Activation of mesangial cells with TNF-alpha stimulates M-CSF gene expression and monocyte proliferation: Evidence for involvement of protein kinase C and protein tyrosine kinase

被引:22
作者
Kamanna, VS [1 ]
Pai, R [1 ]
Bassa, B [1 ]
Kirschenbaum, MA [1 ]
机构
[1] UNIV CALIF IRVINE, DEPT MED, DIV NEPHROL, IRVINE, CA 92717 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 1996年 / 1313卷 / 02期
关键词
TNF-alpha; M-CSF; mesangial cell; monocyte; protein kinase; signal transduction;
D O I
10.1016/0167-4889(96)00064-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In this study, we examined the effect of TNF-alpha on mesangial cell expression of M-CSF, a colony-stimulating factor associated with monocyte differentiation into macrophages and proliferation. Incubation of mesangial cells with TNF-alpha-stimulated mRNA expression and protein synthesis of M-CSF. Mesangial cell activation with PMA, a PKC activator, stimulated M-CSF mRNA expression while PKC depletion decreased M-CSF mRNA expression to control levels. Stimulation of PKC-depleted mesangial cells with either PMA or TNF-alpha inhibited M-CSF mRNA transcripts. Preincubation of mesangial cells with calphostin C, a PKC inhibitor, reduced both PMA- and TNF-alpha-induced M-CSF mRNA transcripts. Specific protein tyrosine kinase inhibitors blocked TNF-alpha-induced mesangial cell M-CSF mRNA expression, Additional studies showed that pertussis toxin, isoproterenol, and dibutyryl (db)cAMP did not induce mesangial cell M-CSF gene expression. However, coincubation of mesangial cells with TNF-alpha and either dbcAMP, forskolin, or pertussis toxin inhibited TNF-alpha-induced M-CSF gene expression. Finally, TNF-alpha-activated mesangial cell conditioned media stimulated monocyte/macrophage proliferation dose-dependently and was prevented by using anti-M-CSF, These data suggested that M-CSF can regulate monocyte differentiation into macrophages and proliferation within the mesangium induced by proinflammatory cytokines such as TNF-alpha. These cellular events appeared to be modulated by signal transduction pathways mediated by PKC and PTK.
引用
收藏
页码:161 / 172
页数:12
相关论文
共 65 条
[1]   COLONY-STIMULATING FACTOR-I IN THE INDUCTION OF LUPUS NEPHRITIS [J].
BLOOM, RD ;
FLORQUIN, S ;
SINGER, GG ;
BRENNAN, DC ;
KELLEY, VR .
KIDNEY INTERNATIONAL, 1993, 43 (05) :1000-1009
[2]  
BOSWELL JM, 1988, J IMMUNOL, V141, P3050
[3]   CHEMOATTRACTANTS PROVOKE MONOCYTE ADHESION TO HUMAN MESANGIAL CELLS AND MESANGIAL CELL INJURY [J].
BRADY, HR ;
DENTON, MD ;
JIMENEZ, W ;
TAKATA, S ;
PALLISER, D ;
BRENNER, BM .
KIDNEY INTERNATIONAL, 1992, 42 (02) :480-487
[4]  
BRENNER BM, 1986, KIDNEY, P107
[5]   PRODUCTION OF MACROPHAGE-COLONY-STIMULATING FACTOR (M-CSF) BY HUMAN ARTICULAR-CARTILAGE AND CHONDROCYTES - MODULATION BY INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR-ALPHA [J].
CAMPBELL, IK ;
IANCHES, G ;
HAMILTON, JA .
BIOCHIMICA ET BIOPHYSICA ACTA, 1993, 1182 (01) :57-63
[6]   MACROPHAGES IN ACUTE GLOMERULAR INFLAMMATION [J].
CATTELL, V .
KIDNEY INTERNATIONAL, 1994, 45 (04) :945-952
[7]   SINGLE-STEP METHOD OF RNA ISOLATION BY ACID GUANIDINIUM THIOCYANATE PHENOL CHLOROFORM EXTRACTION [J].
CHOMCZYNSKI, P ;
SACCHI, N .
ANALYTICAL BIOCHEMISTRY, 1987, 162 (01) :156-159
[8]  
DIAMOND JR, 1991, LAB INVEST, V64, P21
[9]   ESSENTIAL FATTY-ACID DEFICIENCY DURING ACUTE PUROMYCIN NEPHROSIS AMELIORATES LATE RENAL INJURY [J].
DIAMOND, JR ;
PESEK, I ;
RUGGIERI, S ;
KARNOVSKY, MJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (05) :F798-F807
[10]  
DIAMOND JR, 1989, AM J PATHOL, V135, P711