Glycan analysis of normal and wounded corneas from wild type and Galectin-3 knockout mice
CFG Member?
Yes subgroups :2 :Glycans in immune recognition and function
,1 :Glycans in host-microbe interactions ,7 :Glycomics and glycoinformatics
Request Details
Requester First Name:
Chandrassegar
Requester Last Name:
Saravanan
Head of Lab. First Name:
Noorjahan
Head of Lab. Last Name:
Panjwani
Assigned First Name:
Noorjahan
Assigned Last Name:
Panjwani
Requester Email:
noorjahan.panjwani@tufts.edu
Requester Interest:
Dr. Panjwani's laboratory is focusing on the mechanism by which galectins-3 and 7 mediate corneal epithelial cell migration. We are currently performing studies to: (i) identify and characterize the corneal epithelial cell surface and extracellular matrix (ECM) molecules which serve as counterreceptors of galectin-3 and -7, to establish whether the lectins modulate corneal epithelial cell migration by binding to well known integrins, growth factor receptors, and/or ECM molecules and (ii) determine whether galectin-3 mediates corneal epithelial cell migration indirectly by modulating the expression of key adhesion and/or signal transduction molecules by using small interfering RNA, cDNA microarrays and glycogene arrays.
Request Date:
11/18/2005
Institution:
Tufts University School of Medicine
CFG Core:
C2
Amount Requested:
Experiment to be conducted:
Recent studies in our laboratory (Cao et al, 2002) have shown that: (i) galectins-3 and -7, but not galectin-1, are expressed in mouse corneal epithelium at sites of cell-matrix and cell-cell adhesion, (ii) exogenous galectin-3 and -7, but not galectin-1, stimulate re-epithelialization of corneal wounds in the wild-type mouse animal model, and (iii) re-epithelialization of corneal wounds is significantly slower in the gal3-/- mice compared to that in the gal3+/+ mice. In contrast, there was no difference in the rate of re-epithelialization of corneal wounds between galectin-1-deficient and wild-type mice. These data lead us to conclude that galectins-3 and -7, but not galectin-1, play a role in corneal epithelial cell migration and re-epithelialization of corneal wounds. Of particular interest is our finding that exogenous galectin-3 accelerated re-epithelialization of wounds in gal3+/+ mice but, surprisingly, not in the gal3-/- mice. These data may suggest that galectin-3 may modulate the expression of counter receptors of the lectin itself and that gal3-/- corneas may be deficient in the expression of specific cell surface counterreceptors of galectin-3. Glycan profiling in both gal 3+/+ and gal3-/- normal and wounded corneas will provide us the details of the changes in glycan structures, which are influenced by galectin-3 and hence its role in corneal wound healing.
Reference:
Cao Z, Said N, Amin S, Wu HK, Bruce A, Garate M, Hsu DK, Kuwabara I, Liu FT, Panjwani N. Galectins-3 and -7, but not galectin-1, play a role in re-epithelialization of wounds. J Biol Chem. 2002 Nov 1;277(44):42299-305.
Within Scope of Consortium:
Y
if yes, indicate the person responsible for inputing data into core B:
chandrassegar
Specific aims being addressed:
Comments By Investigator
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- The requested reagents did not produce any meaningful results.
- Our experiment did not show a difference in antibody binding to mouse pancreas tissues. We will not be publishing or pursuing the research in this area further.
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