Linked Life Data

12879161

Source:http://linkedlifedata.com/resource/pubmed/id/12879161

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-7-24
pubmed:abstractText
In hypertonicity-stressed (i.e., 600 mOsm) SV40-immortalized rabbit and human corneal epithelial cell layers (RCEC and HCEC, respectively), we characterized the relationship between time-dependent changes in translayer resistance, relative cell volume and modulation of MAPK superfamily activities. Sulforhodamine B permeability initially increased by 1.4- and 2-fold in RCEC and HCEC, respectively. Subsequently, recovery to its isotonic level only occurred in RCEC. Light scattering revealed that in RCEC 1) regulatory volume increase (RVI) extent was 20% greater; 2) RVI half-time was 2.5-fold shorter. However, inhibition of Na-K-2Cl cotransporter and Na/K-ATPase activity suppressed the RVI response more in HCEC. MAPK activity changes were as follows: 1) p38 was wave-like and faster as well as larger in RCEC than in HCEC (90- and 18-fold, respectively); 2) increases in SAPK/JNK activity were negligible in comparison to those of p38; 3) Erk1/2 activity declined to 30-40% of their basal values. SB203580, a specific p38 inhibitor, dose dependently suppressed the RVI responses in both cell lines. However, neither U0126, which inhibits MEK, the kinase upstream of Erk, nor SP600125, inhibitor of SAPK/JNK, had any effect on this response. Taken together, sufficient activation of the p38 limb of the MAPK superfamily during a hypertonic challenge is essential for maintaining epithelial cell volume and translayer resistance. On the other hand, Erk1/2 activity restoration seems to be dependent on cell volume recovery.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-2631
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
193
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-13
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12879161-Adaptation, Physiological, pubmed-meshheading:12879161-Animals, pubmed-meshheading:12879161-Cell Line, pubmed-meshheading:12879161-Cell Size, pubmed-meshheading:12879161-Electric Impedance, pubmed-meshheading:12879161-Enzyme Activation, pubmed-meshheading:12879161-Epithelium, Corneal, pubmed-meshheading:12879161-Homeostasis, pubmed-meshheading:12879161-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:12879161-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:12879161-Mitogen-Activated Protein Kinases, pubmed-meshheading:12879161-Osmosis, pubmed-meshheading:12879161-Osmotic Pressure, pubmed-meshheading:12879161-Rabbits, pubmed-meshheading:12879161-Recovery of Function, pubmed-meshheading:12879161-Rhodamines, pubmed-meshheading:12879161-Saline Solution, Hypertonic, pubmed-meshheading:12879161-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:12879161-Species Specificity, pubmed-meshheading:12879161-p38 Mitogen-Activated Protein Kinases
pubmed:year
2003
pubmed:articleTitle
Hypertonicity-induced p38MAPK activation elicits recovery of corneal epithelial cell volume and layer integrity.
pubmed:affiliation
Department of Biological Sciences, College of Optometry, State University of New York, 33 West 42nd St., New York, NY 10036, USA. vbildin@sunyopt.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't