Ultrastructure of cell junctions in FANFT-induced urothelial tumors in urinary bladder of Fischer rats

B. U. Pauli, Ronald S Weinstein, J. Alroy, M. Arai

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

The ultrastructure of intercellular junctions in normal Fischer rat urothelium was compared with that in noninvasive (stage O) and invasive (stage A-B2) urinary bladder tumors induced with the carcinogen N-(4-(5-nitro-2-furyl)-2-thiazoly) formamide (FANFT). Zonulae occludentes of normal urothelium appeared as a continuous belt of three to five parallel strands interconnected by intramembranous fibrils as seen in freeze-fracture replicas. In noninvasive FANFT tumors, some zonulae occludentes were focally expanded in size whereas others were markedly attenuated. With the progression of these tumors into invasive tumors, zonulae occludentes were discontinuous, thus becoming fasciae or maculae occludentes. Gap junctions of both the PF-1 and PF-2 types were observed in normal Fischer rat bladder urothelium and occurred either separately or in close proximity. In freeze-fracture replicas, the intramembrane particles of PF-1 gap junctions were often in a hexagonal array with a center to center spacing of 9 to 10 nm., whereas those of PF-2 gap junctions were irregularly arranged with a center to center spacing of approximately 20 nm. FANFT tumors contained PF-1 gap junctions which appeared normal but they were devoid of PF-2 gap junctions. Desmosomes, the most frequently encountered type of intercellular junctions in normal and neoplastic urothelium, were morphologically similar to those described in other epithelia. In normal urothelium, the number of desmosomes increased with cell maturation from basal to superficial cells. In FANFT tumors, the average size and number of desmosomes increased with the degree of squamous differentiation. Regional loss of desmosomes was observed in invasive tumors. Similarly, there was a regional loss of hemidesmosomes. The ultrastructure of intercellular junctions is similar for both rat and human noninvasive transitional cell carcinomas and squamous cell carcinomas. Thus, the rat model provides an appropriate system for the study of relationships between junctional alterations and early stages of bladder carcinogenesis.

Original languageEnglish (US)
Pages (from-to)609-621
Number of pages13
JournalLaboratory Investigation
Volume37
Issue number6
StatePublished - 1977
Externally publishedYes

Fingerprint

FANFT
Intercellular Junctions
Inbred F344 Rats
Urothelium
Gap Junctions
Desmosomes
Urinary Bladder
Neoplasms
Hemidesmosomes
Transitional Cell Carcinoma
Fascia
Urinary Bladder Neoplasms
Carcinogens
Squamous Cell Carcinoma
Carcinogenesis
Epithelium

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Ultrastructure of cell junctions in FANFT-induced urothelial tumors in urinary bladder of Fischer rats. / Pauli, B. U.; Weinstein, Ronald S; Alroy, J.; Arai, M.

In: Laboratory Investigation, Vol. 37, No. 6, 1977, p. 609-621.

Research output: Contribution to journalArticle

@article{ae3ee9e8f48547ce8281424ea4dff4dc,
title = "Ultrastructure of cell junctions in FANFT-induced urothelial tumors in urinary bladder of Fischer rats",
abstract = "The ultrastructure of intercellular junctions in normal Fischer rat urothelium was compared with that in noninvasive (stage O) and invasive (stage A-B2) urinary bladder tumors induced with the carcinogen N-(4-(5-nitro-2-furyl)-2-thiazoly) formamide (FANFT). Zonulae occludentes of normal urothelium appeared as a continuous belt of three to five parallel strands interconnected by intramembranous fibrils as seen in freeze-fracture replicas. In noninvasive FANFT tumors, some zonulae occludentes were focally expanded in size whereas others were markedly attenuated. With the progression of these tumors into invasive tumors, zonulae occludentes were discontinuous, thus becoming fasciae or maculae occludentes. Gap junctions of both the PF-1 and PF-2 types were observed in normal Fischer rat bladder urothelium and occurred either separately or in close proximity. In freeze-fracture replicas, the intramembrane particles of PF-1 gap junctions were often in a hexagonal array with a center to center spacing of 9 to 10 nm., whereas those of PF-2 gap junctions were irregularly arranged with a center to center spacing of approximately 20 nm. FANFT tumors contained PF-1 gap junctions which appeared normal but they were devoid of PF-2 gap junctions. Desmosomes, the most frequently encountered type of intercellular junctions in normal and neoplastic urothelium, were morphologically similar to those described in other epithelia. In normal urothelium, the number of desmosomes increased with cell maturation from basal to superficial cells. In FANFT tumors, the average size and number of desmosomes increased with the degree of squamous differentiation. Regional loss of desmosomes was observed in invasive tumors. Similarly, there was a regional loss of hemidesmosomes. The ultrastructure of intercellular junctions is similar for both rat and human noninvasive transitional cell carcinomas and squamous cell carcinomas. Thus, the rat model provides an appropriate system for the study of relationships between junctional alterations and early stages of bladder carcinogenesis.",
author = "Pauli, {B. U.} and Weinstein, {Ronald S} and J. Alroy and M. Arai",
year = "1977",
language = "English (US)",
volume = "37",
pages = "609--621",
journal = "Laboratory Investigation",
issn = "0023-6837",
publisher = "Nature Publishing Group",
number = "6",

}

TY - JOUR

T1 - Ultrastructure of cell junctions in FANFT-induced urothelial tumors in urinary bladder of Fischer rats

AU - Pauli, B. U.

AU - Weinstein, Ronald S

AU - Alroy, J.

AU - Arai, M.

PY - 1977

Y1 - 1977

N2 - The ultrastructure of intercellular junctions in normal Fischer rat urothelium was compared with that in noninvasive (stage O) and invasive (stage A-B2) urinary bladder tumors induced with the carcinogen N-(4-(5-nitro-2-furyl)-2-thiazoly) formamide (FANFT). Zonulae occludentes of normal urothelium appeared as a continuous belt of three to five parallel strands interconnected by intramembranous fibrils as seen in freeze-fracture replicas. In noninvasive FANFT tumors, some zonulae occludentes were focally expanded in size whereas others were markedly attenuated. With the progression of these tumors into invasive tumors, zonulae occludentes were discontinuous, thus becoming fasciae or maculae occludentes. Gap junctions of both the PF-1 and PF-2 types were observed in normal Fischer rat bladder urothelium and occurred either separately or in close proximity. In freeze-fracture replicas, the intramembrane particles of PF-1 gap junctions were often in a hexagonal array with a center to center spacing of 9 to 10 nm., whereas those of PF-2 gap junctions were irregularly arranged with a center to center spacing of approximately 20 nm. FANFT tumors contained PF-1 gap junctions which appeared normal but they were devoid of PF-2 gap junctions. Desmosomes, the most frequently encountered type of intercellular junctions in normal and neoplastic urothelium, were morphologically similar to those described in other epithelia. In normal urothelium, the number of desmosomes increased with cell maturation from basal to superficial cells. In FANFT tumors, the average size and number of desmosomes increased with the degree of squamous differentiation. Regional loss of desmosomes was observed in invasive tumors. Similarly, there was a regional loss of hemidesmosomes. The ultrastructure of intercellular junctions is similar for both rat and human noninvasive transitional cell carcinomas and squamous cell carcinomas. Thus, the rat model provides an appropriate system for the study of relationships between junctional alterations and early stages of bladder carcinogenesis.

AB - The ultrastructure of intercellular junctions in normal Fischer rat urothelium was compared with that in noninvasive (stage O) and invasive (stage A-B2) urinary bladder tumors induced with the carcinogen N-(4-(5-nitro-2-furyl)-2-thiazoly) formamide (FANFT). Zonulae occludentes of normal urothelium appeared as a continuous belt of three to five parallel strands interconnected by intramembranous fibrils as seen in freeze-fracture replicas. In noninvasive FANFT tumors, some zonulae occludentes were focally expanded in size whereas others were markedly attenuated. With the progression of these tumors into invasive tumors, zonulae occludentes were discontinuous, thus becoming fasciae or maculae occludentes. Gap junctions of both the PF-1 and PF-2 types were observed in normal Fischer rat bladder urothelium and occurred either separately or in close proximity. In freeze-fracture replicas, the intramembrane particles of PF-1 gap junctions were often in a hexagonal array with a center to center spacing of 9 to 10 nm., whereas those of PF-2 gap junctions were irregularly arranged with a center to center spacing of approximately 20 nm. FANFT tumors contained PF-1 gap junctions which appeared normal but they were devoid of PF-2 gap junctions. Desmosomes, the most frequently encountered type of intercellular junctions in normal and neoplastic urothelium, were morphologically similar to those described in other epithelia. In normal urothelium, the number of desmosomes increased with cell maturation from basal to superficial cells. In FANFT tumors, the average size and number of desmosomes increased with the degree of squamous differentiation. Regional loss of desmosomes was observed in invasive tumors. Similarly, there was a regional loss of hemidesmosomes. The ultrastructure of intercellular junctions is similar for both rat and human noninvasive transitional cell carcinomas and squamous cell carcinomas. Thus, the rat model provides an appropriate system for the study of relationships between junctional alterations and early stages of bladder carcinogenesis.

UR - http://www.scopus.com/inward/record.url?scp=0017698770&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0017698770&partnerID=8YFLogxK

M3 - Article

C2 - 599905

AN - SCOPUS:0017698770

VL - 37

SP - 609

EP - 621

JO - Laboratory Investigation

JF - Laboratory Investigation

SN - 0023-6837

IS - 6

ER -