitamin A deficiency. Serial sections of the urinary tracts of female mice that had been kept on vitamin A–deficient diets for 8–56 wk (a–f, 8 wk; g and h, 12 wk; and i–l, 16 wk) were stained with hematoxylin and eosin (a, b, and i), AU1 mouse monoclonal antibody to UP IIIa (c, d, and g), a rabbit antiserum to keratin K1 (e, f, and h), and a mouse monoclonal antibody to PCNA (j–l). Panels a, c, and e; b, d, and f; g and h; and I and j were serial sections. Bracket in panel i indicates an area of normal urothelium. Note the formation of small keratinized foci that contained K1-positive and UP-negative suprabasal cells (asterisks in a–h). Also note that the PCNA-positive cells were present in all cell layers in the nonkeratinized epithelium (k) but were mainly restricted to the basal layer in keratinized epithelium (l). L, lumen; asterisks denote keratinized regions in all panels. Bars (i and j), 200 μm; (a–h, k, and l) 100 μm.

Mentions: To identify the target cells that were responsible for the formation of keratinized squamous epithelium during vitamin A deficiency, we stained serial sections of the mouse urinary tract using antibodies to K14 (marker for keratinocyte basal cells), K1 (marker for keratinization), and UPs (markers for urothelial differentiation). We found that as early as 8 wk after the female mice had been fed with a vitamin A–deficient diet, keratinizing epithelial foci that were K14 positive (basal), K1 positive (suprabasal), and UPIIIa negative were formed (Fig. 5, a–h, asterisks). The squamous nature of these epithelia was confirmed by the fact that proliferative cell nuclear antigen (PCNA)–positive cells were restricted to the basal layer (Fig. 5, i, j, and l) unlike the urothelium, where such cells could be associated with all cell layers, including the superficial umbrella cells (Fig. 5, i–k; Kong et al., 2004).


Cellular basis of urothelial squamous metaplasia: roles of lineage heterogeneity and cell replacement.

Liang FX, Bosland MC, Huang H, Romih R, Baptiste S, Deng FM, Wu XR, Shapiro E, Sun TT - J. Cell Biol. (2005)

The initial formation of keratinized foci in the mouse bladder urothelium during vitamin A deficiency. Serial sections of the urinary tracts of female mice that had been kept on vitamin A–deficient diets for 8–56 wk (a–f, 8 wk; g and h, 12 wk; and i–l, 16 wk) were stained with hematoxylin and eosin (a, b, and i), AU1 mouse monoclonal antibody to UP IIIa (c, d, and g), a rabbit antiserum to keratin K1 (e, f, and h), and a mouse monoclonal antibody to PCNA (j–l). Panels a, c, and e; b, d, and f; g and h; and I and j were serial sections. Bracket in panel i indicates an area of normal urothelium. Note the formation of small keratinized foci that contained K1-positive and UP-negative suprabasal cells (asterisks in a–h). Also note that the PCNA-positive cells were present in all cell layers in the nonkeratinized epithelium (k) but were mainly restricted to the basal layer in keratinized epithelium (l). L, lumen; asterisks denote keratinized regions in all panels. Bars (i and j), 200 μm; (a–h, k, and l) 100 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2171294&req=5

fig5: The initial formation of keratinized foci in the mouse bladder urothelium during vitamin A deficiency. Serial sections of the urinary tracts of female mice that had been kept on vitamin A–deficient diets for 8–56 wk (a–f, 8 wk; g and h, 12 wk; and i–l, 16 wk) were stained with hematoxylin and eosin (a, b, and i), AU1 mouse monoclonal antibody to UP IIIa (c, d, and g), a rabbit antiserum to keratin K1 (e, f, and h), and a mouse monoclonal antibody to PCNA (j–l). Panels a, c, and e; b, d, and f; g and h; and I and j were serial sections. Bracket in panel i indicates an area of normal urothelium. Note the formation of small keratinized foci that contained K1-positive and UP-negative suprabasal cells (asterisks in a–h). Also note that the PCNA-positive cells were present in all cell layers in the nonkeratinized epithelium (k) but were mainly restricted to the basal layer in keratinized epithelium (l). L, lumen; asterisks denote keratinized regions in all panels. Bars (i and j), 200 μm; (a–h, k, and l) 100 μm.
Mentions: To identify the target cells that were responsible for the formation of keratinized squamous epithelium during vitamin A deficiency, we stained serial sections of the mouse urinary tract using antibodies to K14 (marker for keratinocyte basal cells), K1 (marker for keratinization), and UPs (markers for urothelial differentiation). We found that as early as 8 wk after the female mice had been fed with a vitamin A–deficient diet, keratinizing epithelial foci that were K14 positive (basal), K1 positive (suprabasal), and UPIIIa negative were formed (Fig. 5, a–h, asterisks). The squamous nature of these epithelia was confirmed by the fact that proliferative cell nuclear antigen (PCNA)–positive cells were restricted to the basal layer (Fig. 5, i, j, and l) unlike the urothelium, where such cells could be associated with all cell layers, including the superficial umbrella cells (Fig. 5, i–k; Kong et al., 2004).

Bottom Line: Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency.During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium.These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia.

View Article: PubMed Central - PubMed

Affiliation: Epithelial Biology Unit, The Ronald O. Perelman Department of Dermatology.

ABSTRACT
Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency. Moreover, these cells remain phenotypically distinct even after they have been serially passaged under identical culture conditions, thus ruling out local mesenchymal influence as the sole cause of their in vivo differences. During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium. These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia.

Show MeSH
Related in: MedlinePlus