10.1002/(SICI)1097-4652(199610)169:1<66::AID-JCP7>3.3.CO;2-7 Gram‐positive bacteria are recognized pathogens in urinary tract infections. Lipoteichoic acids, major components of the cell wall of gram‐positive bacteria, are important virulence attributes, but their mechanism of action is not well understood. We have postulated that infection‐induced altered function of progenitors of urothelial cells (UT) residing in the basal layer is likely to have long‐lasting effects on the architecture and function of the urothelium. Our earlier in vitro studies in UT of basal type, grown under growth restricting conditions, have shown that (1) treatment with lipoteichoic acid from Streptococcus faecalis (LT‐2) stimulates a subpopulation of progenitors of urothelial cells to proliferate, and (2) resulting large colonies differentiated at an increased rate under conditions simulating those in the basal layer of the urothelium. The hypothesis underlying the present studies was that nitric oxide (NO) mediated LT‐2 action on these functions of UT. Immunocytochemical studies using an antibody against inducible nitric oxide synthase (iNOS) confirmed expression of iNOS in LT‐2‐treated UT. Our hypothesis was tested by treating UT grown under growth restricting conditions (0.005% bovine pituitary extract) with LT‐2 (25 μg/ml), in the presence or absence of inhibitors of NOS (1 mM NG‐nitro‐L‐arginine methyl ester (L‐NAME); 1 μM dexamethasone (DEXA)) or 25 μM hemoglobin, a potent inactivator of NO. Treatment with LT‐2 in the presence of these agents prevented the following effects of LT‐2 alone: (1) the stimulatory effect on proliferation of single cells, as well as within the resulting large colonies; (2) the subsequent differentiation of large colonies resulting from this proliferative activity, as indicated by distribution of β1 subunit‐containing integrins to cell‐cell contacts; (3) the inhibitory effect on the subsequent ability of LT‐2‐treated UT to attach to extracellular matrix proteins. These studies suggest that induction of NOS by LT‐2, initially aimed at restricting the replication of infectious agents, may have potential cost of damage to the host bladder by interfering with urothelial differentiation. © 1996 Wiley‐Liss, Inc.
Journal of Cellular Physiology – Wiley
Published: Oct 1, 1996
It’s your single place to instantly
discover and read the research
that matters to you.
Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.
All for just $49/month
Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly
Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.
Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.
Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.
All the latest content is available, no embargo periods.
“Hi guys, I cannot tell you how much I love this resource. Incredible. I really believe you've hit the nail on the head with this site in regards to solving the research-purchase issue.”Daniel C.
“Whoa! It’s like Spotify but for academic articles.”@Phil_Robichaud
“I must say, @deepdyve is a fabulous solution to the independent researcher's problem of #access to #information.”@deepthiw
“My last article couldn't be possible without the platform @deepdyve that makes journal papers cheaper.”@JoseServera