Increased applied pressure enhances the uptake of IgG complexes by macrophages

被引:13
作者
Mattana, J
Sankaran, RT
Singhal, PC
机构
[1] ALBERT EINSTEIN COLL MED,LONG ISL JEWISH MED CTR,DIV NEPHROL,DEPT MED,NEW HYDE PK,NY 11040
[2] ALBERT EINSTEIN COLL MED,BRONX,NY 10467
关键词
macrophages; IgG complexes; hypertension; calcium;
D O I
10.1159/000164004
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Increased pressure, as may occur with hypertension, may alter cellular function by inducing repetitive mechanical strain, However, increased pressure itself may directly alter cellular function independent of stretching of cells, We undertook the present study to determine whether increased applied pressure could alter uptake of IgG complexes by macrophages. Increased pressure was applied to confluent macrophages grown on plastic culture plates using a pressure chamber apparatus kept inside the incubator at 37 degrees C and pressure regulated using a rotator pump and adjustable outlet valve. Macrophages that were subjected to increased pressure were found to have a significantly greater uptake of IgG complexes in a dose-dependent manner. The effect of increased pressure could be abrogated by carrying out experiments in calcium-free medium while this exerted no effect on uptake by macrophages under control conditions. Increased uptake of IgG complexes by macrophages subjected to increased applied pressure could also be attenuated by incubation with the calcium channel blockers amlodipine and cinnarizine. To determine whether the effect of increased pressure was related to the plastic substrate on which the cells are grown; cells were also seeded onto type I collagen gels and uptake of IgG complexes was measured. Uptake by macrophages on the type I collagen substrate was significantly enhanced with increased applied pressure compared to control (p < 0.01). These studies demonstrate that exposure of macrophages to increased pressure enhances their uptake of IgG complexes via a mechanism that appears to involve an increase in intracellular calcium. This effect might play a role in some of the consequences of systemic arterial and glomerular capillary hypertension.
引用
收藏
页码:40 / 45
页数:6
相关论文
共 23 条
[1]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[2]  
DIAMOND JR, 1991, KIDNEY INT, V39, pS29
[3]  
DIAMOND JR, 1992, AM J PATHOL, V141, P887
[4]  
FLOEGE J, 1992, LAB INVEST, V66, P485
[5]   GLOMERULAR HYPERTROPHY IN MINIMAL CHANGE DISEASE PREDICTS SUBSEQUENT PROGRESSION TO FOCAL GLOMERULAR SCLEROSIS [J].
FOGO, A ;
HAWKINS, EP ;
BERRY, PL ;
GLICK, AD ;
CHIANG, ML ;
MACDONELL, RC ;
ICHIKAWA, I .
KIDNEY INTERNATIONAL, 1990, 38 (01) :115-123
[6]  
GERRITY RG, 1981, AM J PATHOL, V103, P181
[7]  
GREEN SA, 1984, J BIOL CHEM, V260, P9867
[8]   VERAPAMIL PROTECTS AGAINST PROGRESSION OF EXPERIMENTAL CHRONIC-RENAL-FAILURE [J].
HARRIS, DCH ;
HAMMOND, WS ;
BURKE, TJ ;
SCHRIER, RW .
KIDNEY INTERNATIONAL, 1987, 31 (01) :41-46
[9]  
HARRIS RC, 1992, LAB INVEST, V66, P548
[10]  
HOSTETTER TH, 1981, AM J PHYSIOL, V241, pF85, DOI 10.1681/ASN.V1261315