Awardee OrganizationBETH ISRAEL DEACONESS MEDICAL CENTER
Description
Abstract Text
The long term goals of this research are to elucidate the structure and
function of porcine gastric mucin and to investigate how this
glycoprotein contributes to gastric physiology, in particular to
protection against acid secretion in the stomach. Two specific
hypotheses will be tested in our experiments: 1) that gastric mucin
peptide (apomucin), although accounting for only 20% of the molecule as
against the 80% sugars, is a major determinant of the unique viscous
properties of gastric mucins: 2) the ability of mucin to polymerize and
form a gel is directly correlated with the protective properties of
gastric mucin against secreted hydrochloric acid and other noxious agent
such as proteases, oxygen radicals and alcohol. Three specific aims are
designed to test our hypotheses using a combination of molecular and
biophysical techniques. Aim 1 is to clone and sequence the major porcin
gastric mucin genes. Purified porcine gastric mucin will be chemically
deglycosylated, antibodies raised against this sugar-free apo-mucin will
be used to screen a gastric cDNA library and positive clones will be
purified and sequenced. Northern blot analysis and in situ hybridizatio
will be used to localize the cells and organs of origin of these apomuci
cDNA clones. Aim 2 is to use these clones to obtain cross-hybridizing
probes to rat gastric mucin, which then can be used to study the
regulation of mucin gene expression in rats after physiologic and
pharmacologic stimuli. Aim 3 is to express truncated mucin genes in
eukaryotic expression vectors to obtain large quantities of truncated
peptides and characterize them as regards to their aggregation and
gelation properties, their ability to bind lipids and retard h+
diffusion. These findings will enable us to determine the contribution
of the various structural regions of apomucin to aggregation and
gelation. These studies will provide unique structural, functional and
physiologic data on gastric mucins. Since these molecules provide a
protective barrier against H+ diffusion in the mammalian stomach, our
results are of direct relevance to human peptic ulcer disease, H. pylori
gastritis and gastric cytoprotection.
National Institute of Diabetes and Digestive and Kidney Diseases
CFDA Code
DUNS Number
071723621
UEI
C1CPANL3EWK4
Project Start Date
01-July-1980
Project End Date
31-December-1999
Budget Start Date
01-January-1998
Budget End Date
31-December-1999
Project Funding Information for 1998
Total Funding
$269,730
Direct Costs
$161,515
Indirect Costs
$108,215
Year
Funding IC
FY Total Cost by IC
1998
National Institute of Diabetes and Digestive and Kidney Diseases
$269,730
Year
Funding IC
FY Total Cost by IC
Sub Projects
No Sub Projects information available for 5R01DK028195-17
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