Gap junctions, homeostasis, and injury

被引:111
作者
De Maio, A
Vega, VL
Contreras, JE
机构
[1] Johns Hopkins Univ, Sch Med, Div Pediat Surg, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA
关键词
D O I
10.1002/jcp.10108
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Gap junctions (Gj) play an important role in the communication between cells of many tissues. They are composed of channels that permit the passage of ions and low molecular weight metabolites between adjacent cells, without exposure to the extracellular environment. These pathways are formed by the interaction between two hemichannels on the surface of opposing cells. These hemichannels are formed by the association of six identical subunits, named connexins (Cx), which are integral membrane proteins. Cell coupling via Gj is dependent on the specific pattern of Cx gene expression. This pattern of gene expression is altered during several pathological conditions resulting in changes of cell coupling. The regulation of Cx gene expression is affected at different levels from transcription to post translational processes during injury. In addition, Gj cellular communication is regulated by gating mechanisms. The alteration of Gj communication during injury could be rationalized by two opposite theories. One hypothesis proposes that the alteration of Gj communication attenuates the spread of toxic metabolites from the injured area to healthy organ regions. The alternative proposition is that a reduction of cellular communication reduces the loss of important cellular metabolisms, such as ATP and glucose. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:269 / 282
页数:14
相关论文
共 208 条
[1]   MYOCARDIAL-FUNCTION IN SEPSIS AND ENDOTOXIN-SHOCK [J].
ABEL, FL .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (06) :R1265-R1281
[2]  
Alvarez-Maubecin V, 2000, J NEUROSCI, V20, P4091
[3]   IDENTIFICATION OF PROXIMAL AND DISTAL REGULATORY ELEMENTS OF THE RAT CONNEXIN32 GENE [J].
BAI, S ;
SPRAY, DC ;
BURK, RD .
BIOCHIMICA ET BIOPHYSICA ACTA, 1993, 1216 (02) :197-204
[4]  
BAI SA, 1995, MOL CELL BIOL, V15, P1439
[5]   Dephosphorylation and intracellular redistribution of ventricular connexin43 during electrical uncoupling induced by ischemia [J].
Beardslee, MA ;
Lerner, DL ;
Tadros, PN ;
Laing, JG ;
Beyer, EC ;
Yamada, KA ;
Kléber, AG ;
Schuessler, RB ;
Saffitz, JE .
CIRCULATION RESEARCH, 2000, 87 (08) :656-662
[6]   Rapid turnover of connexin43 in the adult rat heart [J].
Beardslee, MA ;
Laing, JG ;
Beyer, EC ;
Saffitz, JE .
CIRCULATION RESEARCH, 1998, 83 (06) :629-635
[7]   A network of electrically coupled interneurons drives synchronized inhibition in neocortex [J].
Beierlein, M ;
Gibson, JR ;
Connors, BW .
NATURE NEUROSCIENCE, 2000, 3 (09) :904-910
[8]  
Belluardo N, 1999, J NEUROSCI RES, V57, P740, DOI 10.1002/(SICI)1097-4547(19990901)57:5<740::AID-JNR16>3.0.CO
[9]  
2-Z
[10]   Gap junctions as electrical synapses [J].
Bennett, MVL .
JOURNAL OF NEUROCYTOLOGY, 1997, 26 (06) :349-366