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K+ channels and the cAMP-PKA pathway modulate TGF-beta1-induced migration of rat vascular myofibroblasts.
J Cell Physiol. 2008 Sep; 216(3):835-43.JC

Abstract

Our previous studies have indicated that TGF-beta1 exerts its effect on the expression of A-type potassium channels (I(A)) in rat vascular myofibroblasts by activation of protein kinase C during the phenotypic transformation of vascular fibroblasts to myofibroblasts. In the present study, patch-clamp whole-cell recording and transwell-migration assays were used to examine the effects of TGF-beta1- and phorbol 12-myristate 13-acetate (PMA)-induced expression of I(A) channels on myofibroblast migration and its modulation by the protein kinase A (PKA) pathway. Our results reveal that incubation of fibroblasts with TGF-beta1 or PMA up-regulates the expression of I(A) channels and increases myofibroblast migration. Blocking I(A) channel expression by 4-aminopyridine (4-AP) significantly inhibits TGF-beta1- and PMA-induced myofibroblast migration. Incubation of fibroblasts with forskolin does not result in increased expression of I(A) channels but does cause a slight increase in fibroblast migration at higher concentrations. In addition, forskolin increases the TGF-beta1- and PMA-induced myofibroblast migration but inhibits TGF-beta1- and PMA-induced the expression of I(A) channels. Whole-cell current recordings showed that forskolin augments the delayed rectifier outward K(+) (I(K)) current amplitude of fibroblasts, but not the I(A) of myofibroblasts. Our results also indicate that TGF-beta1- and PMA-induced expression of I(A) channels might be related to increase TGF-beta1- or PMA-induced myofibroblast migration. Promoting fibroblast and myofibroblast migration via the PKA pathway does not seem to involve the expression of I(A) channels, but the modulation of I(K) and I(A) channels might be implicated.

Authors+Show Affiliations

Institute of Brain Science, School of Life Sciences and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18551429

Citation

Liu, Ya-Rong, et al. "K+ Channels and the cAMP-PKA Pathway Modulate TGF-beta1-induced Migration of Rat Vascular Myofibroblasts." Journal of Cellular Physiology, vol. 216, no. 3, 2008, pp. 835-43.
Liu YR, Ye WL, Zeng XM, et al. K+ channels and the cAMP-PKA pathway modulate TGF-beta1-induced migration of rat vascular myofibroblasts. J Cell Physiol. 2008;216(3):835-43.
Liu, Y. R., Ye, W. L., Zeng, X. M., Ren, W. H., Zhang, Y. Q., & Mei, Y. A. (2008). K+ channels and the cAMP-PKA pathway modulate TGF-beta1-induced migration of rat vascular myofibroblasts. Journal of Cellular Physiology, 216(3), 835-43. https://doi.org/10.1002/jcp.21464
Liu YR, et al. K+ Channels and the cAMP-PKA Pathway Modulate TGF-beta1-induced Migration of Rat Vascular Myofibroblasts. J Cell Physiol. 2008;216(3):835-43. PubMed PMID: 18551429.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - K+ channels and the cAMP-PKA pathway modulate TGF-beta1-induced migration of rat vascular myofibroblasts. AU - Liu,Ya-Rong, AU - Ye,Wen-Lei, AU - Zeng,Xi-Min, AU - Ren,Wen-Hua, AU - Zhang,Yu-Qiu, AU - Mei,Yan-Ai, PY - 2008/6/14/pubmed PY - 2008/8/30/medline PY - 2008/6/14/entrez SP - 835 EP - 43 JF - Journal of cellular physiology JO - J Cell Physiol VL - 216 IS - 3 N2 - Our previous studies have indicated that TGF-beta1 exerts its effect on the expression of A-type potassium channels (I(A)) in rat vascular myofibroblasts by activation of protein kinase C during the phenotypic transformation of vascular fibroblasts to myofibroblasts. In the present study, patch-clamp whole-cell recording and transwell-migration assays were used to examine the effects of TGF-beta1- and phorbol 12-myristate 13-acetate (PMA)-induced expression of I(A) channels on myofibroblast migration and its modulation by the protein kinase A (PKA) pathway. Our results reveal that incubation of fibroblasts with TGF-beta1 or PMA up-regulates the expression of I(A) channels and increases myofibroblast migration. Blocking I(A) channel expression by 4-aminopyridine (4-AP) significantly inhibits TGF-beta1- and PMA-induced myofibroblast migration. Incubation of fibroblasts with forskolin does not result in increased expression of I(A) channels but does cause a slight increase in fibroblast migration at higher concentrations. In addition, forskolin increases the TGF-beta1- and PMA-induced myofibroblast migration but inhibits TGF-beta1- and PMA-induced the expression of I(A) channels. Whole-cell current recordings showed that forskolin augments the delayed rectifier outward K(+) (I(K)) current amplitude of fibroblasts, but not the I(A) of myofibroblasts. Our results also indicate that TGF-beta1- and PMA-induced expression of I(A) channels might be related to increase TGF-beta1- or PMA-induced myofibroblast migration. Promoting fibroblast and myofibroblast migration via the PKA pathway does not seem to involve the expression of I(A) channels, but the modulation of I(K) and I(A) channels might be implicated. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/18551429/K+_channels_and_the_cAMP_PKA_pathway_modulate_TGF_beta1_induced_migration_of_rat_vascular_myofibroblasts_ L2 - https://doi.org/10.1002/jcp.21464 DB - PRIME DP - Unbound Medicine ER -