• Port-a-Patch

    世界最小パッチクランプセットアップ
  • Port-a-Patch

    誰でもデータ取得 - 教育ツールとして最適
  • Port-a-Patch

    細胞, オルガネラ, 脂質二分子膜
  • Port-a-Patch

    世界で最も歴史あるプレーナー式パッチクランプ装置
  • Port-a-Patch

    細胞内灌流実験に最適

2021 - L-carnitine suppresses transient receptor potential vanilloid type 1 activity and myofibroblast transdifferentiation in human corneal keratocytes

icon pap Port-a-Patch Publication in Lab Invest (2021)

Authors:
Turan E., Valtink M., Reinach P.S., Skupin A., Luo H., Brockmann T., Salem M.H.O.B., Pleyer U., Mergler S.

Journal:

Lab Invest (2021) doi: 10.1038/s41374-021-00538-0


Abstract: 

Corneal stromal wound healing is a well-balanced process promoted by overlapping phases including keratocyte proliferation, inflammatory-related events, and tissue remodeling. L-carnitine as a natural antioxidant has shown potential to reduce stromal fibrosis, yet the underlying pathway is still unknown. Since transient receptor potential vanilloid 1 (TRPV1) is a potential drug target for improving the outcome of inflammatory/fibrogenic wound healing, we investigated if L-carnitine can mediate inhibition of the fibrotic response through suppression of TRPV1 activation in human corneal keratocytes (HCK). We determined TRPV1-induced intracellular calcium transients using fluorescence calcium imaging, channel currents by planar patch-clamping, and cell migration by scratch assay for wound healing. The potential L-carnitine effect on TRPV1-induced myofibroblast transdifferentiation was evaluated by immunocytochemical detection of alpha smooth muscle actin. RT-PCR analysis confirmed TRPV1 mRNA expression in HCK. L-carnitine (1 mmol/l) inhibited either capsaicin (CAP) (10 µmol/l), hypertonic stress (450 mOsmol/l), or thermal increase (>43 °C) induced Ca2+ transients and corresponding increases in TRPV1-induced inward and outward whole-cell currents. This was accompanied by suppression of injury-induced increases in myofibroblast transdifferentiation and cell migration. In conclusion, L-carnitine contributes to inhibit stromal scarring through suppressing an injury-induced intrinsic TRPV1 activity that is linked with induction of myofibroblast transdifferentiation in HCK cells.


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