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Integrins are heterodimeric transmembrane receptor glycoproteins consisting of alpha and beta subunits that mediate adhesion and interactions between cells and extracellular matrix. Such interactions may be perturbed in various pathologic states, resulting in the altered phenotypic expressions of the integrins in affected tissues. To ascertain the alterations in integrins in various renal diseases, their distribution was investigated in different forms of glomerulonephritis by indirect immunofluorescence and immunoelectron microscopy using specific antibodies directed against beta 1 integrins and integrin alpha v beta 3 (vitronectin receptor). In addition, the distribution of certain extracellular matrix components (ie, fibronectin, vitronectin, and type IV collagen) was examined. Integrin beta 1 and alpha v beta 3 were highly expressed in proliferating mesangial cells in immunoglobulin A nephropathy, membranoproliferative glomerulonephritis type I and diffuse proliferative lupus nephritis. Their putative ligands (ie, fibronectin, vitronectin, and type IV collagen) also were increased in the expanded mesangial regions. In immunoglobulin A nephropathy, integrin beta 1 and alpha v beta 3 were seen by immunoelectron microscopy to be localized to the mesangial cell membranes in close proximity to the immune complex deposits; however, fibronectin and vitronectin immunoreactivities were observed in the mesangial immune complex deposits. Similarly, vitronectin also was detected in the immune complex deposits of other forms of proliferative nephritis, ie, membranoproliferative glomerulonephritis type I and diffuse proliferative lupus nephritis. In diffuse proliferative lupus nephritis, the cellular crescents displayed immunoreactivity toward integrin alpha v beta 3 and vitronectin. In nonimmune complex glomerular disease associated with nephrotic syndrome (ie, minimal change nephrotic syndrome), integrin alpha 3 beta 1, which normally has a linear capillary distribution, was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
January 1975,
Contributions to nephrology,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
July 1993,
Current opinion in nephrology and hypertension,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
April 1969,
Monatsschrift fur Kinderheilkunde,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
August 1993,
Nihon Jinzo Gakkai shi,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
January 1993,
Arkhiv patologii,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
January 1984,
Terapevticheskii arkhiv,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
August 2000,
Biology of the cell,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
October 2011,
Current opinion in cell biology,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
December 1989,
The American journal of physiology,
K Shikata, and
H Makino, and
S Morioka, and
T Kashitani, and
K Hirata, and
Z Ota, and
J Wada, and
Y S Kanwar
January 2009,
Current pharmaceutical design,
