Differential distribution of tenascin and cellular fibronectins in acute and chronic renal allograft rejection.
BACKGROUND
Acute and chronic renal allograft rejection injuries involve, albeit variably, all compartments of the organ and are associated with significant structural changes. We hoped to gain new insights into these phenomena by determining distribution of certain extracellular matrix proteins known to be involved in architectural remodeling processes.


METHODS
Frozen tissue samples from biopsies of acute (n = 14) and chronic (n = 12) human renal allograft rejections were studied to compare distribution of tenascin, the extradomains A and B (EDA, EDB), and oncofetal (Onc) isoforms of cellular fibronectin (cFn). Normal kidneys (n = 4) served as controls. Cryosections were immunostained by the avidin-biotin-complex method with monoclonal antibodies specific for those molecules.


RESULTS
In acute rejection, reactivity for tenascin and EDA-cFn was increased slightly to moderately in glomerular mesangia and in most vessels while it was intensely and diffusely increased in the interstitium. Rarely were focal EDB-cFn and Onc-cFn reactions seen in lesions deemed to reflect acute injury. In chronic rejection, tenascin and EDA-cFn were strongly increased in most glomerular mesangia and in vascular walls but unevenly in the interstitium. In rare glomerular synechiae and vessels, enhanced staining for tenascin and EDA-cFn as well as EDB-cFn and Onc-cFn was noted while in obsolete glomeruli only EDB-cFn and Onc-cFn were detected. The enhanced distribution of tenascin and EDA-cFn partly reflected that noted during nephrogenesis, whereas staining patterns for EDB-cFn and Onc-cFn differed from their fetal counterparts.


CONCLUSIONS
Tenascin and EDA-cFn are strongly and preferentially expressed in the interstitial and vascular compartments of acute and chronic renal rejection injury suggesting that, in these sites, active repair and remodeling occur during both phases of the rejection process irrespective of the changes seen by conventional microscopy. Tenascin, EDA-cFn as well as EDB-cFn and Onc-cFn are all involved, albeit variably, in the glomerular and vascular alterations of chronic rejection. The finding of tenascin and of the three isoforms of cFn in glomerular synechiae with actively proliferating epithelium suggests that certain epithelial cells might partake in the synthesis of these molecules.
Gould
V E
VE
Department of Pathology, Rush Medical College, Chicago, Illinois.
Martinez-Lacabe
V
V
Virtanen
I
I
Sahlin
K M
KM
Schwartz
M M
MM
D000208:Acute Disease; D000911:Antibodies, Monoclonal / Q000276:immunology; D001707:Biopsy, Needle; D015816:Cell Adhesion Molecules, Neuronal / Q000378:metabolism*; D002908:Chronic Disease; D005109:Extracellular Matrix / Q000648:ultrastructure*; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D005353:Fibronectins / Q000378:metabolism*; D006084:Graft Rejection; D006801:Humans; D007668:Kidney / Q000378:metabolism; D016030:Kidney Transplantation / Q000473:pathology*; D019063:Tenascin
D000911:Antibodies, Monoclonal; D015816:Cell Adhesion Molecules, Neuronal; D016326:Extracellular Matrix Proteins; D005353:Fibronectins; D019063:Tenascin