Table 1.

A summary of recent studies using specific inhibitors against different MAPKs to manage the disruptive effects of toxicants, drugs and other causative agents on junction dynamics^a

Causative agents (e.g. drugs, toxicants, viruses, proteins and peptides)	Effects on junction dynamics	Inhibitor(s) used to block and/or reverse the phenotype	Kinase(s) blocked	Organ, tissue or cell line
Adjudin	Disruption of Sertoli–germ cell anchoring junction [58]	U0126	MEK1/2/5	Testes
Cadmium chloride	Disruption of the BTB (e.g. loss of occludin, ZO-1, and N-cadherin from the BTB) [38,50]	SB202190	p38 MAPK	Testes
Aspirin	Disruption of TJ-permeability barrier and a decline in the protein level of claudin-7 [76]	SB203580, but not PD98059 and U0126	p38 MAPK	MKN28 (human gastric adenocarcinoma cell line)
Group B coxsackievirus 3	Disruption of the organization of ZO-1 and F-actin [77]	SB203580	p38 MAPK	HUVEC (human umbilical vein endothelial cells)
HIV-I Tat protein	Decline in tight junction barrier integrity and a decrease in level of claudins, integral membrane proteins of the tight junction [78]	PD98059	MEK1/2/5	D407 (human retinal pigment epithelial cell line)
Overexpression of Ras	Disruption of tight junction and adherens junction [69]	PD98059	MEK1/2/5	MDCK (Madin-Darby canine kidney cell line)

^aThis Table is not intended to be exhaustive: only selected examples are shown to illustrate the use of specific inhibitors to block (or delay) damage to cell junctions (e.g. BTB) in the testes induced by toxicants and other causative agents in other epithelial cell junctions.