Hypertonicity-induced p38MAPK activation elicits recovery of corneal epithelial cell volume and layer integrity.

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  • Author(s): Bildin VN;Bildin VN; Wang Z; Iserovich P; Reinach PS
  • Source:
    The Journal of membrane biology [J Membr Biol] 2003 May 01; Vol. 193 (1), pp. 1-13.
  • Publication Type:
    Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Springer Country of Publication: United States NLM ID: 0211301 Publication Model: Print Cited Medium: Print ISSN: 0022-2631 (Print) Linking ISSN: 00222631 NLM ISO Abbreviation: J Membr Biol Subsets: MEDLINE
    • Publication Information:
      Original Publication: New York, Springer.
    • Subject Terms:
      Epithelium, Corneal/*cytology ; Epithelium, Corneal/*physiology ; Homeostasis/*physiology ; Mitogen-Activated Protein Kinases/*metabolism ; Recovery of Function/*physiology ; Saline Solution, Hypertonic/*pharmacology ; Sodium-Potassium-Exchanging ATPase/*metabolism; Adaptation, Physiological/physiology ; Animals ; Cell Line ; Cell Size/drug effects ; Cell Size/physiology ; Electric Impedance ; Enzyme Activation ; Epithelium, Corneal/drug effects ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Osmosis/drug effects ; Osmosis/physiology ; Osmotic Pressure ; Rabbits ; Rhodamines/pharmacokinetics ; Species Specificity ; p38 Mitogen-Activated Protein Kinases
    • Abstract:
      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.
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    • Grant Information:
      EY04795 United States EY NEI NIH HHS
    • Accession Number:
      0 (Rhodamines)
      0 (Saline Solution, Hypertonic)
      2609-88-3 (lissamine rhodamine B)
      EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
      EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
      EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
      EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
      EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
    • Publication Date:
      Date Created: 20030725 Date Completed: 20040205 Latest Revision: 20230320
    • Publication Date:
      20231215
    • Accession Number:
      10.1007/s00232-002-2002-8
    • Accession Number:
      12879161