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Abstract：
Endogenous electric fields (EFs) serve as a crucial signal to guide cell movement in processes such as wound healing, embryonic development, and cancer metastasis. However, the mechanism underlying cell electrotaxis remains poorly understood. A plausible hypothesis suggests that electrophoretic or electroosmotic forces may rearrange charged components of the cell membrane, including receptors for chemoattractants which induce asymmetric signaling and directional motility. This study aimed to explore the role of Transforming Growth Factor Beta (TGFβ) signaling in the electrotactic reaction of 3T3 fibroblasts. Our findings indicate that inhibiting canonical and several non-canonical signaling pathways originating from the activated TGF-β receptor does not hinder the directed migration of 3T3 cells to the cathode. Furthermore, suppression of TGF-β receptor expression does not eliminate the directional migration effect of 3T3 cells in the electric field. Additionally, there is no observed redistribution of the TGF-β receptor in the electric field. However, our studies affirm the significant involvement of Phosphoinositide 3-Kinase (PI3K) in electrotaxis, suggesting that in our model, its activation is likely associated with factors independent of TGFβ action.
摘要：
内源性电场（EF）作为一个关键的信号，以指导细胞运动的过程中，如伤口愈合，胚胎发育,和癌症转移。然而,细胞电滑行的潜在机制仍然知之甚少。一个合理的假设表明，电泳或电渗力可能会重新排列细胞膜的带电成分，包括诱导不对称信号和定向运动的化学引诱物的受体。本研究旨在探讨转化生长因子β(TGFβ)信号在3T3成纤维细胞电调控反应中的作用。我们的发现表明，抑制源自激活的TGF-β受体的经典和几种非经典信号通路不会阻碍3T3细胞向阴极的定向迁移。此外，抑制TGF-β受体表达并不能消除3T3细胞在电场中的定向迁移效应。此外,在电场中没有观察到TGF-β受体的再分布。然而,我们的研究确认了磷酸肌醇3-激酶（PI3K）在电滑行中的显着参与，这表明在我们的模型中，其激活可能与独立于TGFβ作用的因子有关。
